BI231 Final

PCC BI231

1. Anatomical Variation

• No two humans are exactly alike.

• Variations can occur in organ structure, blood vessels, nerves, and bone shape.

• Important for healthcare professionals to recognize normal variation vs pathology.

Homeostasis

The body’s ability to maintain a stable internal environment.

Negative feedback

Negative Feedback: Reverses a change.

Positive Feedback

Enhances the change.

Anatomical Position

• Body stands upright, facing forward, arms at sides, palms forward.

• Importance: Universal reference for describing locations and directions on the body

Tissues: Structure & Function

1. Epithelial – Covers surfaces, lines cavities, forms glands.

2. Connective – Supports, protects, stores fat, immune responses (bone, blood, cartilage).

3. Muscle – Movement (skeletal, cardiac, smooth).

4. Nervous – Communication (neurons and neuroglia).

Basal Cell Carcinoma

• Most common, least dangerous

Squamous Cell Carcinoma

Can spread if not treated.

Melanoma

Least common, most deadly—originates in melanocytes

1st degree burn

1st Degree: Epidermis only (sunburn).

2nd degree

epidermis + part of dermis (blisters)

3rd degree burn

full skin thickness destroyed, risk of infection, fluid loss, scarring

vitamin D production

1. skin converts choleesterol to cholecalciferol using UV light

2. liver and kidneys convert it to calcitriol. (Active form)

3. important for calcium absorption and bone health

osteoblasts

build bone (bone formation)

osteoclasts

break down bone matrix (resorption)

osteocytes

maintain bone matrix (mature cells)

osteogenic cells

stem cells that become osteoblasts

Calcium Regulation

Needed for muscle contraction, nerve signaling, and blood clotting.

• parathyroid Hormone (PTH): Increases blood calcium (stimulates osteoclasts, kidney reabsorption, and vitamin D activation).

• Calcitriol (Vitamin D): Increases calcium absorption from intestines.

• Calcitonin: Lowers blood calcium (inhibits osteoclasts, increases calcium deposition in bones).

Bone disorders Osteoporosis

weak bones due to low bone mass

osteomalacia (rickets)

sotf bones due to vitamin D deficiency

fracture healing steps

1. hematoma forms

2. soft callus forms

3. hard callus forms

4. bone remodeling

joint disorders osteoarthritis

wear & tear of cartilage common with aging

rheumatoid arthritis

autoimmune attack on joint lining

gout

uric acid buildup in joints

joint strenght vs mobility

inverse relationship = the more mobile the jpint the less stable & less mobile is more stable

Muscle & Muscle Fiber Structure

muscle is made of fascicles

fascicles = made of bundles of muscle fibers ( cells )

muscle fiber (cells) = long, multinucleated cell with myofibrils

myofibrils = contain sarcomeres

muscl cell and sarcomere parts

sarcolemma

cell membrane

sarcoplasm

facilitate muscle contraction and relaxation by regulating calcium levels and providing the necessary building blocks and energy

sarcoplasmic reticulum

store, release, and take up calcium and thereby control muscle contraction

T-Tubules

store, release, and take up calcium and thereby control muscle contraction

sarcomere

facilitates muscle contraction

(z disc to z disc) contains actin and myosin

thin filament

contains actin tropomyosin and troponin

1. Troponin binds Ca2+

2. moves tropomyosin

3. reveals myosin binding sites

thick filament

contains myosin (myosin jheads bind to actin and pull during contraction

muscle dystrophy

Cause = genetic mutation
effect = weakening & breakdown of muscle

motor unit structure and functions

fine control = small motor unit

powerful movement = large motor unit

motor unit & muscle strength

motor units activated = stronger contraction (recruitment)

larger motor units = stronger force

Neuromuscular junction structure

1. synaptic knob (contains ACh vesicles

2. synaptic cleft

3. motor end plate (has ACh receptors)

NMJ function

1. action potential leads to ACh release

2. ACh binds receptors leading to muscle fiber depolarization

3. triggers muscle polarization

phases of muscle contraction (write down before revealing)

1. EXCITATION: action potential arrives to NMJ, Acetylcholine is released and binds to receptors causing depolarization

2. EXCITATION-CONTRACTION COUPLING: action potential travels down t-tubules, calcium is released from sarcoplasmic reticulum, calcium binds to troponin and tropomyosin shifts and actin sites are exposed.

3. CONTRACTION: myosin heads bind to actin (cross bridges), power stroke pulls actin leading to ATP binding and heads detaching and recocking.

4. RELAXATION: Acetylcholine is broken down and calcium is reabsorbed.

steps of contraction phase

1. cross bridge forms: myosin heads bind to actin

2. powerstroke: myosin puls actin inward

3. detachment : ATP binds myosin and detaches it from actin

4. resetting: ATP is hydrolyzed and myosin heads recock

Length tension relationship

too short = filaments overlap

too long = not close enough cross bridges

ideal length = maximum force

Phases of a myogram (muscle twitch)

1. latent period: time between stimulus and contraction

2. contraction phase: cross bridge cycling and tension rises

3. relaxation phase: calcium is reabsorbed and tension fails

factors affecting twitch strength

1. length

2. fatigue

3. temperature

4. hydration

5. stimulus frequency

incomplete tetanus

rapid stimulation leads to muscle partially relaxing between twitches.

complete tetanus

no relaxation leading to smooth sustained contractions achieved with high frequency stimulation

muscle metabolism (energy use)

immediate: creatine phosphate donates P to ADP

short term: anaerobic glycolysis

long term: aerobic respiration

muscle fatigue causes

low ATP, ion imbalance, lactic acid buildup

EPOC (excess post excercise oxygen consumption)

restores ATP/creatine, removes lactic acid, reoxygenate myoglobin

slow twitch muscles

• red color high in myoglobin

• aerobic energy

• resistant

• low power

• posture muscles

fast twitch muscles

• white, low in myoglobin

• anaerobic energy

• fatigues quickly

• high power

• arm muscles for sprinting

smooth muscle cell structure

• spindle shaped

• no sarcomere

• dense body

smooth muscle contraction

1. calcium enters eCF or SR

2. calcium binds to calmodulin

3. activates myosin light chain kinase

4. MLCK phosphorlyates, leading to cross bridges forming

CNS organs & function

• brain, spinal cord

• integrate, and control

PNS organs & function

• nerves outside of CNS

• cimmunication lines

sensory (afferent)

• sends signals to CNS

• somatic (skin and muscles)

• visceral (organs)

motor (efferent)

• somatic motor: voluntary control (skeletal muscle)

• autonomic motor: involuntary (smooth, cardiac, glands)

• sends signals from CNS

sympathetic

flight or fight

parasympathetic

rest and digest

gray matter

• cell bodies, dendrites, synapses

• unmylinated

• outer cortex in brain

• inner H shape

white matter

• myelinated axons

• myelin gives lighter color

• inner areas

• outer ring

parts of a neuron and funtion

• dendrites: receive signals

• cell body: contains nucleus, integrates signals

• axon: seends signals to other cells.

• Axon terminal: reaeases neuotransmitters

• myelin sheath: insulates axon, speeds up signals

• node of ranvier, gaps in sheath allows saltatory conduction

astrocytes (CNS)

blood brain barrier, nutrient transfer. repairs

oligodendrocytes (CNS) and Schwann cells (PNS)

form myelin sheath

microglia (CNS)

immune defense and phagocytosis

ependymal cells (CNS)

line ventricles and make CSF

satellite cells (PNS)

support ganglia and regulate enviornment

saltatory conduction

action potential jumps from node to node

membrane potential

• difference in charge across membrane

• resting membrane potential is -70mv

• created bt Na/K

Na

In cell

K+

leaks out of cell

depolarization

membrane becomes less negative (Na enters(

repolarization

membrane returns to resting state( K+ leaves)

hyperpolarization

membrane becomes more negative than resting membrane potential (repolarized phase)

graded potentials

varies with stimulus

action potential

all or non size

action potential generation steps

1. resting state -70mV

2. threshold reached (-55mV) voltage gated channels open (Na)

3. depolarization: Na enters membrane going to +30 mV

4. repolarization: Na channels close, K+ channels open and leave cell

5. Hyperpolarization: K+ overshoots, dips below resting potential

6. return to resting: na/k pumps restore balance.

absolute refactory period of a neuron

no new action potentials possible Na channel inactive

relative refactory period

stronger stimulus can trigger new AP (K channel still open and membrane hyperpolarized).

acetylcholine

muscle contraction, parasympathetic signals

dopamine

mood and motor control

serotonin

mood sleep apetite

norepinehrine

sympathetic response, alertness

GABA

main inhibitory neurotransmitter in CNS

glutamate

main excitatory neurotransmitter in CNS

excitatory post synaptic potential (EPSP)

depolarization

Inhibitory post synaptic potential (IPSP)

hyperpolarization

summation

one neuron fires repeatedly = temporal

multiple neurons fire at ones - spatial

meninges layer and function

protect brain and spinal cord and contain CSF

dura mater

tough layer

arachnoid mater

web like middle layer

pia mater

this inner layer touching spinal cord

epidural space

between dura mater and vertebrae

subdural space

between dura and arachnoid mater

subarachnoid space

betwween arachnoid and pia mater contains CSF

ascending spinal tract

carry sensory info

descending spinal tract

carry motor commands from the brain to muscles

spinal nerve & nerve structure

31 pairs split into dorsal and ventral root

reflex arc

1. receptor: detects stimulus

2. sensory neurons: send signal to CNS.

3. 3. integration center: spinal cord

4. motor neurons: carry commands

5. effector: muscle/gland responds

muscle spindle

specialized muscle fiber that detects stretch. sends signals to CNS