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BIOS 255 Week 8 Comprehensive Exam Study Guide
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BIOS 255 Week 8 Comprehensive Exam Study Guide
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1. In general, the nervous system does what?Control center of the other systems, communicated and processes commands.
2. What is the main diff btwn positive and neg feedback?
Positive -> increases the effect of the stimulus continuously (platelet formation, childbirth)
3. The ankle joint(tib+fib+talus) is an example of what kind of a joint?
Hinge joint. Actions – inversion/eversion, plantar
flexion/dorsiflexion
4. The characteristics of epithelia include what?
- Regeneration -avascular – polarity – apical vs basal
5. What is NOT a property of synovial joints?
IS a property – free movement, cavity, capsule, synovial fluid, ligaments, articular cartilage
6. The 3 types of protein fibers in Connective tissue
- Collagen (thick) – elastic – reticular (thin)
7. Chondroitin sulfate is abundant in the matrix of what?
- Blood vessels and bones and gives cartilage it’s stiffness, regulate the water and electrolyte balance of tissues
8. The sacrum articulates w/ what?
5th lumbar vertebra + coccyx+ILLIUM
9. The protein that strengthens the stratum corneum and reduces water loss at the skin surface is? (starts w/
K) Keratin
10. Different categories of sweat glands? What is dominant in most body surface and another that is only found in certain
areas?
Eccrine = dominant Apocrine = in hairy skin Ceruminous =modified sweat glands in the ear canal
11. Hard palate of the roof of the mouth is mostly formed by
what? Mostly -> Maxillary bones , the rest = Palatine bones
12. The shaft of the long bone is called what? Starts with
D Diaphysis
13. The smooth rounded articulate process of a bone is termed – chondyle vs articular
cartilage? Rounded knob= chondyle/// Flat = Facet // Rounded expanded end = Head
14. Action of osteoclasts
- Bone dissolving, breaking down bone, remodeling, resorption, release Ca2+
15. Endochondral ossification -> put the steps in an order
1) Development of cartilage model 2) Growth of cartilage 3) Primary ossification center in the diaphysis
4) Medullary/marrow cavity via osteoclasts 5) 2ndary ossification centers in epiphysis
6) articular cartilage and epiphyseal plate
16. The smallest fxnal repeating unit of the skeletal muscle fiber is
what? Sarcomere
, 17. Correct sequence of the events for skeletal muscle contraction -> when does the Ca2+ bind? When does myosin head
bind?
A nerve signal arrives at the axon terminal and opens voltage-gated calcium channels.
Calcium ions enter the terminal. Calcium stimulates the synaptic vesicles to release
acetylcholine (ACh) into the synaptic cleft. One action potential causes exocytosis of
about 60 vesicles, and each vesicle releases about 10,000 molecules of ACh. ACh
diffuses across the synaptic cleft and binds to receptors on the sarcolemma. These
receptors are ligand-gated ion channels. Two ACh molecules must bind to each receptor
to open the channel. When it opens, Na+ flows quickly into the cell and K+ flows out.
The voltage on the sarcolemma quickly rises to a less negative value as Na+ enters the
cell, then falls back to the RMP as K+ exits. This rapid up-and-down fluctuation in
voltage at the motor end plate is called the end-plate potential (EPP). Areas of
sarcolemma next to the end plate have voltage-gated ion channels that open in response
to the EPP. Some of these are specific for Na+ and admit it to the cell, while others are
specific for K+ and allow it to leave. These ion movements create an action potential.
The muscle fiber is now excited.
A wave of action potentials spreads from the motor end plate in all directions, like ripples on a
pond. When this wave of excitation reaches the T tubules, it continues down them into the cell
interior. Action potentials open voltage-gated ion channels in the T tubules. These are linked to
calcium channels in the terminal cisterns of the sarcoplasmic reticulum (SR). Thus, channels in
the SR open as well and calcium diffuses out of the SR, down its concentration gradient into the
cytosol. Calcium binds to the troponin of the thin filaments. The troponin–tropomyosin complex
changes shape and exposes the active sites on the actin. This makes them available for binding to
myosin heads.
The myosin head must have an ATP molecule bound to it to initiate contraction. Myosin ATPase,
an enzyme in the head, hydrolyzes this ATP into ADP and phosphate (Pi). The energy released by
this process activates the head, which “cocks” into an extended, high-energy position. The head
temporarily keeps the ADP and Pi bound to it. The cocked myosin binds to an exposed active site
on the thin filament, forming a cross-bridge between the myosin and actin. Myosin releases the
ADP and Pi and flexes into a bent, low-energy position, tugging the thin filament along with it.
This is called the power stroke. The head remains bound to actin until it binds a new ATP. The
binding of a new ATP to myosin destabilizes the myosin–actin bond, breaking the cross-bridge.
The myosin head now undergoes a recovery stroke. It hydrolyzes the new ATP, recocks (returns
to step 10), and attaches to a new active site farther down the thin filament, ready for another
power stroke.
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