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layers of epidermis(which one is only shown in thick skin)
Stratum corneum
Stratum lucidum(the one only found in thick skin bc it is where there is high friction:callus)
stratum granulosum
stratum spinosum
stratum basel
What are sensory receptors? Which are found superficially or deep?
sensory receptors have to do with light touch, pressure, vibration that we feel
superficial: merkel discs, free nerve endings, and meissner corpuscle
deep: pacinian corpuscle
Difference between the three types of hair
lanugo: fine and non pigmented hair
vallus: short and barely visible hair
terminal: long and heavily pigmented hair
Be able to describe the difference between epidermal and deep wound healing
epidermal: damage to the epidermis
deep: damage to all layers
steps of epidermal wound healing
inflammation: local immune cells coming in the clean up debris
migration: basel cells moving towards each other to seal wound
Proliferation: basel cells are actively dividing to replace what is lost
maturation: once cells come in contact with each other they stop dividing and wound is healed
steps of deep wound healing
hemostasis: the clot forming
inflammation: local immune cells coming in to clean up debris
migration: fibroblast making collagen and scab forms
proliferation: more cell division and fibroblast
scab falls off and collagen is remodeled
burns
1st degree burns: damage to the epidermis no function loss, redness and pain
2nd degree burns: damage to the epidermis and dermis, blistering, redness, pain and may be some function lost
3 degrees burns: damage to all layers of skin, most function lost, may have numbness/tingling
functions of the bone
Support: For body and soft organs
Protection: Protect brain, spinal cord, and vital organs
Movement:Levers for muscle action
Mineral and growth storage: Calcium and growth factors reservoir
Blood cell formation: Hematopoiesis occurs in red marrow cavities of certain bones
Fat storage: Fat, used for an energy source, is stored in bone cavities
Hormones storage: Osteocalcin secreted by bones helps to regulate insulin secretion, glucose levels, and metabolism
Difference between epiphyseal growth plate vs line and tissue present
epiphyseal growth plate: consistently dividing and lets the long bone grow
Epiphyseal line: When the plate becomes a line because the bone has stopped growing
hyaline cartilage
What is bone remodeling? What two cells are responsible for this?
Bone remodeling: where the bone is breaking down and building back up
Osteoblast and osteoclast bc it is in there name
What is the difference between intra-membranous and endochondral ossification?
Intra-membranous | endochondral |
Forms flat bones of skull, mandible and clavicle | Forms most bones(especially long bones) |
has multiple ossification center | has 2 main ossification centers (Primary and Secondary) |
Is more simpler | Has a cartilage model that turns into bone |
steps of intra-membranous ossification
Formation of ossification center: messengers are bringing osteoblast into the center
Calcification: osteoblast stop making the ECM and the osteocytes form in the lacuna. The ECM hardened bc of the calcium and mineral salts
Formation of trabeculae: the trabeculae forms into spongy bone. The is is also where blood vessels are shown
Formation of the periosteum: mesenchyme develops into the periosteum which forms on top of the compact and spongy bone
steps of endochondral ossification
Formation of the cartilage model: mesenchyme cells develop into chondroblast which forms the model
Growth of the cartilage model: chondroblasts form into chondrocytes which grow and once they can not move anymore they reside in the lacunae
Formation of the primary ossification center:where cartilage is replaced by bone in the shaft. And the bone formation is inward. Nutrient artery is formed
Formation of the medullary cavity: osteoclasts are breaking down bone to create the cavity
Formation of the secondary ossification center: occurs in the epiphysis of the bone. There the bone is forming onward
Formation of the articular cartilage and epiphyseal pate: both are made up of hyaline cartilage that covers the epiphysis
Know factors that affect bone development, growth, and repair
Deficiency of Vitamin A: slows down bone development
Deficiency of Vitamin C : results in fragile bones
Deficiency of Vitamin D: rickets, osteomalacia
Insufficient Growth Hormone: dwarfism
Excessive Growth Hormone: gigantism, acromegaly
Insufficient Thyroid Hormone: delays bone growth
Sex Hormones: promote bone formation; stimulate ossification of epiphyseal plates
Physical Stress: stimulates bone growth
What vitamins are needed for normal bone metabolism? What do they contribute to?
Vitamin A stimulates activity of osteoblasts.
Vitamin C is needed for synthesis of collagen.
Vitamin D is essential to healthy bones because it promotes the absorption of calcium from foods in the gastrointestinal tract into the blood.
Vitamins K and B12 are needed for synthesis of bone proteins.
Explain the role of calcitonin, parathyroid hormone, and calcitriol in the regulation of calcium ion blood levels.
calcitonin= uses osteoblasts
High blood/ calcium levels stimulate the thyroid glands, which secretes calcitonin. Then there is a reduce in calcium uptake in kidney and intestines, which brings the calcium levels back to normal
Parathormone(PTH): uses osteoclasts
Low calcium levels stimulate the parathyroid glands, which secretes PTH. then there is an increase in calcium uptake in kidneys and intestines, which restores calcium levels(going back to normal)
steps of fracture repair
Hematoma formation: breaking down of blood vessels,
Fibrocartilaginous callus formation/inflammation:phagocytes come in to clean up debris, fibroblast creating collagen and chondroblast creating cartilage
Bony callus formation:osteoblasts are laying down osteoids and then the bony callus is forming the spongy bone
Bone remodeling: spongy is replaced by compact bone the fracture line may disappear. Osteoclasts are also coming in the cleanup/ reshape the bone
What is a sarcomere?identify the structures on the sarcomere if presented with an image
Sarcomeres: many myofilaments that make up the myofibrils
A bands: the dark regions
H zone: the lighter region in the middle of the a band
M line: line of protein that is in the middle of the H zone
I band: lighter regions that are on either side of the a band
Z line: line of protein that is in the middle of I bands

What is contraction? What happens in the sliding filament model of contraction?
Contraction: the activation of cross bridges to generate force
The thin filaments are moved and the thick filaments are staying in place
The Z lines are moving closer together and the the sarcomere is shortened
The I bands are also getting smaller
steps of cross bridge contraction cycle when there is low calcium and high calcium present.
low calcium: troponin and tropomyosin block active sites on the action so not contraction occurs
The myosin head can not attach to actin
High calcium: Ca2+ binds to troponin which changes its shape. It can then move tropomyosin away from the myosin binding sire
Myosin head is then able to bind to actin, which forms the cross bridge
1. Cross bridge formation: high-energy myosin head attaches to actin thin filament active site
2. Power stroke: myosin head pivots and pulls thin filaments towards M line
3. Cross bridge detachment: ATP attaches to myosin head, which causes the bridge to detach
4. Cocking of myosin head: energy from hydrolysis of ATP cocks myosin head into a high energy state( that energy will then be used for the power stroke next time)
What is the difference between depolarization and repolarization? what are the steps?
Depolarization: when the inside of plasma membrane becomes less negative(if threshold is reached, depolarization happens)
Repolarization: returning to resting membrane potential
a stimulus from a sensory cell or another neuron causes the target cell to depolarize towards the threshold potential
if the change reaches the threshold, all Na+ channels open and the membrane depolarizes
at the peak action potential K+ channels open and it begins to leave cell the cell. at the same time to Na+ channels close
where Repolarization starts to occur
the membrane becomes hyper polarized as K+ ions continue to leave to cell. the hyper polarized membrane is in a refractory period and cannot fire
the K+ channel then close and the Na+/ K+ transporter restores the resting potential
neuromuscular junction
Action potential(AP) travels down axon terminal= voltage gated Ca+ channels open synaptic bulb
Ca+ is released through synaptic bulb, which opens vesicles containing Ach
Ach travels through synaptic cleft to bind to ligand channels on motor end plate(muscle cell)
Na+ now enters the muscle= sarcolemma voltage(more positive coming it)
Voltage change travels down the t tubules → voltage gated Ca+ on the sarcoplasmic reticulum to open and release Ca+ inside the cell
Ca+ binds to troponin → tropomyosin to expose myosin binding site on actin→cross bridge cycle→ contraction
How contraction ends
Ca+ returns to place of storage
acetocholinesterase= breaks down Ach into acetic acid and chlorine(which gets recycled)