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Option B
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What type of tissue is cartilage?
Connective tissue
Cartilage features
Hard, but flexible
Compressible
Elastic
How is cartilage built?
All cartilage built by Chondrocytes - these build a matrix around them
Chondrocytes
Cells responsible for cartilage formation
Found in lacunae
Lacunae
Pockets that they (Chondrocytes) live in within the matrix
Matrix
Made of Chondrin (forms the matrix of cartilage)
Made of proteins (collagen) and glycoproteins
Collagen
A fibrous protein that provides structural support and strength to tissues.
Collagen molecules assemble into fibrils (small strands), which then organise into larger fibres.
True or False
The relative abundance of collagen and glycoproteins varies depending on the type of cartilage.
True
What are the 3 types of cartilage?
Hyaline cartilage
Yellow elastic cartilage
White fibrous cartilage
Hyaline cartilage
It has a high proportion of collagen fibres for added strength
Weakest type of cartilage
Location of Hyaline cartilage
Found in the most different places
Location - as support rings in the trachea and bronchi and as articular cartilage on the bone ends.
Articular cartilage is made of Hyaline cartilage
Hyaline cartilage extra information
Blood vessels do not penetrate cartilage, nutrients and oxygen slowly diffuse through it, leading to slow healing.
Long bones are laid down and grow as cartilage and gradually turn to bone (ossify).
Yellow elastic cartilage
Contains yellow elastic fibres containing elastin - matrix is flexible but retains it’s shape
Can see fibres in matrix
Location of Yellow elastic cartilage
Located in the external ear and end of nose
White fibrous cartilage
The cartilage that has the greatest tensile strength
With added parallel bundles of collagen fibres within Chondrin matrix
Located in discs between the vertebrae
Ossification
Involves the conversion of other types of connective tissue turning into bone
Why does cartilage take a long time to heal?
Because it doesn’t have blood vessels running through it so the oxygen and nutrients have to slowly diffuse through.
Cartilage to bones
Most bone is first deposited as hyaline cartilage
It turns bone (ossifies) during growth
A small plate of cartilage is left near the tips of bone shafts until after puberty
Cartilage is maintained at the bone ends as articular cartilage
Compact bone
Compact bone is in a tube at the edge of the bone shaft. Bars of spongy bone support the heads
Compact bone matrix components
30% organic - mainly collagen, which resists tensile forces and fracture
70% inorganic - Hydroxyapatite, which resists compressive forces
Organic
Has carbon to hydrogen covalent bonds
Hydroxyapatite
Collective name for calcium salts, most abundant in bones is calcium phosphate
Collagen structure
Amino acid → Collagen molecule → Collagen fibre
How are bones so strong?
The combination of the two (high tensile strength and resistance to compressive forces) make bones so strong
Tension is resisted by…
Collagen
Compression is resisted by…
Hydroxyapatite
The properties of tension and compression combine to resist other forces like…
Bending and torsion
Cytoplasmic threads linking osteocytes
Canaliculi
What is bone formation called?
Ossification
Bone cells
Osteocytes - cells that build and destroy bones
Osteoblasts
Secrete layers of bone matrix around the cartilage
Osteoclasts
Break down the cartilage/matrix and bone
Why do osteoclasts break down cartilage?
So it can be replaced by bone
Osteoporosis
A condition that weakens bones, making them more susceptible to fractures
Causes of Osteoporosis
Osteoclasts working more than osteoblasts as we age
Abnormal loss of bone density - as calcium salts dissolve out
More fragile bones
Change in bone mass with age
Bone mass increases up until the age of 30 for both men and woman and then stays the same till 40, where it starts to decrease.
In women, their bone mass is lower than men and decreases more rapidly after 40 due to the menopause.
Symptoms of Osteoporosis
Decline in bone density (seen in x-rays and scans)
Fractures
Collapsed spine
Chronic debilitating pain
Risk factors of Osteoporosis
Age
Family history
Inflammatory conditions
Smoking
Medical conditions or long-term use of drugs that affect hormone levels e.g. steroids
Treatment and Prevention of Osteoporosis
Regular weight bearing exercise
Foods rich in calcium and Vitamin D
Drugs
Stop smoking and reduce alcohol consumption
HRT - Hormone Replacement Therapy
Learning to prevent falls
Osteogenesis imperfecta
Brittle Bone disease
What is Brittle Bone disease?
When collagen is not made properly
Inherited condition
Mutation (various) impacting the gene responsible for collagen
True of False
With Brittle Bone disease, in some forms, glycine is replaced with the bulkier amino acids so the molecule cannot coil as tightly and the hydrogen bonds holding the triple helix together are weaker.
True
Symptoms of Brittle Bone disease
Bone pain
Blue sclera
Hearing loss
Brittle bones that break easily
Weak, brittle misaligned teeth
Loose joints - regularly pop out joints
Difficulty breathing
Why is a symptom of Brittle Bone disease having a blue sclera?
Because collagen has a different structure
What does the treatments for Brittle Bone disease aim to do?
Aims to increase bone strength, prevent fractures and maintain mobility
Treatment for Brittle Bone disease
Drugs
Surgery - insert metal rod in bones
Physiotherapy - increase muscle strength around bones
Rickets
Rickets is a childhood bone disorder in which bones soften and become prone to fractures and deformity
Who does rickets affect?
Affects mainly children, may also affect adults
Name for adults who get rickets
Osteomalacia
Why is the main cause of rickets a lack of Vitamin D?
For proper absorption of calcium and phosphorus from the gut, we need Vitamin D. If Vitamin D levels are low in a child, they may have inadequate calcium and phosphorus bone levels.
Vitamin D sources
Fat soluble vitamin found in butter, eggs, oily fish and liver or liver extracts such as cod liver oil.
Vitamin D may be manufactured by the action of sunlight on the skin.
Symptoms of rickets
Enlarged wrists
Bones break easily
Low calcium blood levels (hypocalcaemia)
Bowed legs or knock knees
Child’s physical growth (height, weight) may be affected
There may be spinal, pelvic or cranial deformities
Causes of rickets
Not having enough calcium in one’s diet
Some childhood kidney and liver diseases
Digestive disorder complication that affects calcium and phosphorus absorption
Lack of Vitamin D
Why do our bodies need Vitamin D?
Our bodies need Vitamin D in order to absorb calcium from the intestines. Ultraviolet light (from sunlight) helps our skin convert Vitamin D from an inactive into an active state.
If we don’t have enough Vitamin D, calcium that we eat is not absorbed properly, causing hypocalcaemia to develop.
Risk factors for rickets
Sunlight - children who don’t get enough sunlight are dependant on excellent nutrition to make sure they are getting enough Vitamin D.
Malnutrition - rickets is more common in areas of the world where severe droughts and starvation occur.
Skeletal/striated muscles
Muscles which are attached to bones by tendons
Individual cells combine to form fibres which have lots of nuclei
Why is a muscle a tissue?
Because it is composed of many similar fibres working together to achieve the same function
Muscle contraction is under…
conscious control by the somatic (voluntary) nervous system
Why do myofibrils have mitochondria lying between them?
To provide ATP for energy for muscle contraction
Myofibril structure
Each myofibril consists of long thin structures called filaments
What are thick filaments made of?
Protein myosin
What are thin filaments made of?
Protein actin, with Tropomyosin and Troponin
Thick myosin filaments make…
dark bands - A bands
Thin actin filaments align to make…
pale bands - I bands
Sliding filament theory
The filaments do not change length - they slide past each other
I band structure
Actin
A band structure
Actin and myosin
H zone structure
Myosin
Sarcomere
From Z line to Z line
Made up of myosin
I band changes during contractions
Shortens
A band changes during contraction
No change
Why is there no change in A band during contraction?
Because it contains the entire length of the thick filaments (myosin), which don’t change length
H zone changes during contraction
Shortens
Sarcomere changes during contraction
Shortens
What happens at the secretory vesicle when an action potential arrives at a neuromuscular junction?
Voltage-gated calcium ion channels open
Calcium ions diffuse rapidly into pre-synaptic knob causing vesicles containing Acetylcholine to move to the pre-synaptic membrane for exocytosis into the cleft
What happens at the motor end plate when an action potential arrives at a neuromuscular junction?
Acetylcholine binds to receptors on the motor end plate, causing ligand gated sodium ion channels to open
Sodium ions diffuse rapidly into the sarcoplasm
Motor end plate is depolarised
What is the motor end plate also known as?
Post-synaptic membrane
What happens at the sarcolemma when an action potential arrives at a neuromuscular junction?
Depolarisation spreads to the sarcolemma
Sarcolemma carries depolarisation to the myofibrils
What is the sarcolemma?
Outer membrane
What happens at the T tubule when an action potential arrives at a neuromuscular junction?
T tubule carries wave of depolarisation into the myofibrils
What happens at the Sarcoplasmic reticulum when an action potential arrives at a neuromuscular junction?
The sarcoplasmic reticulum releases calcium via diffusion, causing the muscles to contract
Function of the sarcoplasmic reticulum
Stores calcium
Stage 1 of the Ratchet mechanism
Role of calcium ions
Role of calcium ions in the Ratchet mechanism
When an action potential arrives, calcium ions are released from the sarcoplasmic reticulum
Calcium ions bind to troponin and change its shape
This causes tropomyosin to change position exposing the myosin binding sites on actin
The myosin heads can now form crossbridges with the myosin binding sites on the actin filaments
Stage 2 of the Ratchet mechanism
Power stroke
Role of Power stroke in the Ratchet mechanism
ADP and Pi attached to the head are released. This changes the angle of the head back to its relaxed shape. The myosin head rotates pulling the actin past the myosin, the power stroke.
Stage 3 of the Ratchet mechanism
Role of ATP
Role of ATP in the Ratchet mechanism
An ATP molecule binds to the myosin head and this breaks the crossbridge with actin.
Hydrolysis of the ATP makes energy available and extends the myosin head again, ready to reattach to actin.
Stage 4 in the Ratchet mechanism
End of contraction
End of contraction in the Ratchet mechanism
The sequence repeats until the calcium ions are pumped back into the sarcoplasmic reticulum and the muscle relaxes
Types of muscle fibres
Slow twitch and fast twitch
Slow twitch and fast twitch muscle fibres occur together in varying combinations depending on…
Genetics of the person
Training
Type of muscle
What type of respiration is used in slow twitch muscle fibres?
Aerobic respiration - more efficient at using oxygen in oxidative phosphorylation to generate more ATP without lactate build up.
What type of respiration is used in fast twitch muscle fibres?
Depend on anaerobic respiration and glycolysis to synthesis ATP
Slow twitch muscle fibre characteristics
Used for slow, continuous muscle contractions over a long time
Contains large numbers of mitochondria
Contains lots of myoglobin
Small diameter of fibres
Has many blood capillaries
Low tolerance of lactate
Colour of slow twitch fibres
Red
Sporting events for slow twitch muscle fibres
Marathon running
Aerobics
Distance cycling/walking/swimming
Fast twitch muscle fibres characteristics
Generate short bursts of strength or speed
Contain few mitochondria
Contain little myoglobin
Has a larger diameter of fibres than slow twitch
Has few blood capillaries
Can tolerate reasonable levels of lactate
Colour of fast twitch fibres
White
Sporting events for fast twitch muscle fibres
100m sprint
Javelin throw
High jump