Physiology Integrative Chapters Flashcards

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created 11 years ago by srigot55
updated 11 years ago by srigot55
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mammalian physiology
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classification of neural reflexes

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look at specific neuron (efferent)
o Autonomic or somatic (always acting in an excitatory way)?
o Where is it happening? Spinal or cranial?
o Innate or learned?
o How many neurons? Mono (direct connection between efferent and afferent sides) or polysynaptic (almost all neurons)?


skeletal muscle reflexes

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 Key thing for mono – Direct synapse from sensory neuron onto efferent neuron
 Poly uses a CNS interneuron which can get very complex, most common (all autonomic neurons)
• Convergence – Many sensory neurons feeding into few interneurons
• Divergence – Few interneurons feeding many efferent neurons
 Contraction = excitation of efferent neuron
 Relaxation = inhibition of efferent neuron


autonomic reflexes

 All are polysynaptic
 At least one synapse between sensory & CNS & synapse between preganglionic w/postganglionic neurons
 AKA visceral reflexes
 All are polysynaptic
 Many show tonic (continuous) activity
 Can be integrated in spinal cord or brain
 Limbic system = emotionally driven reflexes
 Examples: Urination, breathing, eating, body temperature, blushing, getting goosebumps, etc.



 Proprioceptors -> CNS -> Alpha motor neurons (somatic motor neurons that innerve skeletal muscle fibers that contract) -> Extrafusal muscle fibers
o Proprioceptors – sensory receptors that monitor position in space, movement, etc.
o Proprioceptors include: joint receptors, muscle spindles & golgi tendon organs

o - Joint receptors – In capsules & ligaments to detect mechanical distortion around joints


muscle spindles (picture)

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- Sensory receptors that sense muscle length & changes in muscle length
 Present in intrafusal muscle fibers
 Stretch the whole length of the muscle tissue
 Intrafusal muscle fibers have a muscle spindle in them and recognize the change in length of the spindle over time
 Intrafusal fibers are contractile at the end but not in the middle (where muscle spindles lie)
 Sustained contraction requires alpha-gamma coactivation and coactivation)
• Alpha motor neurons (somatic) innervate extrafusal fibers, Gamma innervate contractile portion of intrafusal fibers


golgi tendon organs (picture)

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 Respond to muscle tension during isometric contraction
 Reflex response = relaxation
• Inhibiting muscle neurons causing them to not fire and causing relaxation
 Prevents damage to tissue
 Found in junction of muscle fibers and tendon


patellar tendon (knee jerk) reflex

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• muscles are often arranged in antagonistic muscle groups. If you’re going to flex (contract) one muscle, you must extend (relax) its antagonist.
• Knee jerk example – very simple monosynaptic muscle reflex
• Sensory neuron branches in spinal cord:
o One part directly synapses with somatic motor neurons for quad muscle contraction and the Other part synapses on inhibitory neurons for hamstrings.
o Quad contracts, hamstring relaxes & your leg shoots out.
 Inhibition of hamstring is part of the response


flexion reflex (step-on-a-lego reflex) (picture)

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• Reflex from stepping on something sharp or touching something hot (step-on-a-lego reflex)
• Polysynaptic muscle reflex
• Pulls body away from harmful stimuli


body movement

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 Multiple skeletal muscles signaling CNS that integrates signals and coordinates a response
 All polysynaptic
 Reflex movements
 Voluntary movements
 Rhythmic movements


reflex movements

• Stimulated by sensory receptors
• Simple, integrated in spinal cord or brain stem
• Rapid, inherent response
• Ex: knee jerk, cough
• Brain does receive sensory input to coordinate body-wide responses


voluntary movement

• Stimulated by external stimuli or conscious thought
• Complex, integrated in CNS (usually brain)
• Learned movements
• Ex: playing the piano, swimming, riding a bike
• With practice, learned movements can become subconscious – muscle memory, more like a reflex


rhythmic movement

• Start & stop are voluntary
• Intermediate complexity, integrated in spinal cord with higher level input
• Ex: Running, quiet breathing patterns
• Once started, CNS interneurons called central pattern generators maintain repetitive activity
• Ex: Take an animal that is paralyzed where the “start” signal for walking is blocked. If you support the animal on a treadmill and electrically stimulate the spinal central pattern generator for that movement, the legs will start walking.


neural control of movement (table)

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 3 levels of control:
• Spinal cord – spinal reflexes & has central pattern generators, reflex responses
• Brain stem & cerebellum – control postural reflexes & hand/eye movements, fine tunes movement
• Cerebral cortex & basal ganglia – voluntary movements, higher processing


visualization technique

o Picture yourself doing what you’re about to do
o Psychological process stimulates physiological process
o Presynaptic facilitation- Mental process in cerebral cortex stimulates signals in muscle groups
o Used is sports, any kind of performance, anxiety disorders, cancer treatment & pain management


parkinson's disease

o Has helped researchers understand how basal ganglia integrates signals
o Symptoms: abnormal movements (tremors), speech difficulty, lose facial expression, personality changes
o Dopamine activity is key
 Give patients a precursor of dopamine, L-dopa, that can cross the blood-brain barrier.


visceral (autonomic muscle control)

o Mostly controlled by autonomic nervous system
o Hormones, in addition to neural cues, regulate contraction
o Skeletal muscle is attached to bone, smooth & cardiac are not.
o If you contract smooth or cardiac muscle, you change the shape of the organ
o Often very specific in the way that an organ is controlled, so we will cover that as we discuss those tissues.



o Body is constantly fighting to keep a relatively constant state
o Taking in water & ions, either need to use it or excrete it
 Sweat, Urine, Feces, Ventilation
o Water and salt are two of the most important molecules to regulate
 Ion concentrations in interstitial fluid used for transport
 Mess up concentrations and neural function (and other functions) are messed up
 Key for cell volume


osmolarity and tonicity

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systemic integration (picture, response to low blood pressure or blood volume)

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baroreceptor reflex


myogenic autoregulation

o Decrease in blood pressure past the point of vasoconstriction and reduces the blood flow into the glomerulus
o Kidneys can also adjust for differences in blood pressure
o Keeps GFR (glomerular filtration rate) constant over a wide range of pressures (80-180 mm Hg)


tubuloglomerular feedback (picture)

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increase in blood causes and increase in the amount of fluid being pushed through the tubes


autonomic regulation

o Sympathetic control changes resistance in arterioles
o increase in NE causes either vasoconstriction or vasodilation in arterioles depending on the receptor present
kidneys are slower than cardiac for these changes


hormonal regulation

spreads through the blood for a widespread effect
in the kidneys: affects slits on podycytes that control regulation


water balance

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1/3 water is extracellular, 2/3 water is intracellular
3L of plasma, the rest of water is in interstitial fluid
volume of water in= volume of water out
ccan be disrupted by excessive sweating or diarrhea


water conservation (pictures)

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• happens mostly in the kidneys
• Adjust the GFR, adjust the amount of water that is lost
• Water cannot be replenished by the kidneys, just conserved
• Happens in:Renal medulla (significant amount of reabsorption), Distal tubule (small amount or reabsorption), Collecting duct (most of the regulation of reabsorption)
• Concentration of urine varies between 50 mOsM and 1200 mOsM(based on normal body osmolarity of 300 mOsM), trying to move water without moving solutes


Vasopressin controlling water levels (picture)

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• Peptide neurohormone synthesized in the hypothalamus
• Secreted by the posterior pituitary
• AKA antidiuretic hormone (ADH)
• Neurohormone is released into the blood
• Acts on collecting duct epithelium
• causes a slow change in the microtubule membrane composition (incorporates more aquaporins into the membrane)
• increases reabsorption (urine is concentrated), urine is diluted and more water is excreted in the absence of vasopressin
• Vasopressin binds to a receptor -> activates cAMP second messenger system -> inserts aquaporin into the apical membrane ->water is absorbed by osmosis into the blood


vasopressin regulation (picture)

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 Blood pressure
 Blood volume
 Plasma osmolarity* (more important)
• Receptors in the hypothalamus pick up on signals
• Threshold = 280 mOsM
o Release more vasopressin and increased water resorption if you exceed 280 mOsM
o Absorb more during the day than you do at night (Allows you to urinate less at night)


countercurrent exchange

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 Animals like whales that live in cold water need to circulate blood such that it conserves heat
• Puts blood vessels in close proximity conserves heat and conserve the energy that would be needed to heat the blood
•vasa recta


vasa recta (countercurrent exchange) (picture)

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 Cross section of the renal medulla contains tons of ducts and tubes (vasa recta, loops of henle, collecting ducts, etc.)
 Instead of transferring heat, transfers water and solutes
 No loss to environment, kidney is a closed system
 Countercurrent multiplier to make it more dilute than it could have been on its own

• each dot represents another loop, the image represents a whole tissue
• Picks up solutes as it is moved down the loop of henle (red down) due to concentration gradients and ending the blood
• Normal gradient pumps water in and leaved solute
• Start and end at the same concentration in the blood (300 mOsM) but change concentration within the loop
• interstitial fluid is more concentrated, more dilute levels leaving the loop of henle following the concentration gradient
• urea and salt act as solutes


sodium balance (picture)

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o Addition of salt increases body osmolarity
o Without regulation would create a hypertonic ECF -> cell shrinking
o salt (solutes) increase osmolarity, leads to hypotonicity
o To combat the hypotonicity: Salt addition triggers vasopressin secretion and thirst
o Increased vasopressin triggers water conservation
o Thirst increases water intake
o Regulated only via kidneys
o Changes in blood volume are noticed due to the change in blood pressure
o Key hormone: aldosterone


Aldosterone (picture)

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o Fast response
 Aldosterone secretion stimulated by:
 Increased ECF K+ concentration or Decreased blood pressure Trigger the release of aldosterone
• No aquaporins in the membrane- move solutes without moving water


RAS pathway (picture)

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 Renin-angiotensin system (RAS) pathway
 looks for changes in NaCl that passes through the loop of henle -> drop in NaCl levels= drop in blood pressure
 renin is released in response the to the decrease in blood pressure



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from RAS pathways and aldosterone
o Angiotensin I
o Angiotensin II Effects (active molecule)
 All effects increase blood pressure
• Increases vasopressin secretion (stimulates thirst)- increase in volume= increase in pressure since your body absorbs more water
• Vasoconstrictor
• Increases CVCC sympathetic output
• Increases proximal tubule reabsorption
 Medication (ACE inhibitors) that blocks the production of Angiotensin II which will lower blood pressure but may have significant side effects


Potassium regulation

• Key ion for excitable tissue (without proper regulation the concentration in the membranes will change dramatically)
• Hyperkalemia vs Hypokalemia
• Regulated by pH balance
• Kidney disease, improper eating, diarrhea, dehydration


Hyperkalemia vs Hypokalemia

• Hyperkalemia – too much K+
o Makes membrane more excitable and allows more solutes to pass through, cells cannot fully repolarize to “reset” the signal

• Hypokalemia – too little K+
o similar to hyperkalemia but opposite
o makes the membrane potential higher

weakened tissue and responses for both conditions


control of volume and osmolarity

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• drinking replaces fluid loss- reflex response to increased osmolarity, eating ice chips is effective
• salt appetite- animals lick the ground to increase salt content
• dehydration avoidance- mid afternoon nap helps you stay out of the sun during the hottest part of the day to avoid dehydration
• extreme sweating or blood loss- need to replace both the blood volume and the solutes


responses triggered by changes in volume, blood pressure, and osmolarity

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Acid-base balance

o Body is normally slightly alkaline (pH = 7.40, Usually ECF & ICF pH are similar)
o Important because changes dramatically affect protein function (changes the structure of proteins which will change their function)
o Acidosis vs Alkalosis
o Related to K+ levels
o Source of pH changes (Comes from food & metabolism- biggest acid source, in all cells and plasma, bicarbonate and carbonic anhydrase which produces H+)
 In general, your body takes on more acids than bases


general Acidosis vs Alkalosis

o Acidosis
 Too low pH
 Neurons are less excitable = CNS depression -> coma -> death
o Alkalosis
 Too high pH
 Neurons are hyperexcitable = muscle twitches -> sustained contractions -> tetanus -> death


pH homeostasis mechanisms- buffers

 Moderates but does not prevent changes in pH by interacting with H+
 Proteins, phosphate ions, hemoglobin
 Not a permanent fix
 Reversible reaction
• Will increase levels of CO2
• Increased CO2 levels à increased ventilation


pH homeostasis mechanisms- renal regulation

 Cover remaining 25% of regulation
• occurs in the kidneys
• Excrete or reabsorb H+ ions
• Excrete or reabsorb bicarbonate
• relatively slow


pH homeostasis mechanisms (types)

renal regulation


pH homeostasis mechanisms- ventilation

covers 75% of regulation
 Respiratory acidosis
• Increased plasma CO2 due to hypoventilation
• Alcohol, drugs, asthma, fibrosis, dystrophy
• Need to excrete H+ and reabsorb bicarbonate in kidneys


metabolic acidosis vs alkalosis

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• Dietary & metabolic input increases H+
o Lactic acidosis, ketoacidosis, aspirin, diarrhea
• Respiratory compensation à hyperventilation

• Decrease in H+ concentrations
• Excessive vomiting, excessive antacid consumption
• Respiratory compensation àhypoventilation


respiratory acidosis vs alkalosis

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 Respiratory acidosis
• Increased plasma CO2 due to hypoventilation
• Alcohol, drugs, asthma, fibrosis, dystrophy
• Need to excrete H+ and reabsorb bicarbonate in kidneys


energy sources for exercise

 ATP in muscle cells
 Phosphocreatine (PCr) converting ADP into ATP
 Lasts 10-15 seconds


manufacturing new ATP

• Glycolytic metabolism
o Anaerobic
o 2.5 times faster
o 2 ATP/glucose
o Metabolic acidosis

• Citric acid cycle
o Aerobic
o Slower
o 30-32 ATP/glucose
o Both glucose & fatty acids with O2

store as glycogen. muscle and liveer glycogen stores provide 2000kcal worth of energy (20 miles of running). afterwards can use a combo of fatty acids and glucose for energy


hormone regulation of energy production

• Glucagon, cortisol, growth hormone, epinephrine, and norepinephrine all increase during exercise
o Mobilize liver glycogen (turning it in to glucose) raising blood glucose levels
• Insulin decreases
o If blood sugar is up, why does insulin decrease?
 Keeps glucose free for muscle fibers
 Contracting muscle fibers do not need insulin for glucose uptake (GLUT4 transporter)
 Transported to bring glucose from the blood to cells are independent of insulin


oxygen consumption during exercise

• Oxidative phosphorylation uses up O2
• Can quantify intensity by measuring O2 use (VO2)
• VO2 max, athletes can have musch higher VO2 max than normal people


limiting metabolic factors

• Mitochondria
o Important for ATP generation (oxidative phosphorylation)
o Training increases number of mitochondria in muscle fiber
• Cardiovascular or pulmonary system?
o Which holds you back more?
o When cardiac output is 90% max, ventilation is only 65% max


ventilation response to exercise

 As exercise begins
• Mechanoreceptors and proprioreceptors sense movement and signal motor cortex
• Motor cortex signals medulla oblongata to increase ventilation
• Central, carotid & aortic chemoreceptors monitor CO2, pH & O2
• Increase alveolar ventilation as needed
• Under moderate exercise, levels stay constant


cardiac response to exercise

• Cardiac output increases dramatically
o Resting = 5 L/min, Average person = 20 L/min, Trained athlete = 40 L/min
o Cardiac Output (CO)= heart rate x stroke volume
o CO= (SA node rate + autonomic nervous system input) x (venous return + force of contraction)
o Decrease parasympathetic activity -> rising heart rate
o Sympathetic takes over and stimulates heart
 Increases contractility (more blood per beat)
 Increases heart rate
o Sympathetic division triggers body-wide vasoconstriction
o Skeletal muscle vasodilates
 Due to changes in microenvironment
• Temperature, CO2, O2, H+ concentration
• Overrides vasoconstriction signal


blood flow during exercise

o Muscle gets about 1/4 of the blood (1.2L/min) at rest
o Exercise increases blood flow to muscles to almost 90%
o Trained athletes can increase blood flow to muscles to 22 L/min


blood pressure response to exercise

o Increases slightly
 Skeletal muscle vasodilates
 Cardiac output increases
o How does pressure stay increased?
 New threshold?
 Signal inhibition?
 Muscle chemoreceptors?


temperature regulation during exercise

• As you exercise your body “wastes” energy in the form of heat during metabolism
• Body temperature can reach 104-108°F
• Two responses:
o Increased cutaneous blood flow
o Sweating
 Lowers body temperature through evaporative cooling
 Problems: Dehydration, Reduced blood volume
 Disease: Hyperhidrosis, Hypohidrosis