Koofers

Human Phys Exam 2 - Flashcards

Flashcard Deck Information

Class:KINE 304 - Human Physiology
Subject:Kinesiology & Hlth Sciences
University:William and Mary
Term:Spring 2010
- of -
INCORRECT CORRECT
- INCORRECT     - CORRECT     - SKIPPED
Shuffle Remaining Cards Show Definitions First Take Quiz (NEW)
Hide Keyboard shortcuts
Next card
Previous card
Mark correct
Mark incorrect
Flip card
Start Over
Shuffle
      Mode:   CARDS LIST       ? pages   PRINT EXIT
Sensory Systems (parts) 1. Receptors 2. Neural Pathway 3. Brain
Receptors Specialized cells or specialized endings of afferent neurons
5 Types of Neurons 1. mechanoreceptors (touch) 2. thermoreceptors (temp) 3. nociceptors (pain) 4. electromagnetic (light) 5. chemoreceptors (taste, smell, oxygen, osmolarity, etc)
Transduction Regardless of original form of stimulus, it must be changed into electrical energy (occurs at receptor); results in "receptor potential," this is local graded potential. if receptor potential is of sufficient intensity by the time or arrival at first Node of Ranvier, AP will result
Generated by Koofers.com
Receptor field area of body covered by receptors from a single afferent neuron
Sensory Unit single afferent neuron and all of its receptors; strength of stimulus is proportional to strength of response because more receptor potential exceeds threshold, and the greater the frequency of its APs
acuity telling the difference between two stimuli
Adaptation at constant stimulus intensity, receptors gradually become desensitized (decreased rate of AP firing). Two kinds: 1. Phasic (fast), 2. Tonic (slow)
Generated by Koofers.com
Neural (ascending) Pathways afferent neurons carry info to specific brain regions; several classes based on size and thus speed of conduction; Primary (1st order) neuron synapse w/ interneurons in spinal cord or brain; usually converge or diverge
divergence info from single afferent neuron synapses w/ many interneurons
Convergence info from many afferent neurons arrive at same interneuron
2 Classification schemes of Neural Pathways First: A) Specific ascending pathways (carry info about single type of stimulus) B) Nonspecific ascending pathways (carry info about several different types of stimuli); Second: A) Dorsal column lemniscal system, B) Anterolateral System
Generated by Koofers.com
Speed of synapse through pathway Urgent: 110-120 m/s, Not Urgent: 5 m/s
Second classification scheme of Neural Pathways (A) Dorsal column lemniscal system: carries info in dorsal columns of spinal cord (white matter), info crosses to opposite side in medulla, through brainstem to thalamus via lemniscus, composed of large myelinated nerve fibers (110 m/s), higher degree of spatial orientation (phasic info, position info, touch using spatial accuracy, pain); (B) Anterolateral System: carries info in dorsal horns of cords gray matter, info crosses immediately, transmits to brainstem and thalamus, unmyelinated (40 m/s), poor spatial orentation, carries several different types (pain, thermal, crude touch, pressure)
Brain interprets sensory info, from thalamus and brainstem info delivered to specific parts of cerebral cortex, results in perception, sensory systems code 4 aspects of stimulus: 1. Type, 2. Intensity, 3. Location, 4. Duration
Types of Stimuli a. chemical, b. taste, c. smell, d. somatosensory, e. muscle, f. balance, g. hearing, h. vision
Generated by Koofers.com
Intensity of stimuli determined by frequency of AP firing and # of receptors stimulated
Location of stimuli (acuity of stimulus location), the smaller the receptive field, the greater the acuity; the greater the degree of convergence in ascending pathway, the lower the acuity
Duration of Stimuli receptors have different rates of adaptation, rapidly vs slowly (phasic vs tonic)---> how long do you need to know it?
Hormonal (endocrine) System primarily controls metabolic functions of body; effects of some hormones occur in seconds, other homrones continue to regulate functions for weeks; hormones produced and released by endocrine glands, carried away by blood, and then affect target cells; a single endocrine gland may secret more than one hormone, but single cell type secretes only one type
Generated by Koofers.com
3 Basic types of hormones 1. amine hormones, 2. peptide hormones, 3. steroid hormones, *remember: receptors for hormones are proteins
Amine hormones derived from tyrosine, include thyroid hormones and catecholamines (epi and norepi)
Peptide hormones undergo extensive processing before secretion, easily destroyed, soluble in plasma [preprohormone (ribosome)-->prohormone (ER)-->hormone (Golgi Aparatus), then stored in vesiciles and leave via exocytosis]
Steroid hormones derived from cholesterol, specific steroidogenic enzymes in cell determines which steroids produced, easily diffuse across membrane (no intracellular storage), not soluble in plasma, once in circulation combine w/ binding proteins, only small fraction of "free" (bioactive) steroids, lipid based
Generated by Koofers.com
Mechanism of Endocrine Response A) receptors for catecholamines and peptide hormones are ON cell membrane, upon binding intracellular 2nd messenger is activated (usually cAMP), [binding-->G protein-->increase adenylate cylase-->ATP to cAMP-->protein kinase activation-->phosphorylation of enzyme, biological response fairly swift; B) receptors for steroid and thyroid hormones found withIN cells (cytosol/nucleus), bc lipids can pass thru membrane, upon binding hormone/receptor complex interacts w/ DNA as transcription regulating factor, usually slower biologcial response (new data says that some steroids are fast acting)
Features of hormonal action 1. actions greatly amplified at target cells, 2. regulate rates of existing reactions, not initiate new ones, 3. actions are typically slow and prolonged, esp steroids, 4. in general biolocial effect of hormoneis proportional to circulating concentration of that hormone (circulating levels of any hormone determined by rat)e of secretion and rate of removal--metabolism
Secretion most hormones show pulsatile release (not constant steady dribble, more like heartbeat), show circadian rhythm, types of input affecting release: a)change in plasma concentration of mineral ions, b)change in plasma concentrations of nutrients, c)neurotransmitters released from neurons, d) other hormones or paracrien agents
Metabolism usually occurs in liver and kidneys, to small extent w/in target cells, peptide hormones broken down by specific peptidases, steroids undergo series of reduction reactions that make them water soluble (adding electrons), urine is main route of excretion of hormone metabolism (small amounts of intact hormones also excreted via urine)
Generated by Koofers.com
Hypothalamic-Pituitary pathway Hypothalamus is part of brain (stimulated by neurons), pituitary is gland at base of brain (master gland), hypothalamus conveys info to pituitary either by neurons or by blood vessels, 2 sections of pituitary (hypophysis): a)posterior pituitary (neurohypophysis)-back, b)anterior pituitary (adenohypophysis)-front
Posterior Pituitary receives direct neural input from hypothalamus, releases ADH (vasopressin) and oxytocin into bloodstream, ADH works in renal system to control excretion of H20, oxytocin causes contraction of pregnant uterus and ejection of milk from breasts (remember: prolactin produces milk)
Anterior Pituitary receives input from hypothalamus from blood (portal vessels) carrying hypophysiotropic hormones that control secretion of hormones from anterior pituitary
Thyrotropin releasing hormone (TRH) stimulates release of thyroid stimulating hormone (TSH) and prolactin
Generated by Koofers.com
Corticotropin releasing hormone (CRH) stimulates secretion of adrenocorticotropin (ACTH)
Growth Hormone releasing hormone (GHRH) stimulates release of Growth Hormone (GH)
Somatostatin (SS) inhibits GH secretion
Gonadotropin releasing hormone (GnRH) stimulates secretion of Leutinizing hormone (LH) and follicle stimulating hormone (FSH)
Generated by Koofers.com
dopamine (prolactin release inhibiting hormone--PIH) inhibits secretion of prolactin
Follicle Stimulating Hormone (FSH) stimulates growth and development of ovarian follicles, controls spermatogenesis
Leutanizing Hormone (LH) regulate steroidogenesis of gonads (male and female)
Prolactin enhances breast development and milk production
Generated by Koofers.com
Growth Hormone major stimulus of postnatal growth, affects almost all tissue types; also increases lipolysis and decreases glucose uptake by tissue, and increases protein synthesis
ACTH stimulates adrenal cortex to release cortisol
TSH stimulate thyroid gland to release thyroid hormone
Testosterone responsible for male sexual characteristics, has anabolic affect on tissue
Generated by Koofers.com
Estrogen responsible for female sexual characteristics
Progesterone instrumental during pregnancy and in regulating menstrual cycle (increases body temp)
Thyroid Hormone (T3 and T4) increases metabolic activity of virtually all tissues, increases intestinal glucose absorption, increases lipolysis, (usuall T4 converted to T3 in cell)
Cortisol (glucocorticoid) facilitates response to stress, catabolic (breaks down) effects on protein, fat, stimulates gluconeogenesis (making of glucose from non-carb precursors)
Generated by Koofers.com
Aldosterone (mineralocorticoid) controls rate of Na+ loss in renal systems)
Pancreas islets of Langerhans are endocrine units of the organ, alpha cells: produce and secrete Glucagon, beta cells: produce and secrete insulin
Insulin affects ~ 80% of all cells, most important to muscle, adipose, liver; a) regulates blood glucose levels (decreases), b) increases cellular uptake of glucose, FAs & amino acids, c) glucose taken in and enzymes that control glycogen synth. are stimulated (inhibits glycolysis & glyconeogenesis), d) FAs are transported to and taken in by adipose cells and converted to triglycerides (inhibits lipase activity), e) AAs transported to and taken in by several cell types (muscle); increases protein synth. via increase rate of transcription and translation, decreases rate of proteolysis, anabolic (puts together, stores)
Glucagon typically has opposite effects of insulin, if blood glucose decresased, glucagon secreted to restore glucose levels to normal; a) stimulates glycongenolysis, b) stimulates gluconeogenesis, both occur in liver and increase blood glucose, stimulates lipolysis and release of FAs; catabolic (breaks down for usage)
Generated by Koofers.com
gluconeogenesis making glucose from non-carbohydrate precursors
glucose sugars
glycolysis breaking down sugars (to give ATP)
glycogen stored glucose
Generated by Koofers.com
glycogenolysis break down of glycogen in blood stream (to release glucose)
Adrenal Medulla innermost portion of gland, only 10-20% of total mass, synth. and secretes catecholamines (affect virtually all tissues, prepare for fight/flight, epi, norepi, dopamine), [tyrosine-->DOPA-->Dopamine-->Norepi-->Epi], catecholamines stored w/in glnad and released upon stimulation by sympathetic nervous system or hypoglycemia (low blood sugar) or exercise, (fight/flight: increase blood glucose , increase lipolysis, increase heart rate and stroke volume, vasodilation of coronary & skeletal blood vessels, vasoconstriction at viscera)
Muscle 3 Types: 1. Skeletal, 2. Smooth, 3. Cardiac
Skeletal Muscle composed of individual muscle fibers (polynucleated), fibers developed from myoblasts (mononucleated), each fiber surrounded by endomysium, bundle of fibers form fascidle (encased by perimysium), many faciculi comprise whole muscle (encased by epimysium), each fiber contains several hundred to several thousand myofibrils (imagine a rope made of strands), myofibrils made up of myofilaments (thick and thin)
Generated by Koofers.com
Myofilaments 1. Actin (thin)--troponin, tropomyosin, composed of two chains (double helix), w/in groove is tropomyosin which contains troponin complexes; 2. Myosin (thick)--composed of six chains (2 heavy, 4 light), heavy chains form double helix, at end of each chain MHC forms globular head (cross bridge); thick/thin filaments arranged in highly structured pattern resulting in dArk A bands and lIght I bands
Sarcomere single contractile unit
Muscle contraction caused by sliding of filaments, myosin cross-bridges act as ATPase, when ATP cleaved to ADP & Pi, myosin is "energized," step 1: binding of cross-bridge to binding site on actin, step 2: release of ADP & Pi allowing power stroke (pulls toward M line), step 3: new ATP molecule binds to cross-bridge, dissociates cross-bridge from actin, step 4: myosin ATPase cleaves ATP and again energizes myosin (cross-bridge extends toward new site on actin) **initiated by increase in cytosolic [Ca++]
Cytosolic increase in concentration of Ca++ Ca++ released from SR (sacrocplasmic Reticulum), Ca++ binds to troponin complex (T, I, and C subunits), conformational change in tropomyosin, exposes binding sites on actin; release of Ca++ caused by Excitation-Contraction Coupling
Generated by Koofers.com
Excitation-Contraction Coupling causes release of Ca++ from SR, End Plate Potential (EPP) generated by motor neuron evokes AP at sarcolemma, AP penetrates into fiber to individual myofibrils via T-tubules, membrane of T-tubule abuts that of SR at junctional feet, SR then stimulated to open Ca++ channels in its membrane, increased amounts of Ca++ flood into cytosol (contractile activity continues as long as cystolic Ca++ is increased)
What stops contraction? Ca++ pumps located in SR membrane (pump Ca++ back in--is constantly "on"), w/o additional electrical stimulation, cytosolic Ca++ is decreased, Ca++ binding to troponin decreases and binding sites on actin are masked
Tension force exerted by contracting muscle
Load force (resistance) exerted by object opposing contracting muscle
Generated by Koofers.com
Isometric Contraction (Same Length) tenstion developed w/o movement of load
Isotonic Contraction (Same Resistance) constant tension developed accompanied by movement (change) of load; a) concentric--shortening of muscle (tension>load), b) eccentric--lengthening of muscle (load>tension)
Isokinetic Contraction (Same rate of movement) tension developed w/ constant rate of movement (change) of load
Muscle Twitch mechanical response of muscle to single AP
Generated by Koofers.com
Latent Period duration between AP and muscle twitch, associated w/ EC coupling
Contraction Time period between end of latent period and peak force generation, different among fiber types
Relaxation time period between peak tension and complete relaxation, different among fiber types
Summation duration of twitch ~ 100 times greater than that of AP, second twitch generated whiles first is still occuring, with repetitive APs, muscle contraction maintained (tetanus); unfused: begins to relax, fused: doesnt even begin to relax
Generated by Koofers.com
Motor Unit single motor neuron and all muscle fibers it innervates; (slow oxidative, fast oxidative glycolytic and fast glycolitic--additive: 1 first, if not enough add 2, if still not enough add 3)
Slow Oxidative (Motor Unit) few fibers per unit, slow rate of nervous conduction and contraction, fatigue resistant, small fibers [daily actions] (Type I fibers)
Fast Oxidative Glycolytic (Motor Units) greater # fibers per unit, fairly fatigue resistant, fast conduction and contraction, larger fibers [used sometimes] (Type II A fibers)
Fast Glycolytic (Motor Units) greatest # fibers per unit, fatigue quickly, fast conduction and contraction, large fibers [extreme cases] (Type II B) -- humans dont have type II B, but do have type II X
Generated by Koofers.com
Amount of tension develeped by whole muscle determined by 1. amount of tension developed by each fiber, 2. # of fibers contracting, *force developed determined by # actomyosin complexes (the faster the sliding filaments go, the lower the chances of forming an actomyosin complex. the fewer the complexes, the less force)
Muscle Metabolism ATP needed by muscle to fuel contractile activity: 1. create kinase reaction (PC + ADP <--> ATP + C), 2. Anerobic metabolism (glycolysis), 3. Aerobic metabolism (oxidative phosphorylation); at low-moderate exercise intensity, rely almost exclusively on aerobic metabolism--as exercise intensity increases so does contribution of anerobic metabolism
Smooth Muscle essential for GI tract function, blood flow regulation, bladder function etc; innervated by autonomic (involuntary) nervous system; does contract via cross-bridge formation, but the mechanism and regulation is different than in skeletal muscle; fibers are spindle shaped and smaller than skeletal muscle fibers; fibers are mononucleated, w/ smaller diameter and longer length; different proportions of actin/myosin; contractile filaments are diagonal, w/ contraction fiber shortens/widens, tension developed still affected by length, but range is greater than in skeletal muscle
Mechanisms of Smooth Muscle Contraction initiated by increase in cytosolic [Ca++], but process is different than in skeletal muscle; actin has no troponin or tropomyosin, rather increased Ca++ affects myosin (1. Ca++ binds to calmodium, 2. Ca++/calmodium complex binds to MLCK-myosin light chain kinase, 3. Phosphorylates myosin cross-bridges, 4. Phosphorylated cross-bridges bind to actin, 5. Cross-bridge cycling) *change in myosin, not actin that allows cross-bridge cycling, *myosin x-bridge does have ATPase, but less than skeletal muscle; contraction stops when cytosolic Ca++ decreases & action of myosin phosphatase
Generated by Koofers.com
More Smooth Muscle Contraction Rate of cross-bridge cycling much slower than in skeletal muscle, energetics of cross-bridge cycling much more efficient than in skeletal muscle, "Latch Mechanism"--once full contraction achieved, degree of activation need only be fraction of that needed to initiate contraction
What results in increase of Cytosolic [Ca++] (smooth muscle) 1. Release from SR--(a) no T-tubules, but SR membrane close to cell membrane and electrical excitation of cell membrane opens Ca++ channels of SR, (b) influx of extracellular Ca++ then causes Ca++ channels of SR to open (calcium induced calcium release), (c) hormone binding to cell membrane causes breakdown of PIP2 to IP3 (releases Ca++ from SR); 2. Influx of extracellular Ca++--there are voltage & ligand gated channels on cell membrane so depolarization of membrane opens voltage gated channels and binding of hormones and cytokines open ligand gated channels (most from extracellular)
Causes of Smooth Muscle Stimulation 1. Spontaneous Electrical Activity (Pacemaker Potential); 2. Neural Stimulation; 3. Hormones; 4. Local tissue factors
Spontaneous electrical Activity (Pacemaker Potential) (of smooth muscle) controls contractions of gut, increases leakiness of cell membrane to Ca++, gradually causes AP (not all smuscles have leaky membrane), stimulation transmitted to other fibers via "gap junctions"
Generated by Koofers.com
Neural Stimulation (of smooth muscle) controlled by autonomic nervous system, releases norepi (excite) and acetylcholine (inhibit), (skeletal muscle receives only excitatory input), Neuro-Muscular Juncion (NMJ) has specialized end plate region, rather called "diffuse junction" to release a neurotransmitter to affect several cells, Ca++ channels, not Na+ channels evoke AP, current travels along cell membrane that eventualy abuts membrane of SR **Caveoli: like T-tubules, not as deep, just little pot-holes
Hormones (smooth muscle excitation) virtually all smooth muscle fibers respond to circulating hormones (epi, norepi, oxytocin, histamine, etc), binding of hormone can open membrane channels or activate intracellular 2nd messenger system
Local Tissue Factors (smooth muscle excitation) (smooth muscle in blood vessels), decreased oxygen, increased CO2 and decreased pH (lactic acid) causes smooth muscle relaxation and vasodilation, also increased K+, decreased Ca++ and increased adenosine
Types of Smooth Muscle 1. Multiunit: comprised of independently functioning fibers, mainly controlled by neural input (can be altered by hormones), usually innvervated by single nerve ending (ciliary muscles of eye, iris of eye, large arteries, piloerector muscles); 2. Single Unit: not single fibers, but large groups of fibers that contract as a unit (syncytial contraction), contract together bc joined by gap junctions, contraction initiated by few cells in unit that generate pacemaker potentials (gut, uterus, small blood vessels, most of viscera)
Generated by Koofers.com

List View: Terms & Definitions

  Hide All 92 Print
 
Front
Back
 Sensory Systems (parts)1. Receptors 2. Neural Pathway 3. Brain
 ReceptorsSpecialized cells or specialized endings of afferent neurons
 5 Types of Neurons1. mechanoreceptors (touch) 2. thermoreceptors (temp) 3. nociceptors (pain) 4. electromagnetic (light) 5. chemoreceptors (taste, smell, oxygen, osmolarity, etc)
 TransductionRegardless of original form of stimulus, it must be changed into electrical energy (occurs at receptor); results in "receptor potential," this is local graded potential. if receptor potential is of sufficient intensity by the time or arrival at first Node of Ranvier, AP will result
 Receptor fieldarea of body covered by receptors from a single afferent neuron
 Sensory Unitsingle afferent neuron and all of its receptors; strength of stimulus is proportional to strength of response because more receptor potential exceeds threshold, and the greater the frequency of its APs
 acuitytelling the difference between two stimuli
 Adaptationat constant stimulus intensity, receptors gradually become desensitized (decreased rate of AP firing). Two kinds: 1. Phasic (fast), 2. Tonic (slow)
 Neural (ascending) Pathwaysafferent neurons carry info to specific brain regions; several classes based on size and thus speed of conduction; Primary (1st order) neuron synapse w/ interneurons in spinal cord or brain; usually converge or diverge
 divergenceinfo from single afferent neuron synapses w/ many interneurons
 Convergenceinfo from many afferent neurons arrive at same interneuron
 2 Classification schemes of Neural PathwaysFirst: A) Specific ascending pathways (carry info about single type of stimulus) B) Nonspecific ascending pathways (carry info about several different types of stimuli); Second: A) Dorsal column lemniscal system, B) Anterolateral System
 Speed of synapse through pathwayUrgent: 110-120 m/s, Not Urgent: 5 m/s
 Second classification scheme of Neural Pathways(A) Dorsal column lemniscal system: carries info in dorsal columns of spinal cord (white matter), info crosses to opposite side in medulla, through brainstem to thalamus via lemniscus, composed of large myelinated nerve fibers (110 m/s), higher degree of spatial orientation (phasic info, position info, touch using spatial accuracy, pain); (B) Anterolateral System: carries info in dorsal horns of cords gray matter, info crosses immediately, transmits to brainstem and thalamus, unmyelinated (40 m/s), poor spatial orentation, carries several different types (pain, thermal, crude touch, pressure)
 Braininterprets sensory info, from thalamus and brainstem info delivered to specific parts of cerebral cortex, results in perception, sensory systems code 4 aspects of stimulus: 1. Type, 2. Intensity, 3. Location, 4. Duration
 Types of Stimulia. chemical, b. taste, c. smell, d. somatosensory, e. muscle, f. balance, g. hearing, h. vision
 Intensity of stimulidetermined by frequency of AP firing and # of receptors stimulated
 Location of stimuli(acuity of stimulus location), the smaller the receptive field, the greater the acuity; the greater the degree of convergence in ascending pathway, the lower the acuity
 Duration of Stimulireceptors have different rates of adaptation, rapidly vs slowly (phasic vs tonic)---> how long do you need to know it?
 Hormonal (endocrine) Systemprimarily controls metabolic functions of body; effects of some hormones occur in seconds, other homrones continue to regulate functions for weeks; hormones produced and released by endocrine glands, carried away by blood, and then affect target cells; a single endocrine gland may secret more than one hormone, but single cell type secretes only one type
 3 Basic types of hormones1. amine hormones, 2. peptide hormones, 3. steroid hormones, *remember: receptors for hormones are proteins
 Amine hormonesderived from tyrosine, include thyroid hormones and catecholamines (epi and norepi)
 Peptide hormonesundergo extensive processing before secretion, easily destroyed, soluble in plasma [preprohormone (ribosome)-->prohormone (ER)-->hormone (Golgi Aparatus), then stored in vesiciles and leave via exocytosis]
 Steroid hormonesderived from cholesterol, specific steroidogenic enzymes in cell determines which steroids produced, easily diffuse across membrane (no intracellular storage), not soluble in plasma, once in circulation combine w/ binding proteins, only small fraction of "free" (bioactive) steroids, lipid based
 Mechanism of Endocrine ResponseA) receptors for catecholamines and peptide hormones are ON cell membrane, upon binding intracellular 2nd messenger is activated (usually cAMP), [binding-->G protein-->increase adenylate cylase-->ATP to cAMP-->protein kinase activation-->phosphorylation of enzyme, biological response fairly swift; B) receptors for steroid and thyroid hormones found withIN cells (cytosol/nucleus), bc lipids can pass thru membrane, upon binding hormone/receptor complex interacts w/ DNA as transcription regulating factor, usually slower biologcial response (new data says that some steroids are fast acting)
 Features of hormonal action1. actions greatly amplified at target cells, 2. regulate rates of existing reactions, not initiate new ones, 3. actions are typically slow and prolonged, esp steroids, 4. in general biolocial effect of hormoneis proportional to circulating concentration of that hormone (circulating levels of any hormone determined by rat)e of secretion and rate of removal--metabolism
 Secretionmost hormones show pulsatile release (not constant steady dribble, more like heartbeat), show circadian rhythm, types of input affecting release: a)change in plasma concentration of mineral ions, b)change in plasma concentrations of nutrients, c)neurotransmitters released from neurons, d) other hormones or paracrien agents
 Metabolismusually occurs in liver and kidneys, to small extent w/in target cells, peptide hormones broken down by specific peptidases, steroids undergo series of reduction reactions that make them water soluble (adding electrons), urine is main route of excretion of hormone metabolism (small amounts of intact hormones also excreted via urine)
 Hypothalamic-Pituitary pathwayHypothalamus is part of brain (stimulated by neurons), pituitary is gland at base of brain (master gland), hypothalamus conveys info to pituitary either by neurons or by blood vessels, 2 sections of pituitary (hypophysis): a)posterior pituitary (neurohypophysis)-back, b)anterior pituitary (adenohypophysis)-front
 Posterior Pituitaryreceives direct neural input from hypothalamus, releases ADH (vasopressin) and oxytocin into bloodstream, ADH works in renal system to control excretion of H20, oxytocin causes contraction of pregnant uterus and ejection of milk from breasts (remember: prolactin produces milk)
 Anterior Pituitaryreceives input from hypothalamus from blood (portal vessels) carrying hypophysiotropic hormones that control secretion of hormones from anterior pituitary
 Thyrotropin releasing hormone (TRH)stimulates release of thyroid stimulating hormone (TSH) and prolactin
 Corticotropin releasing hormone (CRH)stimulates secretion of adrenocorticotropin (ACTH)
 Growth Hormone releasing hormone (GHRH)stimulates release of Growth Hormone (GH)
 Somatostatin (SS)inhibits GH secretion
 Gonadotropin releasing hormone (GnRH)stimulates secretion of Leutinizing hormone (LH) and follicle stimulating hormone (FSH)
 dopamine (prolactin release inhibiting hormone--PIH)inhibits secretion of prolactin
 Follicle Stimulating Hormone (FSH)stimulates growth and development of ovarian follicles, controls spermatogenesis
 Leutanizing Hormone (LH)regulate steroidogenesis of gonads (male and female)
 Prolactinenhances breast development and milk production
 Growth Hormonemajor stimulus of postnatal growth, affects almost all tissue types; also increases lipolysis and decreases glucose uptake by tissue, and increases protein synthesis
 ACTHstimulates adrenal cortex to release cortisol
 TSHstimulate thyroid gland to release thyroid hormone
 Testosteroneresponsible for male sexual characteristics, has anabolic affect on tissue
 Estrogenresponsible for female sexual characteristics
 Progesteroneinstrumental during pregnancy and in regulating menstrual cycle (increases body temp)
 Thyroid Hormone(T3 and T4) increases metabolic activity of virtually all tissues, increases intestinal glucose absorption, increases lipolysis, (usuall T4 converted to T3 in cell)
 Cortisol(glucocorticoid) facilitates response to stress, catabolic (breaks down) effects on protein, fat, stimulates gluconeogenesis (making of glucose from non-carb precursors)
 Aldosterone(mineralocorticoid) controls rate of Na+ loss in renal systems)
 Pancreasislets of Langerhans are endocrine units of the organ, alpha cells: produce and secrete Glucagon, beta cells: produce and secrete insulin
 Insulinaffects ~ 80% of all cells, most important to muscle, adipose, liver; a) regulates blood glucose levels (decreases), b) increases cellular uptake of glucose, FAs & amino acids, c) glucose taken in and enzymes that control glycogen synth. are stimulated (inhibits glycolysis & glyconeogenesis), d) FAs are transported to and taken in by adipose cells and converted to triglycerides (inhibits lipase activity), e) AAs transported to and taken in by several cell types (muscle); increases protein synth. via increase rate of transcription and translation, decreases rate of proteolysis, anabolic (puts together, stores)
 Glucagontypically has opposite effects of insulin, if blood glucose decresased, glucagon secreted to restore glucose levels to normal; a) stimulates glycongenolysis, b) stimulates gluconeogenesis, both occur in liver and increase blood glucose, stimulates lipolysis and release of FAs; catabolic (breaks down for usage)
 gluconeogenesismaking glucose from non-carbohydrate precursors
 glucosesugars
 glycolysisbreaking down sugars (to give ATP)
 glycogenstored glucose
 glycogenolysisbreak down of glycogen in blood stream (to release glucose)
 Adrenal Medullainnermost portion of gland, only 10-20% of total mass, synth. and secretes catecholamines (affect virtually all tissues, prepare for fight/flight, epi, norepi, dopamine), [tyrosine-->DOPA-->Dopamine-->Norepi-->Epi], catecholamines stored w/in glnad and released upon stimulation by sympathetic nervous system or hypoglycemia (low blood sugar) or exercise, (fight/flight: increase blood glucose , increase lipolysis, increase heart rate and stroke volume, vasodilation of coronary & skeletal blood vessels, vasoconstriction at viscera)
 Muscle3 Types: 1. Skeletal, 2. Smooth, 3. Cardiac
 Skeletal Musclecomposed of individual muscle fibers (polynucleated), fibers developed from myoblasts (mononucleated), each fiber surrounded by endomysium, bundle of fibers form fascidle (encased by perimysium), many faciculi comprise whole muscle (encased by epimysium), each fiber contains several hundred to several thousand myofibrils (imagine a rope made of strands), myofibrils made up of myofilaments (thick and thin)
 Myofilaments1. Actin (thin)--troponin, tropomyosin, composed of two chains (double helix), w/in groove is tropomyosin which contains troponin complexes; 2. Myosin (thick)--composed of six chains (2 heavy, 4 light), heavy chains form double helix, at end of each chain MHC forms globular head (cross bridge); thick/thin filaments arranged in highly structured pattern resulting in dArk A bands and lIght I bands
 Sarcomeresingle contractile unit
 Muscle contractioncaused by sliding of filaments, myosin cross-bridges act as ATPase, when ATP cleaved to ADP & Pi, myosin is "energized," step 1: binding of cross-bridge to binding site on actin, step 2: release of ADP & Pi allowing power stroke (pulls toward M line), step 3: new ATP molecule binds to cross-bridge, dissociates cross-bridge from actin, step 4: myosin ATPase cleaves ATP and again energizes myosin (cross-bridge extends toward new site on actin) **initiated by increase in cytosolic [Ca++]
 Cytosolic increase in concentration of Ca++Ca++ released from SR (sacrocplasmic Reticulum), Ca++ binds to troponin complex (T, I, and C subunits), conformational change in tropomyosin, exposes binding sites on actin; release of Ca++ caused by Excitation-Contraction Coupling
 Excitation-Contraction Couplingcauses release of Ca++ from SR, End Plate Potential (EPP) generated by motor neuron evokes AP at sarcolemma, AP penetrates into fiber to individual myofibrils via T-tubules, membrane of T-tubule abuts that of SR at junctional feet, SR then stimulated to open Ca++ channels in its membrane, increased amounts of Ca++ flood into cytosol (contractile activity continues as long as cystolic Ca++ is increased)
 What stops contraction?Ca++ pumps located in SR membrane (pump Ca++ back in--is constantly "on"), w/o additional electrical stimulation, cytosolic Ca++ is decreased, Ca++ binding to troponin decreases and binding sites on actin are masked
 Tensionforce exerted by contracting muscle
 Loadforce (resistance) exerted by object opposing contracting muscle
 Isometric Contraction(Same Length) tenstion developed w/o movement of load
 Isotonic Contraction(Same Resistance) constant tension developed accompanied by movement (change) of load; a) concentric--shortening of muscle (tension>load), b) eccentric--lengthening of muscle (load>tension)
 Isokinetic Contraction(Same rate of movement) tension developed w/ constant rate of movement (change) of load
 Muscle Twitchmechanical response of muscle to single AP
 Latent Periodduration between AP and muscle twitch, associated w/ EC coupling
 Contraction Timeperiod between end of latent period and peak force generation, different among fiber types
 Relaxation timeperiod between peak tension and complete relaxation, different among fiber types
 Summationduration of twitch ~ 100 times greater than that of AP, second twitch generated whiles first is still occuring, with repetitive APs, muscle contraction maintained (tetanus); unfused: begins to relax, fused: doesnt even begin to relax
 Motor Unitsingle motor neuron and all muscle fibers it innervates; (slow oxidative, fast oxidative glycolytic and fast glycolitic--additive: 1 first, if not enough add 2, if still not enough add 3)
 Slow Oxidative (Motor Unit)few fibers per unit, slow rate of nervous conduction and contraction, fatigue resistant, small fibers [daily actions] (Type I fibers)
 Fast Oxidative Glycolytic (Motor Units)greater # fibers per unit, fairly fatigue resistant, fast conduction and contraction, larger fibers [used sometimes] (Type II A fibers)
 Fast Glycolytic (Motor Units)greatest # fibers per unit, fatigue quickly, fast conduction and contraction, large fibers [extreme cases] (Type II B) -- humans dont have type II B, but do have type II X
 Amount of tension develeped by whole muscle determined by1. amount of tension developed by each fiber, 2. # of fibers contracting, *force developed determined by # actomyosin complexes (the faster the sliding filaments go, the lower the chances of forming an actomyosin complex. the fewer the complexes, the less force)
 Muscle MetabolismATP needed by muscle to fuel contractile activity: 1. create kinase reaction (PC + ADP <--> ATP + C), 2. Anerobic metabolism (glycolysis), 3. Aerobic metabolism (oxidative phosphorylation); at low-moderate exercise intensity, rely almost exclusively on aerobic metabolism--as exercise intensity increases so does contribution of anerobic metabolism
 Smooth Muscleessential for GI tract function, blood flow regulation, bladder function etc; innervated by autonomic (involuntary) nervous system; does contract via cross-bridge formation, but the mechanism and regulation is different than in skeletal muscle; fibers are spindle shaped and smaller than skeletal muscle fibers; fibers are mononucleated, w/ smaller diameter and longer length; different proportions of actin/myosin; contractile filaments are diagonal, w/ contraction fiber shortens/widens, tension developed still affected by length, but range is greater than in skeletal muscle
 Mechanisms of Smooth Muscle Contractioninitiated by increase in cytosolic [Ca++], but process is different than in skeletal muscle; actin has no troponin or tropomyosin, rather increased Ca++ affects myosin (1. Ca++ binds to calmodium, 2. Ca++/calmodium complex binds to MLCK-myosin light chain kinase, 3. Phosphorylates myosin cross-bridges, 4. Phosphorylated cross-bridges bind to actin, 5. Cross-bridge cycling) *change in myosin, not actin that allows cross-bridge cycling, *myosin x-bridge does have ATPase, but less than skeletal muscle; contraction stops when cytosolic Ca++ decreases & action of myosin phosphatase
 More Smooth Muscle ContractionRate of cross-bridge cycling much slower than in skeletal muscle, energetics of cross-bridge cycling much more efficient than in skeletal muscle, "Latch Mechanism"--once full contraction achieved, degree of activation need only be fraction of that needed to initiate contraction
 What results in increase of Cytosolic [Ca++] (smooth muscle)1. Release from SR--(a) no T-tubules, but SR membrane close to cell membrane and electrical excitation of cell membrane opens Ca++ channels of SR, (b) influx of extracellular Ca++ then causes Ca++ channels of SR to open (calcium induced calcium release), (c) hormone binding to cell membrane causes breakdown of PIP2 to IP3 (releases Ca++ from SR); 2. Influx of extracellular Ca++--there are voltage & ligand gated channels on cell membrane so depolarization of membrane opens voltage gated channels and binding of hormones and cytokines open ligand gated channels (most from extracellular)
 Causes of Smooth Muscle Stimulation1. Spontaneous Electrical Activity (Pacemaker Potential); 2. Neural Stimulation; 3. Hormones; 4. Local tissue factors
 Spontaneous electrical Activity (Pacemaker Potential) (of smooth muscle)controls contractions of gut, increases leakiness of cell membrane to Ca++, gradually causes AP (not all smuscles have leaky membrane), stimulation transmitted to other fibers via "gap junctions"
 Neural Stimulation (of smooth muscle)controlled by autonomic nervous system, releases norepi (excite) and acetylcholine (inhibit), (skeletal muscle receives only excitatory input), Neuro-Muscular Juncion (NMJ) has specialized end plate region, rather called "diffuse junction" to release a neurotransmitter to affect several cells, Ca++ channels, not Na+ channels evoke AP, current travels along cell membrane that eventualy abuts membrane of SR **Caveoli: like T-tubules, not as deep, just little pot-holes
 Hormones (smooth muscle excitation)virtually all smooth muscle fibers respond to circulating hormones (epi, norepi, oxytocin, histamine, etc), binding of hormone can open membrane channels or activate intracellular 2nd messenger system
 Local Tissue Factors (smooth muscle excitation)(smooth muscle in blood vessels), decreased oxygen, increased CO2 and decreased pH (lactic acid) causes smooth muscle relaxation and vasodilation, also increased K+, decreased Ca++ and increased adenosine
 Types of Smooth Muscle1. Multiunit: comprised of independently functioning fibers, mainly controlled by neural input (can be altered by hormones), usually innvervated by single nerve ending (ciliary muscles of eye, iris of eye, large arteries, piloerector muscles); 2. Single Unit: not single fibers, but large groups of fibers that contract as a unit (syncytial contraction), contract together bc joined by gap junctions, contraction initiated by few cells in unit that generate pacemaker potentials (gut, uterus, small blood vessels, most of viscera)
36, "/var/app/current/tmp/"