Lab E1 Flashcards
Anatomy
is the study of the structure and description of the human body.
Micro-anatomy vs. macro-anatomy
Physiology
is the study of biological functions and processes of the human body under basal (normal) conditions.
homeostasis
the dynamic constancy of the internal physiological environment while buffering the challenges of the external environment.
-It reflects the ability of the human body to maintain relatively constant (internally), despite the changes in our surrounding environment.
Feedback Control Mechanism
- Stimulus
- change detected by receptor
- input: information afferently sent to control center
- output: information sent efferently to effector
- response of effector leads to influence of magnitude of stimulus and returns to variable homeostasis
Negative Feedback System
The response of the control system is negative or opposing to the stimulus.
Examples:
Regulation of blood pressure
Decrease in blood volume ->decrease in blood pressure ->detected by baroreceptors in carotid arteries ->sent to the brain ->vessels constrict, heart rate increases, etc.
Positive Feedback System
The response of the control system is positive or promoting the stimulus.
Positive feedback systems act to amplify the initial response to the stimulus.
Only 2
Child birth
Blood coagulation
When the head of a fetus is positioned appropriately, the increased pressure on the cervix stimulates sensory receptors. The excited sensory receptors then send a neural message to the brain. The brain responds by triggering the release of the hormone oxytocin from the posterior pituitary gland. Oxytocin travels through the blood stream to the uterus and promotes increase in contractions. This process will continue and the cervix becomes further stimulated and the uterine contractions become stronger until birth occurs.
Plasma Membrane
Serves as an external cell barrier
The plasma membrane is selectively permeable.
The phospholipid bilayer marks the boundaries of the cell and is amphipathic in nature.
Each lipid molecule contains a hydrophilic and a hydrophobic region.
Transport Mechanisms:Passive – Simple
Simple Diffusion
Natural movement from high to low concentrations
Unassisted transport (does not use an integral protein)
Transport Mechanisms:Passive – Facilitated
Channel mediated
Special transport proteins create hydrophilic tunnels in the lipid bilayer
Facilitated the transport of small, polar molecules and ions
Transport Mechanisms:Passive – Facilitated
Carrier mediated
Special transport proteins “carry” the substance across
Facilitates the transport of large, polar molecules
Transport Mechanisms:Osmosis
Water moves to side with higher solute concentration
Transport Mechanisms:Active Transport
Primary Active Transport
Carrier proteins “pump” the molecules against the concentration gradient
Direct use of cellular energy
Transport Mechanisms:Active Transport
Secondary Active Transport
Downhill movement of one molecule drives the uphill movement of another molecule
Indirect use of energy
Utilizes the established concentration gradient of molecule A to power the transport of molecule B
Transport Mechanisms:Vesicular Transport
Endocytosis
Vesicular transport is the bulk transport of substances into or out of the cell.
Substances are taken into the cell by modifying the plasma membrane structure
Phagocytosis
- “Cell eating”
- The cell engulfs a large particle by forming projecting pseudopods (“false feet”) around it and enclosing it within a membrane sac called a phagosome.
Pinocytosis
- “Cell drinking”
- Infolding of the plasma membrane carries a drop of the extracellular fluid containing solutes into the cell in a tiny membrane-bound vesicle
Transport Mechanisms:Vesicular Transport
Exocytosis
Vesicular transport is the bulk transport of substances into or out of the cell.
Substances are released from the cell into the extracellular environment
Account for most secretion processes
Tonicity of Solutions
Tonicity is a measure of the potential difference in osmotic pressure gradient of two solutions separated by a semipermeable membrane.
It is only influenced by non-penetrating solutes (i.e. solutes that cannot cross the membrane and exert an osmotic pressure).
Isotonic Solution
Both solutions have the same concentration of solutes.
No net movement of water
Hypertonic Solution
A solution in which the concentration of solute is higher than the solution it is being compared to.
water moves to high solute concentration to dilute.
Cell with crenate(water leaves cell to hypertonic solution)
Hypotonic solution
A solution in which the concentration of solute is lower than the solution it is being compared to.
water moves into cell. Cell will lyse.
The skin performs a variety of functions:
Protection
Body temperature regulation
Excretion
Production of vitamin D
Sensory reception
Skin has 2 distinct regions:
Epidermis
Dermis
-Hypodermis
Skin is the largest of all organs, accounting for about 7-15% of total body weight.
Skin varies in thickness from 1.5 to 4 mm or more in different regions of the body.
skin is largest organ
liver is 2nd largest
Vitamin D
calcium and phosphorous reabsorbption
Epidermis
Four Distinct Types of Cells
Keratinocytes
Melanocytes
Merkel cells (also called tactile epithelial cells)
Langerhans cells (also called dendritic cells)
Layers of the Epidermis
“come lets get sun burned”
Stratum corneum Stratum lucidum Stratum granulosum Stratum spinosum Stratum basale
Epidermis Cell Types
Keratinocytes
most abundant
starts in basal then takes 35-45 days to move up and die off
keratin is a strong protein
helps with the integrity of the skin
Epidermis Cell Types
Melanocytes
secretes melanin in space between keratinocytes
protects nucleus from UV rays which damage the DNA
Epidermis Cell Types
Merkel cells (also called tactile epithelial cells)
sensory for touching
Epidermis Cell Types
Langerhans cells (also called dendritic cells)
phagocytic
help with immune response
receptor mediated endocytosis
Layers of the Epidermis
Stratum corneum
“come lets get sun burned”
dead cells
Layers of the Epidermis
Stratum lucidum
“come lets get sun burned”
only on thick skin(palms and heels)
remember this
Layers of the Epidermis
Stratum granulosum
“come lets get sun burned”
flattened
Layers of the Epidermis
Stratum spinosum
“come lets get sun burned”
greatest concentration of keratinocytes
Layers of the Epidermis
Stratum basale
“come lets get sun burned”
where formation starts
Dermis
Papillary
top 20% of dermis(towards epidermis)
Reticular
bottom 80% of layer
Dermis
Papillary
Adjacent to the stratum basale
Dermal papilla is folded
—reason is to maximize the nutrient exchange between dermis and epidermis
epidermis is not blood supplies = no nutrients which is why the top layers start to die
Dermal papillae
- Fingerlike projections which attach to the epidermis above
- Increase the surface area for exchange of gases, nutrients, and waste products between these layers
- Form the ridges and whorls of the skin surface in the fingers, palms, toes, and soles
Dermis
Reticular
Deep region of the dermis
Accounts for about 80% of the total dermal thickness
Dense irregular connective tissue containing collagen fibers, elastic fibers, and blood vessels
Dermis
Hypodermis
not a layer of skin
Consists of both areolar and adipose connective tissue
Serves as thermal insulation, protective padding, and energy storage
Vitamin D function
Calcium and phosphorous reabsorption
The major function of vitamin D is to maintain normal blood levels of calcium and phosphorus. It helps the body absorb calcium that is necessary for building and maintaining healthy bones.
Vitamin D and UV
UV rays stimulate the deep epidermis to produce a vitamin D precursor.
Ends with kidneys(know that)
UV rays stimulate skins -> create precursor to vitamin D - > precursor sent to liver -> precursor sent to kidney where is becomes actual Vitamin D form - > active form of Vitamin D is sent to intestine for absorption of calcium and phosphorous
The more melanin in skin means Vitamin D exposure would need to be longer to get stimulation from UV for Vitamin D production
darker skin = longer time in sun for same daily dose of vitamin D stimulation
know this for exam “there is no set amount of time”
Melanin
Produced by melanocytes from an amino acid called tyrosine
Accumulate on the superficial, or “sunny,” side of keratinocytes
Shields the nucleus from ultraviolet radiation
Tyrosine - > tyrosinease forms melanin so if the enzyme is missing then no melanin
this is Albinism
More melanin to protect keratinocytes is why your skin tans
it shows as skin getting darker
know for exam
Carotene
Yellow-orange pigment that is obtained from vegetable sources
Carrots, keratin, and stratum cornea
this is for Carotene
Hemoglobin
The pink hue of Caucasian reflects the crimson color of oxygenated hemoglobin in the capillaries of the dermis
Caucasian skin contains little melanin, the epidermis is nearly transparent and allows the color of blood to show through
Note: Black and blue marks represent discolored blood that is visible through the skin. Such bruises reveal sites where blood has escaped from the circulation and clotted below the skin. The clinical term for this is called a hematoma.
4 oxygen for 1 hemoglobin
in red blood cells
makes a red/pink hue
know for exam
Sebaceous Glands(oil)
oil protects skin
antibacterial
Sudoriferous Glands(sweat)
Eccrine and Apocrine
Sudoriferous Glands(sweat)
Eccrine
everywhere
concentrated palms, soles, forehead
secrete straight up into sweat pore
Sudoriferous Glands(sweat)
Apocrine
axillary and anogenital
secrete into a hair follicle then comes out at hair root
becomes active during puberty and gives body odor
Sensory receptors
Chemoreceptors
chemical response
taste, smell
Photoreceptors
light
eyes
Thermoreceptors
temperature
Mechanoreceptors
touch
Nociceptors
pain
First 4 go through adaptation
after a while you no longer think about it(temperature becomes fine, touching something a long time becomes dull)
advantageous so the body is not overloaded by stimulus
Nociceptors
pain does not adapt because it is a constant need to know your body is hurting
don’t want to have adaptation to encourage fixing the pain
Skin Receptors
Meissner’s corpuscles
Light and intermittent
Distributed on various areas of the skin but are concentrated in areas sensitive to light touch, such as fingertips, lips, and nipples
Skin Receptors
Pacinian corpuscles
deep and intermittent
- shaving
Respond to deep pressure or vibration
Skin Receptors
Ruffini’s corpuscles
Deep and Sustained
- deep tissue massage
Respond to skin stretching and torque
Skin Receptors
Merkel discs
Light and Sustained
Provide information about an object’s qualities like edges or its curves
Meissners, Pacinian, and Ruffini
encapsulated by a connective tissue
Merkel
not encapsulated
Skin Cancer types
Basal cell carcinoma
Squamous cell carcinoma
Melanoma
Skin Cancer types
Basal Cell Carcinoma
Least malignant and most common of the skin cancers
Over 30% of all Caucasians get it in their lifetime!
Cells of the stratum basale proliferate, invading the dermis and hypodermis, and causing tissue erosions there
Most common lesions of this cancer are dome-shaped, shiny nodules
Grows relatively slowly, metastasis seldom occurs
99% full cure rate
Skin Cancer types
Squamous cell carcinoma
Arises from keratinocytes of the stratum spinosum
Appears as a scaly, irregular, reddened, round elevation
Grows rapidly and will likely metastasize if not removed
99% full cure rate
Skin Cancer types
Melanoma
Cancer of the melanocytes
Most dangerous kind of skin cancer
Can originate wherever there is pigment, but it often arises from existing moles
Metastasizes rapidly into surrounding circulatory vessels
Key to survival is early detection; survival rate decline with increasing thickness, degree of involvement of nearby lymph nodes, and extent of metastasis
Melanoma detection ABCDE
Review the three types
Rules
A – asymmetry(symmetry for regular mole)
B – border – defined rigid border
C – color – normal brownish(blotchy is bad)
D - diameter – normal up to 6mm
E – evolution and elevation
evolution = change over time(if changing then check)
elevation = how far raised above skin – normal is not as high
Types of muscle tissue
Smooth muscle is unicellular with ONE nucleus
Cardiac muscle
intercalated disk assist in contraction so it contracts in unison
Skeletal muscle peripheral located with multiple nucleie
on periphery to pack the rest of the cell densely with fibers for contractions
Know skeletal muscle for test
Organization of Skeletal Muscle
Epimysium
Surrounds muscle group
Perimysium
Surrounds fascicle
Endomysium
Surrounds muscle fiber/cell
Striations in a longitudinal section of skeletal muscle
Know longitudinal and cross sections of skeletal muscle differentiation
know thick or thin skin slides too
Striations in a longitudinal section of skeletal muscle
Know longitudinal and cross sections of skeletal muscle differentiation
know thick or thin skin slides too
know underlined and boxed in red for test
H band is ONLY myosin
no actin
A band spans the entire myosin area
myosin AND actin
A for Actin and And
I band is ONLY actin
no myosin
M line is middle of myosin
in middle
Sarcomere is the functional unit of the muscle
smallest unit that can perform a contraction
Z disk to Z disk on myofibril
On contraction(HI disappear but A stays same) H zone will disappear upon contraction
A zone stays same size
I zone disappears
Protein fibers Actin and Myosin DO NOT change length on contraction but do overlap
the entire Sarcomere does change length on contraction
know underlined and boxed in red for test
H band is ONLY myosin
no actin
A band spans the entire myosin area
myosin AND actin
A for Actin and And
I band is ONLY actin
no myosin
M line is middle of myosin
in middle
Sarcomere is the functional unit of the muscle
smallest unit that can perform a contraction
Z disk to Z disk on myofibril
On contraction(HI disappear but A stays same) H zone will disappear upon contraction
A zone stays same size
I zone disappears
Protein fibers Actin and Myosin DO NOT change length on contraction but do overlap
the entire Sarcomere does change length on contraction
Anatomy of Myofibrils
A band – dark region of the sarcomere,myosin filaments plus some overlapping actin
I band – light region of the sarcomere, containing only actin filaments
H zone – in the center of the each A bandis a portion of the myosin filament with no overlap of actin
Z line – howsarcomeres are divided from each other, found in the center of each I band
M line – in the center of each A band
Anatomy of Myofibrils fiber types
Thick = myosin
Thin = actin
Tropomyosin is wrapped around by tropomyosin
Located on the actin molecule itself are two additional proteins, troponin and tropomyosin. These proteins make up only a small portion of the muscle, but they play an important role in the regulation of the contraction process.
Sarcolemma
Sarcolemma = membrane of the sarcomere
Sarcolemma then endomysium
The T tubules send the signal of action potential to all microfibrils in an area so unified contraction across multiple myofibrils
Sarcoplasmic Renticulum is the internal Ca2= storage
Excitation-Contraction Coupling
Ach is released at the NMJ and binds to receptor site on the sarcolemma
Action potential in muscle membrane
Depolarization of T tubules causes Ca2+ channels to open
Intracellular concentration of Ca2+ increases
Ca2+ binds to troponin on the thin filaments
Tropomyosin moves to allow the interaction of actin and myosin
Cross-bridge cycling begins and force is generated
Ca2+ reaccumulated by the SR and the muscle relaxes
Troponin and Tropomyosin
When [Ca2+] is low
- Tropomyosin blocks the myosin binding site on actin
- Contraction will not occur
When [Ca2+] is present -Ca2+ binds troponin complex -Conformational change of tropomyosin allows myosin to bind to actin -Contraction can occur ----- Myosin has a high affinity for actin tropomyosin blocks the spots if not then muscle contraction all the time TnC = binds to calcium TnI = binds to actin TnT = binds to tropomyosin
Once calcium bind then it causes a conformational change which moves the tropomyosin out of the actins way
Actin and myosin can then bind
Sliding Filament Theory
- Release
- Cocked
- Cross Bridge
- Power stroke
- attached
- ATP causes the release of myosin binding to actin
- ATP is hydrolyzed and gets cocked
- ATP binds
- ATP – phosphate is released and myosin pulls the actin
- ADP is release
Motor Unit & Precision of Muscle Movement
Motor unit
the motor neuron and all the muscle fibers it innervates
only what the axon terminals are touching
pic has 6 fibers but only 4 are touched by axon terminals
Fine motion will have a greater density of motor neurons but each motor neuron will innervate less motor units
small motor units = fine motor activities
large motor units = gross motor activities
Skeletal Muscle Actions
Isometric
length stays the same
holding a tray with or without glasses = same muscle length
the tone changes because of weight but not muscle length
Isotonic
concentric = bicep curl
eccentric = contract but lengthen(trying to lift something but it doesn’t move)
Skeletal Muscle Actions parts
Agonist – the primary mover
Synergistic – muscles that assist the agonist group
Antagonistic- muscles that oppose the agonist
Classification of Skeletal Muscle Fibers
Structural and histological features determine the type of fibers based on size, diameter, and myoglobin. (Myoglobin is the oxygen binding molecule that facilitates oxygen transport into myocytes.)
Type 1 = slow twitch
Type 2 = fast twitch
Slow twitch endurance activities(long run) myoglobin binds to oxygen and doesn’t let it go keeps oxygen in muscles(oxygen storage) high mitochondria = energy production need ATP to release the muscle contraction fatigue resistance so you can go longer
Fast twitch
power lifter
exert a lot of energy at one time then done
Classification of Skeletal Muscle Fibers
Slow twitch – Type I
Myoglobin rich
Contain large numbers of oxidative enzymes
High mitochondrial volume
Surrounded by more dense capillary networks
Fatigue resistant
Slower maximal shortening velocity
Highly efficient
Classification of Skeletal Muscle Fibers
Fast twitch - Type IIX and Type IIA
Type IIX -Small number of mitochondria -Less resistant to fatigue -Rich in glycolytic enzymes Generate the highest power output
Type IIA
- Intermediate fibers
- Mixture of Type I and Type IIX
Exercise Physiology
Hypertrophy
increasing muscle size but not the number of muscle number
Gender difference
if a male and female muscle fiber is exactly the same diameter then they will be exactly as strong
can do the same work
on average male has a bigger diameter and therefore would be stronger because the fiber size
Exercise Physiology
Hypertrophy
An increase in muscle fiber diameter due to an increase in myofibril size
The amount of force that can be generated by a muscle group is proportional to the cross-sectional area of the muscle.
Thus, physiological adaptations as a result of strength training are a result an increase in muscle size, not muscle number (i.e. hyperplasia).
Exercise Physiology
Muscle soreness
Result from microscopic injury to the muscle fibers
Delayed Onset Muscle Soreness (DOMS) appears 24-48 hours post microscopic injury
NOT a result of lactic acid accumulation
Exercise Physiology
Gender Differences
When absolute strength (the total amount of force applied) is compared in untrained men and women, men are typically stronger.
This apparent sex difference in strength is often obsolete when force production in men and women is compared on the basis of the cross-sectional area of the muscle.
Sarcopenia
Aging
aging losing muscle mass
know the numbers for slow and rapid phase for muscle decline
generally see a shift from Type 2 to Type 1 muscle fibers go from fast twitch to slow twitch
Sarcopenia
Age related decline in muscle mass begins around age 25 and occurs across the lifetime.
The rate of age related muscle loss occurs in two distinct phases
- Slow phase – 10% of muscle mass is lost from 25 to 50 years
- Rapid phase – An additional 40% of muscle mass is lost from 50 to 80 years
- Generally see in a shift in fiber type (heavy loss of fast twitch, increase of slow twitch).
Rigor Mortis
Postmortem muscle stiffness resulting from rigor crossbridges in the absence of adenosine triphosphate
Muscular Dystrophy
A group of hereditary muscle diseases that weaken skeletal muscle
Characterized by defects in muscle proteins or lack of a protein called dystrophin that results in a progressive muscle weakness and a loss of muscle fibers
Dystrophin holds the cell membrane up
in muscular dystrophy the dystrophin is missing then the cells start to collapse
impacts males more because on X chromosome
males have only one X so if impacted they are impacted
