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Year 1 Semester 1 > Cell Biology > Flashcards

Cell Biology Flashcards

1
Q

What is a cell always derived from?

A

Another cell!

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2
Q

What can all life forms be traced back to?

A

Last Universal Common Ancestor (LUCA), a single-celled organism

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3
Q

What do all Eukaryotes share as an ancestor?

A

An ancestor that possessed a bacterial endosymbiont that evolved into modern mitochondria

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4
Q

What is a Phylogenetic or genealogic tree?

A

A tree showing the evolutionary history of a group of organisms. It can be inferred indirectly from nucleotide or amino acid sequence data.

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5
Q

What is the most widely used phylogenetic marker?

A

The small subunit ribosomal RNA gene (SSU rRNA)

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6
Q

What characterise Eukaryotic cells?

A

A complex endomembrane, with both endogenous (eg nucleus and RER) and exogenous (eg Mitochondria and Plastids) origins.

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7
Q

What is the exogenous source of Mitochondria?

A

Alpha-proteobacteria

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8
Q

What is the exogenous source of Chloroplasts?

A

Cyanobacteria

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9
Q

What is the plasma membrane of a cell?

A

-It encloses the cell content, separating it from the external environment, and allows for different concentrations of substances to be maintained.
-Allows for communication with environment and other cells.

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10
Q

What its the function of cytosol?

A

Gives many metabolic pathways and where protein synthesis occurs.

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11
Q

What is the function of the Nucleus?

A

Contains the main genome, where DNA and RNA synthesis (transcription) occur

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12
Q

What is the function of the endoplasmic reticulum?

A

Synthesis of most lipids, synthesis of proteins for distribution to many organelles and to the plasma membrane and secretions.

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13
Q

What is the function of the Golgi apparatus?

A

Modification, sorting, and packaging of proteins and lipids for various organelles, PM or secretion

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14
Q

What is the function of Lysosomes?

A

Intracellular degradation

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15
Q

What is the function of Endosomes?

A

Sorting of endocytose (internalised) material

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16
Q

What is the function of Peroxisomes?

A

Oxidation of toxic molecules

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17
Q

What is the function of the Mitochondria?

A

Oxidative Phosphorylation and FeS cluster biosynthesis

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18
Q

What are all the lipids in the Plasma membrane?

A

Ampiphillic, meaning they have a hydrophilic head and hydrophobic tail

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19
Q

In terms of mass of the plasma membrane, what percentage is made up of lipids and what percentage is made up of proteins.

A

Each are around 50%

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20
Q

What are there four major phospholipids in mammalian plasma membrane?

A

-Phosphatidylethanolamine
-Phosphatidylserine
-Phosphatidylcholine
-Sphingomyelin

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21
Q

Which Phospholipids in the plasma membrane point outwards?

A

Phosphatidylcholine and Sphingomyelin

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22
Q

Which Phospholipids in the plasma membrane point inwards?

A

Phosphatidylethanolamine and Phosphatidylserine

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23
Q

What are glycolipids and what are they important for?

A

Sugar containing lipids. They face away from the cytoplasm, and allow for cell-recognition and as an entry point for some bacterial toxins and viruses.

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24
Q

Why is membrane fluidity required?

A

Some transporter and enzyme activities are modulated by the fluidity of the membrane they are associated with.

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25
Q

Give the functions of some membrane proteins.

A

Transporters - Move nutrients, metabolites or ions across membranes
Linkers - Join membranes to intra or extracellular molecules
Receptors - Transduce signals from environment or transport Ligands
Enzymes - catalyse reactions at membrane surfaces

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26
Q

What is the glycocalix?

A

A cell coat made up of glycoproteins and glycolipids that protect cells against chemical, physical and biological damages.

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27
Q

What are N-Glycans?

A

Glycoproteins that are Asparagine-linked

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28
Q

What are O-Glycans

A

Glycoproteins that are Serine/Threonine linked

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29
Q

What can Glycans affect?

A

Glycans can affect health and disease in numerous ways, eg modulate inflammatory response, enable viral immune escape, promote cancer cell metastasis

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30
Q

Give some functions of the Glycocalyx?

A

Protection - can keep unwanted interactions at distance
Adhesion - Carbohydrate binding proteins on other cell surfaces
Recognition - Cell type specific Glycosylation patterns
Storage - Bind and release growth factors

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31
Q

What are the three major cytoskeletal filaments?

A

-Intermediate filament
-Actin filaments
-Microtubules

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32
Q

What is the function of the cytoskeleton?

A

Dynamically organises distinct membrane bound compartments to maintain cell shape as well as facilitate intracellular movement.

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33
Q

Describe Intermediate filaments features?

A

-Found in both cytoplasm and nucleus
-Provides mechanical strength and prevent overstretching
-Diameter of 10 nm
-Polymer

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34
Q

Describe Intermediate filament’s structure.

A

-Core structure is an alpha-helical coil
-Two helical monomers make up a dimer
-These dimers work together to create a long tetramer.
These tetramers make lateral associations, with multiple associations making up a filament.

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35
Q

Describe intermediate filaments in the nucleus

A

-Known as nuclear lamins
-Meshwork lining the inner membrane.
-Act as anchorage points for chromosomes and nuclear pores.

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36
Q

Give the categories of intermediate filaments.

A

Cytoplasmic which include
-Keratins (in epithelia)
-Vimentin (in connective tissue, muscle cells and neuroglial cells)
-Neurofilaments (in nerve cells)
Nuclear which include
-Nuclear lamins (in all animal cells)

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37
Q

How do all intermediate filaments differ (and stay similar)

A

The Tail tends to differ massively in size due to different functions (eg much larger in neurofilaments), but the rod tends to stay the same size.

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38
Q

What are the protein subunits of intermediate filaments?

A

Lamins

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39
Q

What are Lamins (IF)

A

Protein subunits that line the inner face of nuclear envelope. They provide structural support and attachment sites for binding proteins and chromosomes.

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40
Q

What is Keratin?

A

Intermediate filaments that are indirectly connected to neighbour cells through desmosomes.

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41
Q

Describe Microtubules features

A

-Diameter of 25nm
-Tube
-Polymers made up of globular monomers (known as tubulins)
-Appear only in the cytoplasm
-Rigid
-Dynamic
-Have a plus end (Beta) and minus end (alpha)
-Form cylinder of 13 protofilaments (using GTP)

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42
Q

Where do Microtubules assemble from?

A

-Centrosomes (normal cell)
-Spindle poles (Mitotic spindle)
-Basal body (Cilia/flagella)

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43
Q

What are the two microtubule Motor proteins?

A

Kinesins and Dyneins

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44
Q

Describe how Kinesins and Dyneins move along the microtubule?

A

(Globular) Head binds to the microtubule, as well as ATP. This ATP is hydrolysed, releasing the energy required to move along the microtubule. The “cargo” is attached to the tails.

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45
Q

In which direction do Kinesins move along the microtubule?

A

Towards the (Beta) Plus end

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46
Q

In which direction do Dyneins move along the microtubule?

A

Towards the (Alpha) Minus end.

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47
Q

Which motor proteins drive/move cilia and flagella?

A

Moved by Dyneins. This is done by producing microtubule sliding by moving two against each other.

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48
Q

Describe Cilia

A

-Numerous and short
-Stick out of a cell surface
-Flip back and forth to push material over the surface
-Locomotion of the cell

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49
Q

Describe Flagella

A

-Few and long (often longer than the cell)
-Locomotion of the entire cell.

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50
Q

Describe the features of Actin filaments.

A

-Diametert of 6-8nm
-A polymer made up of actin monomers, which require ATP to build.
-Act in the cytoplasm, with a cortex, in bundles, in 2D networks or 3D Gels
-Flexible

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51
Q

Describe the formation of actin filaments.

A

-Globular (G-actin) monomers add to either end, forming polarised filaments (F-actin)
-Polymerisation associated with ATP hydrolysis.
-Filament assembly and organisation is regulated by actin binding proteins.

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52
Q

Give examples if actin filaments in cells.

A

-Microvilli in Intestine
-Contractile bundles in cytoplasm
-Sheetlike and fingerlike protrusions
-Contractile ring during cell division

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53
Q

What are the Actin filament’s motor proteins?

A

Myosins

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54
Q

Describe Myosins

A

Globular heads that bind to actin filaments and ATP (with this hydrolysis driving movement). Tails bind to cargo.

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55
Q

Describe Myosin I

A

MOVEMENT

-In all cells
-One head and Tail
-Used in intracellular organisation
-Moves cargo along the actin filament

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56
Q

Describe Myosin II

A

CONTRACTION

-Primarily in Muscle cells
-Dimer
-Forms filaments
-Act as contractile structures

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57
Q

What is Spectrin?

A

Cytoskeletal protein that lines the inner plasma membrane, crucial for mechanical strength, stability and shape. Links membranes to the motor proteins and all major filament systems.

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58
Q

What are the 6 stages of mitosis?

A

Prophase
Prometaphase
Metaphase
Anaphase
Telophase
Cytokinesis

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59
Q

What happens during Prophase (Mitosis)

A

Chromosomes condense and mitotic spindles form

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60
Q

What happens during Prometaphase (Mitosis)

A

Nuclear membrane breaks down and spindles attach to chromosomes.

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61
Q

What happens during Metaphase (Mitosis)

A

Chromosomes align at the centre of the cell

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62
Q

What happens during Anaphase (Mitosis)

A

Sister chromatids are pulled to their poles of the cell

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63
Q

What happens during Telophase (Mitosis)

A

Nuclear membrane builds around decondensing chromosomes, and actin creates a contractile ring.

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64
Q

What happens during Cytokinesis (Mitosis)

A

Actin contracts, splitting the two cells.

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65
Q

What stages make up interphase?

A

G1, S, G2

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66
Q

What is G1 (Interphase)

A

First growth phase
-recovery from previous division
-Preparation for DNA synthesis
-Doubles the cells organelles
-Synthetase proteins for DNA replication

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67
Q

What is S (Interphase)

A

-Synthesis of proteins associated with DNA
-DNA is replicated

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68
Q

What is G2 (Interphase)

A

-Second growth phase
-Preparation for mitosis - synthesis of proteins required for division

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69
Q

Where are checkpoints located in the cell cycle?

A

G1, G2 and Mitosis

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70
Q

What is being checked during the G1 Checkpoint in interphase?

A

-Is the cell big enough?
-Is the environment favourable?
-Is the DNA damaged?
-Is there enough space?

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71
Q

What is being checked during the G2 checkpoint in interphase?

A

-Is the DNA replicated?
-Is the DNA correct?
-Is the cell big enough?
-Is the environment favourable?

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72
Q

What is being checked during the M checkpoint?

A

Are all chromosomes attached to the spindle?

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73
Q

What controls passage through the checkpoints in the cell cycle?

A

Cyclin-dependent kinases (Cdk), which require cyclins to work. These enzymes phosphorylate an amino acid in a protein, giving the signal to proceed to the next stage in the cycle.

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74
Q

What happens to cyclins as they cell cycle advances?

A

They are destroyed

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75
Q

What is Quiescence in the cell cycle?

A

A Pause. Cells enter the G0 phase.

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76
Q

What happens during the G0 phase of the cell cycle.

A

-No growth, only maintenance.
-Can last days, weeks, years (eg skin cells) or be indefinite (neurons, muscle)
-Can reenter G1

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77
Q

What are growth factors?

A

Molecules that stimulate cell growth, division and differentiation.
-Only low concentrations are required (10^-10M), and many have receptors in the plasma membrane.
-Without it cells enter G0
-Found in blood

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78
Q

Give examples of Growth factors.

A

-Platelet-derived growth factor (PDGF)
-Fibroblast growth factor (FGF)
-Epidermal growth factor (EGF)

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79
Q

What is apoptosis?

A

Regulated and programmed cell death/suicide.

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80
Q

What happens during apoptosis?

A

-Activation of built-in suicide pathway.
-Cell shrinks
-Nuclear condensation and fragmentation
-Membrane changes trigger phagocytes to digest the cells.

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81
Q

When is apoptosis triggered?

A

By the body to maintain or grow, her due to a pathogenic infection.

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82
Q

How does pathogenic activation cause apoptosis?

A

Viral infections triggers this, with cytotoxic T-cells toxins or heat shock killing the cell. It can also be done when DNA in the nucleus is damaged or misfolded proteins accumulate in ER.

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83
Q

Give some key events in apoptosis.

A

-Activation of the p53 gene, which codes for a transcription factor preventing progression at G1 checkpoint.
-Mitochondrial membrane ruptures, leaking cytochrome c, activating caspases.

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84
Q

What do activated caspases do?

A

-Cleave nuclear lamins, leading to nuclear fragmentation
-Activate DNase, which cuts cell DNA into fragments
-Cleave cytoskeleton, leading to the cell detaching from neighbours, extracellular matrix and the cell rounds up.

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85
Q

What is cell death by necrosis?

A

Accidental cell death due to injury.

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86
Q

Describe cell death by necrosis.

A

-Nucleus swells
-Cell swelling causes membrane damage
-Cell bursts (lysis)
-Cell contents released into tissues, triggering an inflammatory response.

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87
Q

What do the body fluid compartments include?

A

Extracellular fluid (Plasma and interstitial fluid) and Intracellular fluid

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88
Q

Describe the capillary epithelium between the interstitial fluid and plasma.

A

It is porous, allowing the movement of substances between the different compartments.

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89
Q

Describe the distribution of Na+, K+, Cl- and proteins between the body fluid compartments.

A

-Intracellular fluid has a high conc of K+ and proteins
-Extracellular fluid has a high conc of Na+, Cl-
-Plasma has a higher conc of proteins compared to ISF

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90
Q

What allows for the chemical disequilibrium between the body fluid compartments?

A

-Membranes act as barriers to solutes
-Active transport of solutes fights against diffusion to create disequilibrium.

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91
Q

What are the two major classes of transport proteins?

A

Carrier proteins - Bind solute on one side of membrane and deliver it to other side by confirmation change protein.
Channel proteins - Form hydrophilic pores in membrane through which solutes (mainly ions) can diffuse

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92
Q

What is Primary active transport?

A

Uphill transport coupled directly to hydrolysis of ATP (usually pumps called ATPases)

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93
Q

What is secondary active transport

A

A generated solute gradient is used by a cotransporter protein to drive uphill transport of a second molecule.

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94
Q

Describe the pumping cycle of Na+/K+-ATPase

A

-3 Na+ bind to cytosolic binding sites
-ATP is hydrolysed
-Protein undergoes conformational change, Na+ is released outside
-2 K+ bind to extracellular binding site
-Dephosphorylation occurs and protein returns to original confirmation, releasing K+ into the cytosol

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95
Q

What is symported secondary active transport?

A

When both transported molecules move in the same direction.

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96
Q

What is antiported secondary active transport?

A

When the transported molecules move in opposite directions.

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97
Q

What four components make up the neuronal cell?

A

-Dendrites
-Axon
-Axon terminal
-Cell body

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98
Q

What maintains the resting membrane potential?

A

-High permeability of the membrane to K+
-Active transport of Na+ out of the cell

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99
Q

What different values add up to make the resting membrane potential?

A

All the potentials generated by the different ion gradients add together to make the RMP

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100
Q

What are the different stages of an action potential?

A

-RMP
-Stimulus
-Depolarisation
-Repolarisation
-Hyperpolarisation
-RMP

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101
Q

Describe Stimulation during an action potential.

A

-Some voltage gated sodium ion channels open
-Na+ diffuses into the cell

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102
Q

Describe depolarisation during an action potential.

A

-If the threshold voltage (-55mV) is reached, all voltage gated Na+ ion channels open, allowing Na+ to diffuse into the cell.

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103
Q

Describe repolarisation during an action potential.

A

-K+ ion channel opens and K+ diffuses out of the axon
-Na+ ion channels inactivated

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104
Q

Describe hyperpolarisation during an action potential.

A

Some Voltage gated K+ ion channels remain open, so excess K+ ions diffuse out of the cell, reducing the voltage of the axon to below the RMP.

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105
Q

Describe the relative refractory period.

A

The period in which the membrane can generate another action potential, but only if the stimulus is bigger than normal, as some Na+ channels have recovered and some K+ channels are still open.

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106
Q

Describe the absolute refractory period.

A

The period in which the membrane cannot generate another action potential no matter how big the stimulus, as the Na+ ion channels are inactivated.

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107
Q

At what part of the neuronal cell does an action potential start?

A

At the axon hillock.

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108
Q

What is the velocity of the action potential relative to?

A

The square root of Diameter x Rm

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109
Q

How does a larger diameter increase the speed of an action potential?

A

Higher diameter = more room for local current flow in current loops.

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110
Q

How does higher membrane resistance increase the speed of an action potential?

A

The higher the membrane resistance, the less current is lost by leaking out of the cell. More current therefore stays in current loops.

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111
Q

What can be found in a high density in the nodes of Ranvier.

A

Voltage gated Na+ ion channels

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112
Q

Describe saltatory conduction

A

An action potential starts at the node of ranvier, which jumps to the next node, and so on. This allows the impulse to travel much more rapidly as it doesn’t have to generate an action potential along the entire length.

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113
Q

Describe synaptic transmission.

A

1)When AP invades the axon terminal, the presynaptic membrane is depolarised
2) this depolarisation opens voltage gated Ca2+ ion channels, allowing ions to diffuse in
3) this release of ions triggers vesicles to release neurotransmitters through exocytosis
4) neurotransmitters diffuse across the cleft, and bind to stereospecific receptors in the post synaptic neurone
5) this binding changes the shape of the ligand gated ion channels, allowing Na+ to diffuse in (this channel is also permeable to K+)
6) The postsynaptic membranne potential reaches a level halfway between the equilibrium ptoentials of the 2 ions (The endplate potential)

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114
Q

What is a Mini-EPP?

A

Small potentials (with the same shape as the EPP) that occur when the nerve and muscle are at rest. These occur due to the random fusion of vesicles with the cell membrane (releasing neurotransmitters).

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115
Q

How many vesicles are required for synaptic transmission (and how many are often released)?

A

Approximately 100, but 200-300 are released in response to normal action potentials, with this extra margin being the safety factor.

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116
Q

What enzyme breaks down acetylcholine that is released into the synaptic cleft?

A

Acetylcholinesterase which cleaves it into acetate and choline.

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117
Q

What is skeletal muscle made up of?

A

Muscle cells (called muscle fibres). They contain several nuclei, with many mitochondria. Each fibre contains many myofibrils.

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118
Q

What is the I-band and where is it located?

A

The I-band is located where there is only actin (the thinner filament) and is attached to the Z-line. More light can pass through as it is thinner, making it lighter.

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119
Q

Describe how the different bands, zones and lines change during muscular contraction.

A

A band - Thick filaments stay the same
I band - Thin filaments alone decrease in length
H zone - Area of thick filaments alone descreases in length
Z line - Distance between each line decreases

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120
Q

What is the H-band and where is it located?

A

Attached to the M-line, it is a darker band due to Myosin’s thickness, meaning less light passes through.

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121
Q

What is the A-band?

A

The darkest area of the sarcomere, that contains the overlap of both myosin and actin, meaning the least light can pass through.

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122
Q

Describe the thin filament in a muscle.

A

-Made up of actin, tropomyosin and troponin
-G-actin molecules form F-actin strands. Each G-actin has 1 myosin binding site.
-2 F-actin strands wind together in a double helix
-Long filaments of tropomyosin wind around the F-actin double helix
-Troponin molecules bind to actin and tropomyosin.

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123
Q

Describe troponin.

A

-Consists of 3 subunits (trimeric) - T,C,I
-T and I subunits its bind to tropomyosin and actin, blocking the myosin binding site
-When Ca2+ bind to the C subunit, the muosin binding site is uncovered.

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124
Q

What are T-tubules?

A

Invaginations of the sarcolemma, deep into the muscle fibre

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125
Q

What is each myofibril surrounded by?

A

The sarcoplasmic reticulum - a tubular structure that enlarges into terminal cisternae near the T-Tubules.

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126
Q

What does an action potential trigger in the terminal cisternae?

A

An AP in the T-tubules triggers Ca2+ release from the TCs. This rise in intracellular Ca2+ concentration causes contraction

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127
Q

Describe excitation-contraction coupling.

A

-Ca2+ binds to troponin-C, uncovering the myosin binding site on the actin molecule. This leads to cross-bridge formation.
-Myosin is in its high energy state (having hydrolysed ATP)
-Myosin heads rotate, pulling thin filaments toward centre of sarcomeres (the power stroke)
-ATP binds to myosin head, breaking actin-myosin bond and releasing ADP+Pi
-ATP is split, returning myosin to its high energy state.

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128
Q

Describe muscular relaxation

A

Relaxation of a muscle requires
-Removal of Ca2+ by the SR (via a Ca2+ ATP pump)
-ATP binding to myosin.

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129
Q

What two systems make up the human nervous system?

A

The central nervous system and the peripheral nervous system.

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130
Q

What three types of neurones are found in the human nervous system.

A

-Motor (efferent) neurones
-Interneurones
-Sensory (afferent) neurones

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131
Q

What is true of all neurones?

A

-Conduct electrical impulses along their plasma membranes and fire action potentials
-Communicate with neighbouring cells via a synapse
-Do no divide
-Longevity - Can live and function for a lifetime
-High metabolic rate - require abundent oxygen and glucose

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132
Q

What are the two types of electrical impulse generated in neurones?

A

-Action potentials
-Graded potentials

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133
Q

Describe graded potentials.

A

-Variable strength signals that travel over short distances and lose strength
-Occur in dendrites, cell bodies or axon terminals (NOT IN AXONS)
-Postsynaptic
-Amplitude is directly proportional to the strength of the triggering event

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134
Q

What is a depolarising graded potential known as?

A

An excitatory postsynaptic potential

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135
Q

What is a hyperpolarising graded potential known as?

A

An inhibitory postsynaptic potential

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136
Q

What is it called when 1 presynaptic neurone branches and affects a large number of post-synaptic neurones?

A

Divergence

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137
Q

What is it called when a large number of presynaptic neurones converge to affect a smaller number of post-synaptic neurones?

A

Convergence

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138
Q

Describe an example of spatial summation.

A

1 Three excitatory neurones fire, with their graded potentials separately being subthreshold
2 Subthreshold EPSPs arrive at trigger zone together and sum to create a suprathreshold signal
3 An action potential is generated.

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139
Q

Can summation occur from 1 presynaptic neurone?

A

Through temporal summation, if multiple graded potentials fire close enough together in time the threshold potential can be reached and an action potential generated.

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140
Q

Give examples of secreted neurotransmitters

A

-Amines (eg adrenaline, dopamine, histamine)
-Amino Acids (Glutamate, GABA, Glycine)
-Polypeptides (Cholecystokinin, enkephalins)
-Purines (ATP, AMP)
-Gases (Nitric oxide)

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141
Q

What are the two mechanisms used for neurotransmitter receptors?

A

-Ligand-gated ion channels (ionotropic receptors)
-G-protein coupled receptors that activate second messenger systems (metabotropic receptors)

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142
Q

What is the difference in speed of response between ionotropic and metabotropic receptors?

A

-Ionotropic are rapid and short-acting
-Metabotropic are slower and longer-acting

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143
Q

Some neurotransmitters have both ionotropic and metabotropic receptors. Give an example and name all receptors.

A

Acetylcholine has ionotropic (nicotinic) and metabotropic (Muscarinic) receptors.

144
Q

What is long-term potentiation?

A

The process by which repetitive stimulation at a synapse increases the efficacy of transmission at that synapse.

145
Q

Describe the process of long-term potentiation.

A

-Glutamate is released
-Glutamate binds to two ionotropic receptors
-The AMPA receptor is a Na+ channel and so triggers an EPSP. The EPSP may or may not trigger an action potential, the NMDA receptor is blocked by Mg2+ so has no effect
-Repetitive stimulation results in greater depolarisation and Mg2+ is ejected from the NMDA receptor
-Ca2+ flows through the NMDA receptor
-This causes the postsynaptic cell to become more sensitive to glutamate and alsp enhances glutamate release.

146
Q

Name the components of a signalling pathway.

A

-Signal
-Reception
-Transduction
-Amplification
-Response

147
Q

How can the activity of proteins in a signalling pathway be altered?

A

-Changing the level of the protein
-Changing the activity of a fixed amount of protein by either conformational shape changes or covalent modification.

148
Q

Give the different signalling methods used to transmit signals between cells.

A

-Gap Junctions
-Contact-Dependent
-Autocrine and Paracrine signalling
-Endocrine signalling
-Synaptic signalling

149
Q

Describe Gap junctions in cell signalling

A

-Allow small signalling molecules to pass directly from cell to cell
-Allows ions and metabolites (eg sugars, amino acids, ATP) but not macromolecules (proteins, polysaccharides)
-Utilises diffusion

150
Q

Describe contact dependent cell signalling

A

-Membrane-bound signalling molecule on cell surface interacts directly with receptor on target cell
-Important for immune signalling and during development

151
Q

Describe Paracrine cell signalling.

A

-Local mediators act on different cell types in close proximity (eg cytokines)

152
Q

Describe Autocrine cell signalling

A

“Self-signalling” ie the cells is able to bind to the signal it secretes, acting on other cells of the same type

153
Q

Which types of cell signalling molecules can work on intracellular receptors?

A

Small hydrophobic molecules (that can cross the cell membrane) eg Steroid hormones and NO gas

154
Q

Which types of cell signalling molecules can work on cell-surface receptors?

A

Hydrophillic signalling molecules that cannot cross the cell membrane eg Cytokines, neurotransmitters

155
Q

What are the three classes of Cell-surface receptors?

A

-Ion channel coupled (alters membrane permeability)
-Gprotein coupled
-Enzyme coupled (Intrinsic enzyme activity or assoicates with an enzyme to catalyse reaction)

156
Q

What biological processes are G-protein linked receptors involved in?

A

-Vision (eg Rhodopsin)
-Smell (Olfactory receptors)
-Neurotransmitters (eg Serotonin)
-Immune Regulation (chemokines, histamine)
-Autonomic nervous system (eg blood pressure, heart rate)

157
Q

Give the steps in G-protein linked receptor signalling via cAMP

A

-Signal molecule binds to G-protein linked receptor activating the G-protein
-G-protein activates Adenylyl cyclase (an amplifier enzyme)
-Adenylyl cyclase converts ATP to cAMP
-cAMP activates Protein Kinase A
-Protein Kinase A phosphorylates other proteins, ultimately leading to a cellular response.

158
Q

What two types of G-proteins are there?

A

Trimeric - Transduce signals from G-protein linked receptors
Monomeric - Transduce signals from enzyme linked receptors

159
Q

What is the ⍺ subunit in a trimeric G-protein?

A

A GTPase enzyme (which binds GDP in its resting state)

160
Q

What are the 2 key proteins activated by trimeric G-proteins?

A

-Adenylyl cylase (creates cyclic AMP)
-Phospholipase C (creates Inositol triphosphate IP3, and Diacylglycerol DAG)

161
Q

How does cAMP pass information down the signalling pathway?

A

By activating cAMP dependent protein kinase (PKA) by inducing a conformational shape change. This causes the release and activation of PKA subunits which phosphorylate other proteins.

162
Q

What does Phospholipase C cleave, and produce?

A

It cleaves Phosphoinositol 4,5Biphosphate (PIP2) to produce IP3 and DAG

163
Q

What does IP3 and DAG do in the cell-signalling pathway?

A

-IP3 causes Ca2+ release from the endoplasmic reticulum
-Ca2+ and DAG act together to activate Protein Kinase C

164
Q

Why is Ca2+ a commonly used second messenger?

A

-Small changes in Ca2+ are easily detected as cytosolic levels are maintained at a low compared to extracellular levels.

165
Q

What is Calmodulin?

A

A Ca2+ binding protein that serves as a primary intracellular receptor for Ca2+

166
Q

Describe Enzyme linked receptors.

A

-Single span transmembrane proteins
-Cytosolic domain has intrinsic enzymatic activity or is associated with an enzyme.

167
Q

What are receptor Tyrosine Kinases?

A

-The most common type of enzyme linked receptors
-RTK family includes Insulin and growth factor receptors
-Growth factor receptors control cell proliferator

168
Q

How is the RAS signalling pathway linked to cancer?

A

-RAS is a proto-oncogene
-Most common RAS mutations reduce GTP hydrolysis activity
-GTP stays bound longer and the signalling pathway is continuously switched on
-Leads to cell proliferation, even in the absence of growth factors such as EGF

169
Q

Describe the G-protein coupled receptor-phospholipase reaction.

A

-Signal molecule activates receptor and associated G protein
-G protein activates phospholipaseC (PL-C), an amplifier enzyme
-PL-C converts membrane phospholipids into diacylglycerol (DAG), which remains in the membrane and IP3 which diffuses into the cytoplasm.
-DAG activates protein kinase C which phosphorylates proteins
-IP3 causes release of Ca2+ from organelles, creating a Ca2+ signal

170
Q

Describe how activation of the G-protein linked receptor results in dissociation of the trimeric G-protein.

A

-Signal binding induces conformational shape change in receptor and ⍺-subunit
-⍺-subunit releases GDP and binds GTP
-Activated ⍺ and βy subunits.

171
Q

Describe Trimeric G-proteins.

A

-Bind directly to receptor
-Receptor activates GDP release
-GTP hydrolysis by intrinsic GTPase activity alone.

172
Q

Describe Monomeric G-proteins.

A

-Not directly linked to receptor
-GDP release activated by GEF (guanine nucleotide exchange factor)
-Weak intrinsic GTPase activity - needs GAP (GTPase activating protein) to drive GTP hydrolysis.

173
Q

What mediates the binding between RAS and Receptor Tyrosine Kinases (RTK)?

A

The adapter protein Grb-2

174
Q

RAS is the main signal-transduce protein for which growth factors?

A

Fibroblast growth factor (FGF) and Epidermal growth factor (EGF)

175
Q

How can different cells respond differently to the same signal?

A

By using different receptors or by activating different intracellular machinery

176
Q

What does Acetylcholine cause when bound to ionotropic vs muscarinic receptors?

A

Ionotropic - Membrane depolarisation inducing contraction of skeletal muscle
Muscarinic - Hyperpolarisation of membrane reduces rate of contraction of heart muscle.

177
Q

Describe how Acetylcholine can affect intracellular machinery within the endothelial cell.

A

-Acetylcholine binds to G-protein receptor, activating Phospholipase C
-Leading to IP3 release, activating Ca2+ release and Calmodulin binding.
-This leads to activation of NO synthase activation
-NO binds to guanylyl cyclase (producing cyclic GMP)
-Which leads to rapid relaxation of smooth muscle.

178
Q

Give an example of how signals may combine to alter the activity of signalling protein.

A

-Epinephrin leads to the production of cyclic AMP
-This cAMP activates protein Kinase A, which phosphorylates Glycogen synthase (leading to decreased glycogen synthase) and Glycogen phosphorylase kinase (which phosphorylates Glycogen phosphorylase - leading to glycogen breakdown)
-This leads to the release of energy, allowing for an effective fight or flight response.

179
Q

What are (and describe) the three different types of signalling complexes.

A

Stable - Components of thhe signalling pathway are linked by a scaffold protein
Transient - The signalling complex assembles after the receptor is activated
Transient - Relies on modification of plasma phospholipd molecules

180
Q

Describe the assembly of a signalling complex following receptor stimulation.

A

-An intrinsic inactive receptor remains in the plasma membrane, with inactive intracellular signalling proteins remaining in the cytosol.
-Upon signal binding to the receptor, the intracellular signalling proteins bind to the receptor, activating it, leading to downstream signals.

181
Q

Describe the assembly of transient signalling complexes on phosphoinositide docking sites

A

-An intrinsic inactive receptor and phosphoinositides remain in the plasma membrane, with inactive intracellular signalling proteins remaining in the cytosol.
-Upon signal binding to the receptor, the receptor activates and the phosphoinosites are hyperphosphorylates, activating intracellular signalling proteins, leading to downstream signals.

182
Q

How are signals switched off?

A

-Removal/inactivation of signal
-Removal/inactivation of receptor
-Inactivation of activated signalling proteins
-GTP hydrolysis
-(De)Phosphorylation
-Allosteric
-Degradation/removal of second messengers

183
Q

Describe how signals are removed (to switch the signal off)?

A

-By degradation (eg hydrolysis of acetylcholine)
-By recycling of signalling molecule (eg neurotransmitters, serotonin, dopamine)
-By sequestration by other proteins (eg soluble TNF receptor)

184
Q

Give a common mechanism for removal of receptors.

A

Ligand-dependent receptor-mediated endocytosis

185
Q

What enzyme removes secondary messengers such as cAMP and cGMP.

A

Phosphodiesterase

186
Q

What causes water polarity?

A

Because of the high electronegativity of Oxygen.

187
Q

How does hydrophobicity act as a major driver of protein folding.

A

The protein folds in aqueous solution so that hydrophobic variable groups point inwards, and hydrophillic variable groups point outwards, producing specific shapes.

188
Q

What is Brownian motion?

A

Molecules in solution move due to thermal energy, randomly and collide with other molecules in solution.
-Smaller particles collide less often so move faster

189
Q

Describe the equation to find the flux/diffusion (movement rate) across membrane

A

Flux = Permeability x (High conc - Low conc)

190
Q

How is diffusive motion quantified as opposed to distance?

A

Area covered.

191
Q

How is energy stored internally in a system?

A

Internal energy is stored
-Within chemical bonds
-Between molecules (eg Hbond)
-As Motion

192
Q

Define an exothermic reaction

A

When the internal energy of the products is less than the reactants

193
Q

Define an endothermic reaction

A

When the internal energy of the products is greater than the reactants.

194
Q

What is the first law of thermodynamics?

A

The change in the internal energy of a system is equal to the energy transfer to the system by work + the energy transfer to the system by heat.

ΔU = w + q

195
Q

Define enthalpy change.

A

The energy released by a reaction (- work released to the surroundings)

196
Q

What is the second law of thermodynamics?

A

The entropy of an isolated system will increase or remain the same.

197
Q

What is the Boltzmann formula?

A

S = Kb x lnW
Entropy = Boltzmann constant x ln(number of accessible microstates

198
Q

What are the microstates of a gas?

A

All the possible positions and velocities of all the gas molecules.

199
Q

What happens to the number of microstates in a system as temperature drops?

A

As temperature/KE of a system drops, the number of microstates (entropy) drop.

200
Q

Give the Gibbs Free energy change reaction.

A

ΔG = ΔH - TΔS
Gibbs free energy = Enthalpy change - (Temp x Entropy change)

201
Q

At a constant temperature and pressure, what must the Gibbs free energy be equal to?

A

Less than or equal to 0

202
Q

Give the equation to find the average kinetic energy?

A

KEavg = 3/2 x Kb x T
Average kinetic energy = 3/2 x Boltzmann constant x Temperature

203
Q

Describe how entropy change drives protein folding due to hydrophobic interactions.

A

-Water “freezes” around a non-polar surface creating a highly ordered clathrate shell.
-Hiding non-polar groups reduces amount of ordered water molecules, maximising entropy.
-ie the water doesnt need to order itself around as

204
Q

What determines the rate of a reaction?

A

-Temperature
-Enzymatic catalysis
-Concentration

205
Q

What is the rate of reaction?

A

The change in concentration of a reactant or product with time.

206
Q

How is rate of reaction calculated?

A

Rate = -Δ[R] / Δt

207
Q

What is the order in this reaction?
rate = k[A]x[B]y

A

x + y

208
Q

What is the order of a reaction determined by?

A

By the rate limiting step of a reaction

209
Q

Give the Kc for this equation.
A + B => AB

A

Kc [AB] / [A][B]

210
Q

Give the Kc for this equation.
A+2B => 3C+D

A

Kc = [C]³x[D] / [A]x[B]²

211
Q

What is Le Chatelier’s principle?

A

When a system at equilibrium is subjected to disturbance, the composition of the system adjusts to minimise the disturbance

212
Q

Give the equilibrium constant for water dissociation.

A

Kw = [H+]x[OH-]

213
Q

Give the equation to find the pH of a solution.

A

pH = -log10[H+]

214
Q

What are the two methods of preparing a buffer.

A

-Mixing a large volume of a weak acid with its conjugate base
OR
-Mixing a large volume of weak base with its conjugate acid

215
Q

Give the equation to find the acid dissociation constant.

A

Ka = [A-]x[H+] / [HA]

216
Q

Give the equation to find the pKa.

A

pKa = -log10 x Ka

217
Q

The lower the pKa the?

A

Stronger the base.

218
Q

How can you find the pH of a solution using pKa?

A

pH = pKa + log10([A-]/[HA])

219
Q

If pH < pKa, what form will the molecule typically be in?

A

In the weak acid form.

220
Q

If pH > pKa, what form will the molecule typically be in?

A

In the conjugate base form.

221
Q

What is the Nernst potential?

A

The voltage difference across the membrane created by transferring just enough permanent ions to create an electrostatic barrier against further flow of ions.

222
Q

What is the Donnan equilibrium?

A

The Donnan potential is the sum of the distribution potential and the term dependent on the concentration of the impermeable ion R

223
Q

Give the classical definition of the endocrine system.

A

Endocrine cells within endocrine glands release hormones which are conveyed by the blood stream and act on distant cells.

224
Q

Give some classic endocrine tissues.

A

-Pineal
-Hypothalamus
-Pituitary
-Thyroid
-Parathyroids
-Thymus
-Adrenals
-Pancreas
-Ovaries or Testes

225
Q

Give some non-classical endocrine tissues.

A

-Kidney
-Heart muscle
-Endothelium
-Platelets
-Adipocytes
-White blood cells

226
Q

What is a hormone?

A

A chemical messenger, synthesised by specialised cells, secreted into the blood in small amounts which act on a specific receptor in target organs to regulate cellular function.

227
Q

Give the different types of hormones

A

-High affinity
-Synergistic
-Permissive
-Antagonistic
-Competitive

228
Q

What is a high affinity hormone?

A

A hormone effective at low concentrations.

229
Q

What is a synergistic hormone?

A

The effect of two hormones is greater than one alone (eg thyroid hormone and norepinephrine on heart rate)

230
Q

What is a permissive hormone?

A

The presence of one hormone is necessary for another to have an effect (eg thyroid hormone and aldosterone on Na+/K+ pumps in kidney)

231
Q

What are Antagonistic hormones?

A

Two hormones that oppose each other’s effects (eg insulin vs glucagon)

232
Q

What are competitive hormones?

A

Two hormones, similar in structure, that compete for the same receptor.

233
Q

What are the 3 classes of hormones based on chemical structure?

A

-Steroids
-Peptides
-Amino acids

234
Q

What are steroid hormones synthesised from?

A

From Cholesterol

235
Q

What are peptide hormones synthesised from?

A

From Amino acids

236
Q

What are Amino acid hormones synthesised from?

A

Tyrosine

237
Q

Describe Steroid hormones

A

-Small hydrophobic molecules synthesised from cholesterol
-Release immediately following synthesis
-Circulate in bound form
-Act on intracellular receptors which then bind to DNA and regulate gene transcription
-Has slow, long lasting effects

238
Q

Describe steroid hormones action on receptors.

A

Receptors consist of a hormone binding site attached (by a hinge region) to a DNA binding domain (blocked by the inhibitory protein complex), which are bound to a transcription activating domain.
-Upon steroid binding, the hinge region undergoes a conformational shape change, releasing an inhibitory protein complex (eg Hsp90), exposing the DNA binding site, allowing for DNA transcription

239
Q

Describe Peptide hormones.

A

-Peptide hormones are between 3 and 332 amino acids in length
-Synthesised as preprohormones and stored prior to release
-Act on cell surface receptors then via 2nd messenger systems to cause effect in target cells.

240
Q

Describe Amino acid hormones.

A

-Amino acid hormones include thyroid hormone and epinephrine
-Mostly synthesised from tyrosine
-Stored for instant release
-Different modes of action (TH has intracellular receptor, others act on cell surface)

241
Q

Give the different mechanisms of hormone release (and give examples).

A

Continuous - eg Thyroid hormone
Pulsatile - eg Gonadotrophin releasing hormone
Circadian - eg Melatonin
Excytosis on stimulus - eg Insulin

242
Q

Give examples of post-hormonal release modification.

A

Steroids - androgens -> oestrogens
Vitamin D
Angiotensinogen -> Angiotensin II

243
Q

Give examples of how the effects of hormones are controlled.

A

Modification - increases/decreases hormone activity
Degradation - Hormone broken down or excreted
Receptor down-regulation - desensitisation
Termination of intracellular effects
Negative feedback

244
Q

How can hormones be controlled by negative feedback?

A

-By the regulated metabolite (eg glucose/insulin)
-By the hormone itself (eg cortisol)
-By the tropic hormone released by the pituitary.

245
Q

Where is the hypothalamus and pituitary gland found?

A

In the brain

246
Q

What is the Hypothalamic-Pituitary axis.

A

The major site of interaction between the nervous and endocrine system, exerting control over several endocrine glands and a number of physiological activities.

247
Q

What is the hypothalamus?

A

The region of the brain which plays a key role in homeostasis.

248
Q

What two lobes does the pituitary gland consist of ?

A

The Posterior and Anterior pituitary

249
Q

Describe the Posterior pituitary.

A

It is of neural origin, consisting of axons and nerve endings whose cell bodies reside in the hypothalamus.

250
Q

Where are the hormones in the posterior pituitary produced.

A

The hormones are produced in the paraventricular and supraoptic nuclei, transported down the axon into the posterior pituitary and will release these hormones upon stimulation into capillaries.

251
Q

Describe how hormones are produced and released from the anterior pituitary.

A

Parvocellular neurones (in the hypothalamus) send signals down the pituitary stalk to the secretory cells in the AP, which release the hormones into the bloodstream.

252
Q

Give the posterior pituitary hormones and their major functions.

A

Antidiuretic hormone (ADH) - Water retention by the kidney
Oxytocin - Uterine smooth muscle contraction
- Breast myoepithelial contraction

253
Q

Give the hypothalamic hormones.

A

-Thyrotropin releasing hormone (TRH)
-Gonadotropin releasing hormone (GnRH)
-Corticotropin releasing hormone (CRH)
-Growth hormone releasing hormone (GHRH)
-Growth hormone inhibiting hormone (somatostatin)
-Dopamine

254
Q

What is the Target tissue and function of Thyroptropin releasing hormone (TRH)?

A

-Thyrotrophs (stimulates thyroid stimulating hormone TSH release)
-Lactotroph (Stimulates Prolactin release)

255
Q

What is the Target tissue and function of Gonadotropin releasing hormone (GnRH)?

A

Gonadotrophs - Stimulates follicle stimulating hormone (FSH) and Luteinising hormone (LH) release

256
Q

What is the Target tissue and function of Corticotropin releasing hormone (CRH)?

A

Corticotrophs - Stimulates Adenocorticotropic hormone (ACTH) hormone and prolactin release.

257
Q

What is the Target tissue and function of Growth hormone releasing hormone?

A

Somatotrophs - Stimulates growth hormone (GH) release

258
Q

What is the Target tissue and function of Dopamine?

A

Lactotrophs - Inhibits prolactin release

259
Q

Give the anterior pituitary hormones.

A

-Thryroid stimulating hormone (TSH)
-Follicle-stimulating hormone (FSH)
-Luteinising hormone (LH)
-Adrenocorticotropic hormone (ACTH)
-Growth hormone (GH)
-Prolactin

260
Q

What is the function of Thyroid stimulating hormone (TSH)?

A

Stimulates thyroid hormone release

261
Q

What is the function of follicle stimulating hormone (FSH)?

A

Stimulates sex steroid production

262
Q

What is the function of Luteinising hormone (LH)?

A

Stimulates sex steroid production

263
Q

What is the function of adrenocorticotropic hormone (ACTH)?

A

Stimulates cortisol release

264
Q

What is the function of Growth hormone?

A

Stimulates growth

265
Q

What is the function of prolactin?

A

Stimulates milk production

266
Q

Describe growth hormone.

A

-A 191 Amino acid peptide hormone synthesised by somatotrophs in the anterior pituitary.
-Stimulates growth, cell reproduction and regeneration
-Functions of growth hormone can be direct or indirect via insulin-like growth factor (IGF1)

267
Q

What are the Acute/Direct metabolic actions of GH?

A

-Release fatty acids from adipose tissue and enhances their conversions to acetyl coA
-Reduced glucose metabolism and uptake in to cells, especially the liver
-Increased gluconeogenesis in the liver
-Increased production of insulin-like growth factor (IGF1)

268
Q

What are the long term effects of Growth hormone?

A

-Growth promoting action on bone, epiphyseal cartilage, soft tissue, gonads, viscera
-Promotes amino acid uptake anf protein synthesis
-Insulin-like endocrine effects on tissues.

269
Q

What does the thyroid play an important role in regulating?

A

-Cardiovascular system
-Metabolism
-Neurological state
-Growth and development

270
Q

What are the products of the thyroid?

A

-Thyroxine T4
-Triiodothyronine T3 (most active hormone)
-Calcitonin (calcium homeostasis)

271
Q

Describe the thyroid gland.

A

-About 15-20g in adults
-Consists of two lobes with connecting isthmus
-Right lobe>Left in size
-Rich blood cell
-Usually 2 pairs of parathyroids on rear of thyroid

272
Q

Describe the cells of the thyroid gland.

A

-Functional units are the follicular cells
-Single layer of cells surrounding a pool of colloid
-Production and storage of thyroid hormones in colloid
-The size of the thyroid varies with its state of stimulation
-C cells secrete Calcitonin

273
Q

What is Thyroglobulin?

A

-Glycoprotein synthesised by follicular cells and released into the colloid by exocytosis.
-At the apical follicular-colloid border, tyrosine residues within thyroglobulin are iodinated in the presence of the enzyme thyroperoxidase
-These act as precursors to form thyroid hormones.

274
Q

Which tissue releases thryotropin-releasing hormone?

A

The Hypothalamus

275
Q

Describe how thyroid hormones are formed.

A

-Precursors monoidotyrosine (T1) and diidotyrosine (T2) are coupled under the control of thyroperoxidase to form active hormones Thyroxine (T4) and Triiodothyronine (T3)

276
Q

How is iodide transported into the cell?

A

Through transport with 2 Na+, down the sodium’s concentration gradient.

277
Q

How much T4 and T3 are secreted daily?

A

100nmoles of T4 and 5nmoles of T3

278
Q

How much T3 and T4 is free within the blood?

A

About 0.4% of T3 and 0.04% of T4

279
Q

What are the three major thyroid transporting proteins?

A

-Thyroxine-binding globulin
-Thyroxine-binding prealbumin
-Albumin

280
Q

How much Thyroid hormone is bound to thyroxine-binding globulin?

A

~70% of T3 and T4 bound with high affinity

281
Q

How much Thyroid hormone is bound to thyroxine-binding prealbumin?

A

~10-15% of T4, tenfold greater affinity for T4 than T3

282
Q

How much Thyroid hormone is bound to Albumin?

A

~15-20% circulating T3 and T4, rapid dissociation makes it major source of free hormone to tissues

283
Q

Which product of the thyroid gland is most biologically active?

A

T3/Triiodothyronine

284
Q

Describe how the Hypothalamic-pituitary-thyroid axis interacts.

A

-The hypothalamus releases thyrotropin-releasing hormone which acts on the anterior pituitary
-TRH causes the anterior pituitary to release thyroid stimulating hormone (TSH) into the blood.
-In response to TSH the thyroid releases thyroid hormones
-Negative feedback by T3 and T4

285
Q

Describe how Thyroid stimulating hormone works on the thyroid gland.

A

Increases
-Iodide uptake
-Thyroglobulin synthesis
-Iodination of thyroglobulin
-Pinocytosis of colloid
-Lysosomal activity
-Size of thyroid cells (cuboidal to columnar)

286
Q

What is most plasma T3 derived from (and how much)?

A

80% of plasma T3 is derived from peripheral metabolism of T4 produced by the thyroid.

287
Q

What enzymes metabolise T4?

A

Type 1 deiodinase - results in active or inactive T3
Type 2 deiodinase - Results in active T3
Type 3 deiodinase - Results in inactive T3 or reverse T3

288
Q

What part of T4 does Type 1 and Type 2 deiodinase act on?

A

On the outer ring of T4 to produce active T3

289
Q

What part of T4 does Type 1 and Type 3 deidonase act on?

A

On the inner ring to produce inactive rT3

290
Q

What are the 4 Thyroid hormone receptors?

A

TR Alpha 1 and 2, and TR Beta 1 and 2

291
Q

What does TR alpha 2 not bind to?

A

T3

292
Q

What is the key target of thyroid hormone binding?

A

Increased transcription of genes encoding mitochondrial uncoupling proteins.

293
Q

What enzyme decreases thyroid hormone activity in the periphery?

A

Type 3 Deiodinase

294
Q

Where are the adrenal glands located, and how large are they?

A

Directly above the kidneys, and are between 8-10g in mass.

295
Q

What types of hormones does the adrenal cortex produce?

A

Steroid hormones

296
Q

What types of hormones does the adrenal medulla produce?

A

Amino acid hormones

297
Q

What are the three regions of the adrenal cortex (going from inside to out)?

A

-Zona reticularis
-Zona fasciculata
-Zona glomerulosa

298
Q

What do the adrenal glands consist of?

A

A medulla in the centre, with the adrenal cortex surrounding this. A protective capsule surrounds this.

299
Q

What causes Adrenal-hormone secreting cells to not differentiate?

A

Large concentrations of cortisols.

300
Q

How much of the adrenal gland consists of the cortex.

A

~80-90% of the adrenal mass.

301
Q

What does the zona glomerulosa produce, and how much of the cortex does it take up?

A

-It produces aldosterone.
-It takes up ~15% of the cortical volume.

302
Q

What does the zona fasiculata produce, and how much of the cortex does it take up?

A

-Produces cortisol and androgens
-It takes up ~75% of the cortical volume, and is made up of large lipid containing cells

303
Q

What does the zona reticularis produce, and how much of the cortex does it take up?

A

-Produces cortisol and androgens
-It takes up ~10% of the cortical volume, and consists of compact cells with less lipid.

304
Q

What does the medulla produce, and how much of the adrenal gland does it take up?

A

-Major product is epinephrine
-Comprises ~10-12% of adrenal mass

305
Q

What enzyme does the zona glomerulosa lack that leads to production of Aldosterone?

A

17 ɑ-hydroxylase

306
Q

Describe Aldosterone.

A

-Major mineralocorticoid
~50-70% bound to albumin in plasma
-Half life of 15-20 minutes

307
Q

Describe the primary action of aldosterone.

A

-Primary action on kidney, colon and salivary glands to maintain normal Na+ concentration and extracellular fluid volume.
-Binds to mineralocorticoid receptors within target cells
-Upregulates ENaC
-Upregulates and activates Na+/K+ ATPase
-Increasing Na+ reabsorption.

308
Q

What does adrenocorticotropic hormone stimulate?

A

The release of cortisol.

309
Q

Describe the pathway from ACTH binding to its receptor to the activation of the P450 gene.

A

ACTH activates a G-protein, activating cAMP. This activates protein Kinase A which:

-Phosphorylates StAR protein
-Phosphorylates Cholesterol ester hydrolase, which converts cholesterole ester into free cholesterol

These lead to activation of the P450 gene

310
Q

What gene do the zona fasciculata and reticularis lack that leads to production of androgens and cortisol?

A

The CYP11B2 gene

311
Q

Describe Cortisol

A

-Major glucocorticoid
>90% bound to plasma proteins
-Half life 60-90 minutes
-Effects virtually all tissues mainly by controlling gene transcription.

312
Q

What are the effects of cortisol?

A

-Stimulates hepatic gluconeogenesis
-Inhibits glucose uptake in muscle and adipose tissue
-Stimulates muscle catabolism
-Inhibits bone formation
-Leads to loss of collagen and connective tissue
-Increases vascular sensitivity to epinephrine and norepinephrine
-Can modulate behaviour and cognitive function
-Inhibits gonadal release of testosterone, oestrogen and progestins

313
Q

What effects do glucocorticoids have on the immune system?

A

-Anti-inflammatory and immunosuppressive effects by
-inhibiting cytokine production and thus T cell proliferation
-inhibits prostaglandin and leukotriene production.

314
Q

What is the dual function of the gonads?

A

Secreting sex hormones and gametogenesis.

315
Q

What sex hormones do the testes secrete?

A

-Large amounts of androgens
-Small amounts of oestrogens

316
Q

What sex hormones do the ovaries secrete?

A

-Large amounts of oestrogens
-Small amounts of androgens
-Progesterone when preparing uterus for pregnancy.

317
Q

What process produces ovum?

A

Oogenesis

318
Q

What process produces sperm cells?

A

Spermatogenesis

319
Q

Describe ovum secretion.

A

Ova are secreted into the pelvic space, where they are gathered by fimbriae and travel through the fallopian tube to the uterus. If implantation doesn’t occur the endometrium is shed.

320
Q

Where are oocytes formed, and where do they exist?

A

Oocytes are formed in the developing ovary, arresting in prophase of division 1 and existing within primordial follicles.

321
Q

How many Primordial follicles exist
-At birth
-At menarche
-Develop further
-Are released by ovulation

A

~7,000,000 at birth
~300,000 at menarche
~30,000 develop further
~500 are released by ovulation

322
Q

Describe the ovarian cycle.

A

-Maturation of oocytes and release of an ovum
-Regular cycle of ~28 day duration on average (21-35 days)
-Occurs in line with uterine cycle as part of menstrual cycle.
-Consists of three phases.

323
Q

What are the three phases of the ovarian cycle?

A

-Follicular phase (lasting several months)
-Ovulation (lasting a few hours)
-Luteal phase (lasting 12-15 days)

324
Q

What are the three phases of the follicular phase?

A

Pre-antral phase
Antral phase
Pre-ovulatory phase

325
Q

Describe the pre-antral phase of the follicular phase, of the Ovarian cycle.

A

-The primordial follicule matures into a primary follicle, which matures into a mature pre-antral follicle
-A large number are recruited to develop each cycle
-Paracrine factors stimulate growth
-Antimullerian hormone limits the number developing at the same time.

326
Q

Describe the antral phase of the follicular phase, of the Ovarian cycle.

A

-Appearance of fluid filled atria
-Increased layers of zona granulosa
-Thicker zona pellucida
-Theca interna is more apparent
-Growth dependent on pituitary FSH
-Dominant follicle selected and becomes a significant steroidogenic gland.

327
Q

What do Theca cells do in a primary follicle?

A

Theca cells are able to catalyse androgen production from cholesterol, forming androsteredione

328
Q

What do Granulosa cells do in a primary follicle?

A

Granulosa cells contain aromatase so they can convert the androgen to oestrogen.

329
Q

Describe the pre-ovulatory phase of the follicular phase, of the Ovarian cycle.

A

-Dominant (Graafian) follicle responds to a surge in LH by completing 1st meiotic division and arresting in metaphase of meisosis II
-Haploid secondary oocyte (egg) and polar body.
-FSH increases LH receptor and enzyme suppression in granulosa cells - increasing progesterone production
-Inflammatory cytokines and hydrolytic enzymes released by theca and granulosa cells.

330
Q

Describe the ovulation phase of the ovarian cycle.

A

-Involves an inflammatory event that erodes the wall of the ovary and follicle
-Oocyte, zona pellucida and corona radiata released in to peritoneal cavity before being captured by the oviduct
-Corona radiata is crucial for capture of te oocyte by the fimbriae and movement through the oviduct
-Remnants of the follicle in the ovary go on to form the corpus luteum.

331
Q

Describe the Luteal phase of the ovarian cycle.

A

-Corpus luteum develops
-Granulosa cells fill with lipid
-Major product is progesterone, and oestrogen initially decreases due to LH surge but then rebounds
-If no pregnancy, degenerates in to corpus albicans. Oestrogen and progesterone levels fall allowing FSH and LH levels to rise.
-If pregnancy, placenta releases human chorionic gonadotrophin wwhich enables the corpus luteum to persist.

332
Q

What hypothalamic hormone is involved in the female reproductive system.

A

-Gonadotropin releasing hormone (GnRH), which has a pulsatile release.
-High frequency = LH
-Low frequency = FSH

333
Q

What pituitary hormones are involved in the female reproductive system.

A

-Follicle stimulating hormone (FSH)
-Luteinising hormone (LH)

334
Q

What does Follicle stimulating hormone (FSH) do?

A

-Stimulates recruitment and growth of immature follicles
-Upregulates CYP19 (aromatase) gene expression and activity
-Induces expression of LH receptors in granulosa cells (in the late follicular phase)
-Prevents apoptosis of antral follicles.

335
Q

What does Luteinising hormone (LH) do?

A

↑Androgens + Progesterone

-Acts on theca cells (in follicles) to promote androgen production
-“Surge” last 1-2 days and triggers ovulation
-Acts on granulosa cells (late follicle & corpus luteum) to secrete progesterone
-Maintains the corpus luteum

336
Q

What important ovarian hormones are involved in the female reproductive system?

A

-Oestrogens (oestradiol, oestriol, oestrone)
-Progesterone
-Inhibin A and B

337
Q

What do oestrogens do in the female reproductive cycle?

A

-Prepares reproductive tract for potential fertilisation and pregnancy.
-Is the dominant hormone secreted pre-ovulation (follicular phase)

338
Q

What does progesterone do in the female reproductive cycle?

A

-Promotes uterine and uterine tube secretions to maintain and support potential fertilisation and implantation of an egg
-Is the dominant hormone secreted post-ovulation (luteal phase)

339
Q

What do Inhibin A and B do in the female reproductive cycle?

A

-Secreted by granulosa cells and represses FSH secretion

340
Q

Describe the hormonal changes that occur during the early follicular phase of the female reproductive cycle.

A

↑Low amounts of Oestrogen
↓Progesterone + FSH

-Follicles produce low levels of oestrogen
-Oestrogen negatively feeds back on FSH
-Loss of progesterone and higher oestrogen increases frequency of GnRH pulses
-LH to FSH secretion ratio decreases.
-Decreased FSH leads to follicular atresia leaving the dominant follicle.

341
Q

Describe the hormonal changes that occur during the late follicular phase of the female reproductive cycle.

A

↑OESTROGEN + PROGESTERONE

-Dominant follicle produces >oestrogen
-High oestrogen levels (>200pg/ml) positively feedback on LH
-LH surge enhances progesterone

342
Q

Describe the hormonal changes that occur during the Luteal phase of the female reproductive cycle.

A

↑
↓FSH + LH + PROGESTERONE + OESTROGEN

-Corpus luteum forms.
-FSH and LH levels drop.
-Corpus luteum begins to regress
-Progesterone and oestrogen levels fall
-Negative feedback lifted and FSH rises.

343
Q

From which tissue is growth hormone released?

A

Anterior pituitary

344
Q

What can insufficient growth hormone lead to?

A

Hypo-pituitary dwarfism

345
Q

Give some features of growth hormone excess in adults.

A

-Enlarged jaw, hands and feet
-Growth of lips, nose and skin above eyes
-Growth of viscera
-Impaired glucose tolerance

346
Q

What conditions can excessive growth hormone lead to?

A

-Pituitary gigantism (excessive GH secretion in early life)
-Acromegaly (excessive GH secretion in adulthood)

347
Q

What does Hypothyroidism lead to in children?

A

-Decreased mental capacity and growth

348
Q

What does Hypothyroidism lead to in adults?

A

-General tiredness and lethargy
-Cold intolerance
-Weight gain
-Bradycardia
-Mental slowness
-Depression
-Puffy hands and face.

349
Q

What is Hypothyroidism treated with?

A

Levothroxine (T4)

350
Q

What does hyperthyroidism lead to?

A

-Heat intolerance
-Weight loss
-Warm moist skin
-Tachycardia
-Fine tremor of fingers.

351
Q

Describe Graves disease.

A

-A common cause of thyrotoxicosis
-Autoimmune condition in which auto-antibodies stimulate the TSH receptor
-Upper eyelid retraction
-Swelling of muscles in orbit pushing eyeball out
-Enlarged thyroid due to overstimulation

352
Q

Describe Addison’s disease.

A

-Adrenocorticoid insufficiency, mostly caused by autoimmune response leading to adrenal atrophy

-Cortisol deficiency
-Weakness
-Fatigue
-Decreased appetite
-Hypoglycaemia

-Mineralocorticoid deficiency
-Excessive renal Na+ loss
-Dehydration
-Hypotension
-Hyponatraemia
-Hyperkalaemia
-Acidosis

353
Q

Describe Cushing’s syndrome

A

-Chronic cortisol excess
-Can result from pituitary or adrenal abnormality, or ectopic ACTH
-Cushing’s disease results from a pituitary tumour.

Leads to
-Weight gain (mainly central)
-moon face
-Atrophy of epidermis
-Hypertension
-Psychological disturbances
-Osteoporosis
-Acne, Amenorrhea and hirsutism

354
Q

What is the name given to the structure which forms in the ovaries as a result of an egg not being fertilised?

A

Corpus albicans

355
Q

What type of G-protein is Ras?

A

Monomeric

356
Q

How many membrane spanning domains do G-protein linked receptors have?

A

7

357
Q

Intracellular receptors are located inside the cell. Are the signals that bind to these receptors hydrophobic or hydrophilic?

A

Hydrophobic

Year 1 Semester 1 (4 decks)

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