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305 Cards in this Set
- Front
- Back
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physiology |
studyof how living organisms function |
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pathophysiology |
thestudy of the mechanisms of disease states |
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cells |
simpleststructural units of an organism that can retain the functions characteristic oflife |
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cell differentiation |
process of transforming an unspecialized cellinto a specialized cell About 200 types of cells |
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4 categories of cells |
muscle,neurons, epithelial, connective |
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3 types of muscle cells |
skeletal,cardiac, smooth |
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neuron |
cellof the nervous system that is specialized to initiate, integrate, and conductelectrical signals to other cells |
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nerve |
carriessignals between nervous system and rest of body |
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function of epithelial |
Selectivesecretion and absorption of ions and organic molecules and for protection |
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basement membrane |
extracellularprotein layer that anchors the epithelial cells |
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basolateral |
sideof cell towards basement membrane |
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apical |
sideof cell opposite basement membrance |
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function of connective tissue |
onnect,anchor, support structures of the body |
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loose connective |
loosemeshwork underlying epithelial layers |
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dense connective |
tough,rigid; tendons/ligaments |
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extracellular matrix |
Mixture of proteins, polysaccharides, minerals |
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function of extracellular matrix |
cellularattachments; transmits information through chemical messengers to regulateactivity, migration, growth, differentiation |
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organ systems |
circulatory, digestive, endocrine (glands), immune (WBC and producing organs), integumentary(skin), lymphatic, musculoskeletal, nervous, reproductive, respiratory, urinary |
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intracellular fluid |
fluid within cells 67% of fluid in body |
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extracellular fluid |
fluid outside cells 20-25% Plasma: fluid portion of blood (7% oftotal body water) 75-80% Interstitial fluid |
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homeostasis |
stateof reasonably stable balance between physiological variables dynamic constancy |
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general chacteristics of homeostatic control systems |
steady state feedback systems resetting of set points feedforward regulation |
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steady state |
asystem in which a particular variable is not changing but in which energy mustbe added continuously to maintain a constant condition |
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negative feedback |
increase/decrease in the variable beingregulated brings about responses that tend to move the variable in the oppositedirection to the original change |
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positive feedback |
accelerates a process- explosive system |
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feedforward |
changesin regulated variables are anticipated and prepared for before they actuallyoccur |
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reflex |
specific,involuntary, unpremeditated response to a particular stimulus |
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afferent pathway |
-brings signal from receptor to integrating center |
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effector |
receives a command from integrating center toalter activity Muscles and glands, mostly |
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hormone |
type of chemical messenger secreted into bloodby cells of endocrine system |
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local homeostatic responses |
initiated by a change in the external/internalenvironment and induce an alteration of cell activity with the net effect ofcounteracting the stimulus Different from a reflex because of the localeffect |
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4 categories of messengers |
hormones,neurotransmitters, paracrine, autocrine substances |
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neurotransmitters |
chemical messengers released from endings ofneurons onto other neurons, muscles cells, or gland cells Diffuses through extracellular fluid to targetcell |
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paracrine substances |
chemicalmessengers involved in local communication |
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autocrine substances |
chemical secreted by a cell into extracellularfluid acts upon the same cell |
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gap junctions |
physical linkages connecting cytosol between 2cells Mlcs move directly between cells w/o enteringextracellular fluid |
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adaptation |
survival in specific environments (short term) |
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acclimatization |
improvedfunctioning of an already existing homeostatic system (long term) |
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circadian rhythm |
cycles approximately once every 24 hours Waking/sleeping; body temp; hormoneconcentrations Feedforward system |
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free running rhythm |
whena cycle persisted in the complete absence of environmental cues |
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general principles of physiology |
Homeostasis is essential for health and survival Functions of organ systems are coordinated witheach other Most physiological functions are controlled bymultiple regulatory systems, often working in opposition Information flow between cells, tissues, andorgans is an essential feature of homeostasis and allows for integration ofphysiological processes Controlled exchange of materials occurs betweencompartments and across cellular membranes Physiological processes are dictated by the lawsof chemistry and physics. Physiological processes require the transfer andbalance of matter an energy Structure is a determinant of and has coevolvedwith function. |
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muscle fiber |
skeletal muscle cell |
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myoblasts |
undifferentiated mononucleated muscle cells Fuse to form muscle fibers Skeletal muscle differentiation completed aroundtime of birth |
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satellite cells |
undifferentiatedstem cells- aid in muscle repair Normally Quiescent (inactive) and locatedbetween plasma membrane and basement membrane Upon injury, divide into myoblasts that fusewith existing, damaged tissue or create new muscle fiber |
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quiescent |
inactive |
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myosin |
thick filament 2 large polypeptide heavy chains and foursmaller light chains Combine to form a molecule with 2 globular headsand a long tail (made from entwined heavy chains 2 Binding sites- for ATP and actin |
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thin filament |
Composed of actin, troponin, and tropomyosin Cross bridge binding sites on actin covered bytropomyosin |
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sarcomere |
oneunit of repeating pattern of thick and thin filaments |
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A band |
Thickfilaments in the middle create wide, dark band |
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H zone |
1. in middle of thick filament- only thick filament(no thin overlapping |
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M line |
incenter of A band- proteins linking together 2 adjacent thick filaments |
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Z line |
anchorsone side of thin filament; other end overlaps with thick filament |
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I band |
:area of thin filaments only (lighter in color); bisected by Z line |
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titin |
proteinextending from M line to Z line; maintain alignment of thick filaments inmiddle of sarcomere |
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1 thick filament is surrounded by how many thin filaments |
6 |
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sarcoplasmic reticulum |
endoplasmic reticulum for muscle fibers; forms aseries of sleevelike segments around each myofbril |
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terminal cisternae |
storesCa and releases into cytosol after membrane excitation |
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transverse tubule |
between terminal cisternae of adjacent segments Continuous with sarcolemma (plasma membrane formuscle fibers) Lumen continuous with extracellular fluid Brings Action potentials to interior of musclefiber |
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motor neurons |
(somaticefferent)- axons innervate skeletal muscle fibers; cell bodies in brain stem/SC myelinated axons and large diameter- high velocity signals |
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motor unit |
motor neuron and all the muscles fibers itinnervates When motor neuron activated- all muscles fibersit innervates stimulated |
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motor end plate |
plasmamembrane that lies directly under terminal portion of axon |
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neuromuscular junction |
Axon terminal of motor neuron Vesicles containing acetylcholine (Ach) motor end plate always excitatory |
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explain the steps of membrane excitation |
1. Action potential in motor neuron arrives at axonterminal and depolarizes plasma membrane 2. Voltage sensitive Ca channels open and allow Cainto axon terminal 3. Ca binds to proteins that enable membranes ofACh vesicles to bind to neuronal plasma membrane 4. ACh is released into extracellular cleft anddiffuses to motor end plate. 5. Nicotinic ionotropic receptors bind ACh andopens ion channel in each receptor protein (Na and K can pass) 6. More Na enters motor end plate than K leaving sodepolarizes (end-plate potential- EPP) 7. Action potential propagated across muscle fiberand into T-Tubules |
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acetylcholinesterase |
enzyme in synaptic junction that breaks down ACh Choline transported back into axon terminals tobe reused for new ACh As less ACh available for receptors becausebeing broken down, ion channels in end plate will close End plate returns to resting potential |
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curare |
deadlyarrowhead poison; binds to nicotinic ACh receptors and doesn’t open ionchannels; not destroyed by acetylcholinesterase; no contraction |
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inhibited acetylchoinesterase (nerve gases and organophosphates) |
ACh not removed from synaptic junction Ion channels desensitived to ACh and causesmuscle paralysis Build up of ACh at muscarinic synapses,parasympathetic, slow HR |
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pralidoxime |
reactivatesacetylcholinesterase |
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atropine |
a. muscarinic receptor antagonist |
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succinylcholine |
a. antagonist to ACh receptors- acts likeacetylcholinesterase inhibitors |
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rocuronium and vecuronium |
act like curare bindsto nicotinic ACh receptors and doesn’t open ion channels |
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Clostridium Botulinum toxin |
Blocks release of ACh from axon terminals Breaks down proteins of SNARE complex which arenecessary for fusion of vesicles to plasma membrane |
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excitation contraction coupling |
Sequence of events by which an action potentialin the plasma membrane activates the force generating mechanisms |
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3 subunits of troponin |
I (inhibitory), T (Tropomyosin-binding), C (Cabinding) |
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function of ca in cross bridge formation |
When Ca binds to troponin, changes shape whichallows tropomyosin to move away from myosin binding site on actin Ca concentration determines number of actinsites available for cross bridges |
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Dihydropyridine(DHP) receptor |
T-tubuleprotein that is a voltage sensitive Ca channel- voltage sensor |
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ryanodine receptor |
proteinin sarcoplasmic reticulum membrane; connects to DHP and forms Ca channel |
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cystolic increase in Ca |
During action potential changes to DHP receptortrigger opening of Ca channel in ryanodine receptor Ca released from terminal cisternae into cytosolwhere it can bind to troponin |
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what happens to Ca when it is removed from troponin |
a. Ca-ATPases pump Ca ions from cytosol back intolumen of reticulum |
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cross bridge cycle |
timea cross-bridge binds to a thin filament, moves, and repeats |
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how are cross bridges detached? |
a. Another ATP molecule detaches actin and myosin-allosteric modulator (doesn’t actually utilize energy from ATP) |
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rigor mortis |
i. gradual stiffening of skeletal muscles thatbegins several hours after death ATP no longer being supplied and so links ofcross bridges cannot be broken |
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tension |
forceexerted on an object by a contracting muscle |
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load |
forceexerted on muscle by an object |
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twitch |
i. mechanical response of a muscle fiber to asingle action potential |
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latent period |
i. time between action potential and tension inmuscle fiber begins to increase |
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contraction time |
i. time from beginning of tension development atend of latent period to peak tension |
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summation |
-increase in muscle tension from successive action potentials occurring duringthe phase of mechanical activity |
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tetanus |
maintainedcontraction in response to repetitive stimulation |
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unfused tetanus |
tensionoscillates as the muscle fiber partially relaxes between stimuli |
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fused tetanus |
no oscillations- produced at higher stimulationfrequencies 3-5x greater tension than isometric twitchtension Ca remains elevated in cytosol (successiveaction potentials don’t give it enough time to be pumped back in tosarcoplasmic reticulum) |
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optimal length |
lengthat which the muscle fiber develops the greatest isometric active tension |
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creatine phosphate |
i. Small molecule produced from 3 amino acids andcapable of functioning as a phosphate donor ii. Phosphorylates ADP to supply ATP in demand atskeletal muscle |
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where is ATP obtained for muscle contractions |
Creatine phosphate oxidative phosphorylation glycolysis |
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oxygen debt |
increasedproduction of ATP by oxidative phosphorylation following exercise is used torestore the energy reserves in the form of creatine phosphate and glycogen |
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muscle fatigue |
declinein muscle tension as a result of previous contractile activity decreased shortening velocity slower rate of relaxation |
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central command fatigue |
appropriateregions of the cerebral cortex fail to send excitatory signals to motor neurons |
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myoglobin |
-oxygen binding protein; increases rate of oxygen diffusion into fiber andprovides small store of O2 |
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oxidative fibers |
contain numerous mitochondria- high capacity foroxidative phosphorylation Dependent on blood flow for O2- surrounded bysmall blood vessels |
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glycolytic fibers |
few mitochondria; high concentration of glycolyticenzymes and large store of glycogen larger diameters than oxidative- greater ability to develop tension |
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3 types of skeletal muscle fibers |
Slow oxidative fibers (Type I) fast oxidative glycolytic fibers (Type IIa) fast glycolytic fibers (type IIb) |
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effect of motor unit size |
Smaller motor units for finer control, moredelicate tasks; addition of motor unit doesn’t cause a huge increase in tension |
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order motor units are activated |
slow oxidative--> fast oxidative glycolytic--> fast glycolytic |
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denervation atrophy |
denervatedmuscle fibers become progressively smaller in diameter and the amount ofcontractile proteins they contain decreases |
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disuse atrophy |
atrophyof muscles from disuse for a long period of time |
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effect of low intensity exercise |
long duration- aerobic Increases in number of mitochondria in fibersrecruited Increase in capillaries around fibers Leads to increase in capacity for enduranceactivity with min fatigue |
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effect of high intensity exercise |
short duration- strength training Affects primarily fast twitch fibers Increase in diameter (hypertrophy) fromsatellite cell activation and increased actin and myosin Exercise doesn’t have a lg effect on type ofmuscle fiber Does effect synthesis of metabolic enzymes socan change from oxidative to glycolytic |
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myostatin |
regulatory protein produced by skeletal musclecells and binds to receptors on those same cells; negative feedback to preventexcessive muscle hypertrophy |
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effect of aging on muscle |
Max force a muscle can generate decreases by30-40% from age 30-80 |
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exercise induced muscle soreness |
Damage to muscle cells causing inflammatoryresponse Histamine released by immune system activateendings of pain neurons Lengthening contractions (eccentriccontractions) cause Eccentric contractions linked to more strength |
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poliomyelitis |
viral disease that destroys motor neuronsleading to paralysis of skeletal muscle (bad for muscles of respiration) |
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muscle cramps |
involuntary tetanic contraction of skeletalmuscle Action potentials fire at abnormally high rates |
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hypocalcemic tetany |
involuntary tetanic contraction of skeletalmuscles that occurs when the extracellular Ca concentration decreases to about40% of its normal value EXTRACELLULAR (not sarcoplasmic reticulum Ca) Low Ca increases opening of Na channels inexcitable membranes- depolarization |
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muscular dystrophy |
genetic disease affecting one in 3500 males(fewer females)- progressive degeneration of skeletal and cardiac musclefibers, weakening muscles and leading to death from respiratory/cardiac failure |
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cause of muscular dystrophy |
absence/defect of one/more proteins that make upthe costameres in striated muscle |
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costamere |
cluster of structural and regulatory proteinsthat link the Z disks of the outermost myofibrils to the sarcolemma andextracellular matrix |
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duchenne muscular dystrophy |
sexlinked recessive disorder caused by mutation in a gene on the X chromosome thatcodes for dystrophin (costamere protein) Fibers subjected to repeated structuraldeformation during contraction susceptible to membrane rupture and cell death Condition progresses with muscle use and age proteins |
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dystrophin |
formslink between actin and proteins of the sarcolemma |
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myasthenia gravis |
neuromuscular disorder characterized by musclefatigue and weakness that progressively worsen as the muscle is used cause: destruction of nicotinic ACh receptor proteins of motor end plate by antibodiesof immune system |
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pyridostigmine |
(acetylcholinesteraseinhibitor): Compensates for reduction in available ACh receptors by prolongingtime ACh in synapse |
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thymectomy |
removalof thymus= reduces production of antibodies |
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plasmaheresis |
replacingplasma of blood that contains antibodies |
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treatment for myasthenia gravis |
pyridostigmine glucocorticoids thymectomy plasmapheresis |
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caldesmon |
in smooth muscle associates with thin filaments |
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dense bodies |
cytoplasmicstructures in smooth muscle that are functionally similar to Z lines inskeletal muscle |
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cross bridge activation for smooth muscle |
1. Cross bridge cycling controlled by CA regulatedenzyme that phosphorylates myosin 2. CA binds to calmodulin 3.Ca calmodulin complex binds to myosin lightchain kinase (protein) and activates the enzyme 4. Active myosin light chain kinase uses ATP tophosphorylate myosin light chains in globular head of myosin 5. Phosphorylation of myosin drives cross bridgeaway from thick filament backbone allowing it to bind to actinSlower muscle shortening velocity; not fatigable |
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latch state |
tensionremains even though rate of ATP hydrolysis declines ability to maintain tension with little ATP consumption |
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varicosities |
swollenregions at the end of axons of autonomic neurons |
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nitric oxide |
paracrine signal smooth muscle relaxation |
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single unit smooth muscle |
Cells undergo synchronous activity- responds tostimulation as single unit Some are pacemaker cells that spontaneouslygenerate action potentials- to all though gap junctions Axon terminals located close to pacemaker cellsusually Contract in response to stretch |
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multiunit smooth muscle |
Each cell responds independently Richly innervated Contraction of whole muscle dependent on numberof cells activated and frequency of stimulation Hormones can increase/decrease contractileactivity |
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desmosomes |
holdcells together and are where myofibrils attach in cardiac muscle |
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excitation contraction coupling in cardiac muscle |
L-type Ca channels- voltage gated ca channels onplasma membrane Triggers release of Ca in sarcoplasmic reticulum Cross bridge formation like skeletal muscle Dependent upon extracellular Ca influx likesmooth muscle Graded muscle contractions Cant undergo tetanic contractions- prolongedpotential and twitch from Ca Pacemaker cells |
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motor program |
1. pattern of neural activity required to properlyperform the desired movement |
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descending pathways |
takes information determined by the motorprogram to the local level of the motor control hierarchy |
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sensorimotor cortex |
includes all parts of the cerebral cortex that act together to control musclemovement |
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proprioception |
afferentinformation about the position of the body and its parts in space |
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voluntary movement |
actions that have the following characteristics:1) he movement is accompanied by a conscious awareness of what we are doing andwhy we are doing it; 2) our attention is directed toward the action or itspurpose |
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interneurons |
90% of spinal cord neurons Local interneurons- near motor neuron theysynapses upon Interneurons with longer processes aid incomplex movements Integrate inputs and determine which muscles areactivated wheni |
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afferent input |
Carry info from sensory receptors located inskeletal muscles controlled by motor neurons, other nearby muscles(antagonists), tendons, joints, skin of body parts affected by action |
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muscle spindle |
- areceptor organ, made up of specialized muscle fibers that detects stretch ofskeletal muscles |
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intrafusal fibers |
modified muscle fibers within the spindle |
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2 kinds of stretch receptors in a muscle spindle |
nuclear chain fiber- how much a muscle is stretched nuclear bag fiber- magnitude and speed of stretch |
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extrafusal fibers |
skeletalmuscle fibers that form bulk of muscle and generate its force and movement Connective tissue attaches to intrafusal sostretch of extrafusal also stretches intrafusal |
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alpha-gamma coactivation |
simultaneous firing of action potentials alongalpha motor neurons to extrafusal fibers of a muscle and along gamma motornerons to the contractile ends of intrafusal fibers within that muscle coactivation- muscle spindle doesn't go slack- continuously able to receive muscle length info |
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stretch reflex |
afferent fibers form excitatory synapsesdirectly onto motor neurons that return to the muscle that was stretched |
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monosynaptic reflex |
a. directly onto motor neurons withoutinterneurons- only in stretch reflexes |
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reciprocal innervation |
activation of neurons to one muscle with thesimultaneous inhibition of neurons to its antagonistic muscle Synapses on inhibitory interneuron |
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golgi tendon organs |
monitors how much tension the contracting motorunits are exerting- endings of afferent nerve fibers that wrap around collagenbundles in the tendons near their junction with the muscle controls muscle tension |
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withdrawal reflex |
1. activates flexor muscles and inhibits extensorsof ipsilateral (side that encountered harmful stimulus)c |
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cerebral cortex |
planning and control of voluntary movements |
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subcortical and brainstem nuclei |
important in planning/monitoring movements sequence of movements for action to occur |
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basal nuclei |
Present in circuit from sensorimotor cortex tobasal nuclei to thalamus to cortical areaSuppress or facilitate movement |
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parkinson's disease |
input to basal nuclei diminished, interplay offacilitatory and inhibitory circuits unbalanced, reduced activation of motorcortex |
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Parkinson's disease effect on movement |
akinesia, bradykinesia muscular rigidity, resting tremor |
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substantia nigra |
brainstem nucleus- dark pigment- project tobasal nuclei and release dopamine |
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cerebellum |
Receives input from sensorimotor cortex andvestibular system, eyes, skin, muscles, joints, tendons provides timing signals planning movements |
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cerebellar disease |
absence of a cerebellum- actions not smooth,with tremor Intention tremor- increases as movement getscloser to target Unstable posture, awkward gait |
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2 types of descending pathways |
Corticospinal pathways- originate in thecerebral cortex Brainstem pathways- originate in the brainstem |
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corticospinal pathway |
pyramidal tracts/ pyramidal system) Cell bodies in sensorimotor cortex; terminate inSC Cross (decussate) at the level of the medullaoblongata fine isolate movements |
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corticobulbar pathway |
from sensorimotor cortex to brainstem accompanies corticospinal pathway Control motor neurons that innervate muscles ofthe eye, face, tongue, throat |
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brainstem pathways |
extrapyramidal system) Mostly uncrossed Distinct clusters in the spinal cord named fororigination Coordination of large muscle groups (posture,locomotion) |
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muscle tone |
slightand uniform resistance when it is stretched by an external force From passive elastic components of muscle andongoing alpha motor neuron activity |
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hypertonia |
abnormally high muscle tone increased alpha motor neuron activity disorders of the descending pathways that inhibit motor neurons |
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upper motor neurons |
descending pathways and neurons of the motor cortex |
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spasticity |
type of hypertonia- muscles don’t developincreased tone until stretched a bit Clasp-knife phenomenon- period of “give” afterresistance |
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rigidity |
form of hypertonia- increased muscle contractionis continual; constant resistance to passive stretch |
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hypotonia |
low muscle tone- weakness, atrophy, decreasedreflex responses |
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endocrine system |
consistsof endocrine glands that secrete hormones and hormone secreting cells in thebrain, heart, kidneys, liver, stomach |
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endocrine glands |
ductless glands that secrete hormonesbrain, heart |
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amine hormones |
Derivatives of amino acid tyrosine Thyroid hormones, epinephrine, norepinephrine,dopamine |
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adrenal medulla |
secretes catecholamines (epinephrine andnorepinephrine, dopamine) More epinephrine than norepinephrine secreted |
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Phenylethanolamine-N-methyltransferase |
enzyme that catalyzesreaction of norepinephrine to epinephrine |
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peptide hormones |
allhormones that are composed of amino acids (peptides and proteins) |
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synthesis path of peptide hormone |
1. Ribosomes on endocrine cells make preprohormones 2. Cleaved to be called prohormones by enzymes inrough ER 3. Prohormone packed into secretory vesicles ingolgi apparatus 4. Prohormone is cleaved to make an active hormoneand other peptides which are packaged in vesicle |
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where are steroid hormones produced |
byadrenal cortex and gonads |
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synthesis path of steroid hormones |
1. Hormone producing cell stimulated by anteriorpituitary gland hormone biding to its plasma membrane receptor 2. Receptors linked to Gs proteins-activate adenylyl cyclase and cAMP production 3. cAMP activates protein kinase A- phosphorylationof intracellular proteins 4. final hormone depends on cell type andtypes/amounts of enzymes |
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what are steroids derived from? lipophilic or hydrophilic? |
cholesterol lipophilic |
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what happens to steroid hormones after they are synthesized |
diffuse across plasma membrane into circulationimmediately after formation attach to carrier proteins because not solublein blood |
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what hormones does the adrenal cortex produce |
aldosterone cortisol DHEA androstenedione |
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mineralocorticoid |
effects on salt (mineral) balance, mainly on kidneys handling of Na, K, H+ ions |
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what controls the production of aldosterone |
Production controlled by angiotensin II Binds to plasma membrane receptors in adrenalcortex to activate inositol trisphosphate second messenger pathway |
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functional purpose of aldosterone |
Stimulates Na and H2O retention; K and H+excretion in urine |
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glucocorticoids |
effects on metabolism of glucose |
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purpose of cortisol in body |
facilitationsof body’s responses to stress, regulation of immune system |
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androgens |
hormones with testosterone like actions |
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layers of the adrenal cortex |
zona glomerulosa zona fasciculate zona reticularis |
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zona glomerulosa |
outer layer of the adrenal cortex- enzymes required for corticosteroneand convert to aldosterone |
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zona fasciculate |
producescortisol, primarily but some androgens |
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zona reticularis |
producesandrogens, primarily but some cortisol |
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congenital adrenal hyperplasia |
excessadrenal androgen production results in virilization of the genitalia of femalefetuses |
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aromatase |
enzyme that converts androgens to estrogens |
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corpus luteum |
in ovary produces progesterone |
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progesterone |
hormone responsible for uterine maturation during menstrual cycle and maintaining a pregnancy |
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location of hormone receptors for water and lipid soluble |
water soluble (peptide and catecholamines) on plasma membrane lipid soluble- located in the cell |
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up regulation |
increasein number of hormone’s receptors in a cell, resulting in a prolonged exposureto a low concentration of hormone; target- cell responsiveness |
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down regulation |
decrease in receptor number- exposure to highconcentrations of the hormone- temporarily decreases target-cell responsivenessto hormone- prevents overstimulation |
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permissiveness |
hormone Amust be present in order for hormone B to exert its full effect Hormone A binds to receptors for Hormone B tocause up-regulation Or changes in the signal pathway mediatesactions of a hormone |
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what happens when hydrophilic hormones reach receptors |
(peptide and catecholamines) Enzyme activity of receptor Activity of cytoplasmic janus kinases associatedwith receptor G proteins coupled in plasma membrane ofeffector proteins (ion channels and enzymes) generate second messengers (cAMPand Ca) Ca channel opens- electrical potential- changein cystolic Ca |
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effects of steroid and thyroid hormones |
alters transcription of genes- change in synthesis rate of proteins from those genes |
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secretion |
release by exocytosis from the cell |
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insulin's response to plasma glucose concentration |
Secretion stimulated by increase in plasmaglucose concentration Insulin acts on skeletal muscle and adipose topromote facilitated diffusion of glucose into cytosol Restores plasma glucose concentration |
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tropic hormone |
hormone that stimulates the secretion of another hormone |
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hyposecretion |
too little hormone is secreted |
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primary hyposecretion |
too little hormone because gland is not functioningnormally Ex: partial destruction of a gland, enzymedeficiency, dietary deficiency of iodine (decreased thyroid hormone) |
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secondary hyposecretion |
endocrine gland is receiving too littlestimulation by its tropic hormone Eventually leads to atrophy of gland |
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hypersecretion |
too much hormone |
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how can a cell by hyporesponsive |
Deficiency/ loss of function of receptors forhormone Deficiency of enzymes that catalyze metabolicactivation of a hormone |
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pituitary gland |
hypophysis Lies in sella turcica of sphenoid bone below thehypothalamus Connects to hypothalamus by infundibulum (hasaxons from neurons in hypothalamus and small blood vessels) |
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adenohypophysis |
anterior pituitary gland No neural connections to hypothalamus; vascularconnection exists |
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median eminence |
junction of hypothalamus and infundibulum |
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hypothalamo-phyophyseal portal vessels |
capillaries in median eminence recombine Allows hormones from hypothalamus to directlyinfluence anterior pituitary w/o going into general circulation |
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portal |
veins that connect 2 sets of capillaries |
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hypophysiotropic hormones |
hypothalamic hormones that regulate anteriorpituitary gland function |
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coricotropin releasing hormone |
CRH secretion of ACTH |
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growth hormone releasing hormone |
GHRH)- secretion of growth hormone |
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somatostatin |
SST)-inhibits secretion of growth hormone |
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thyrotropin releasing hormone |
TRH)- secretion of thyroid stimulating hormone(thyrotropin) |
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gonadotropin releasing hormone |
GnRH)- secretion of luteinizing hormone andfollicle stimulating hormone |
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dopamine |
DA inhibits secretion of prolactin |
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follicle stimulating hormone luteinizing hormone |
FSH LH gonadotropic hormones growth and developent of ova/sperm |
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gonadotropic hormones |
stimulategonads to secrete sex hormones (estradiol and progesterone or testosterone |
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growth hormone |
GH)(somatotropin) 1. Target: Liver and other cells- Function: secrete insulin-like growth factor 1(IGF-1)- effects on bone and metabolism 2. Target: organs/tissues-Function: protein synthesis, carbohydrate and lipidmetabolism |
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thyroid stimulating hormone |
TSH (thyrotropin) 1. Target: thyroid Function: stimulate thyroid to secretethyroxine, triiodothyronine increasesprotein synthesis in follicular epithelial cells, increases DNA replication andcell division, increases amount of rough endoplasmic reticulum |
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Prolactin |
Function: stimulate development of mammaryglands during pregnancy and lactation During lactation- prolactin inhibits gonadotropinsecretion, decreases fertility when woman is nursing |
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adrenocorticotropic hormone |
ACTH (corticotropin) Target: adrenal cortex Function: stimulate adrenal cortex to secretecortisol |
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long loop negative feedback |
thirdhormone in a sequence exerts negative feedback effect over ant pituitary and/orhypothalamus Ex: Cortisol- negative feedback to hypothalamus(decrease CRH) and ant pituitary (decrease ACTH) |
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short loop negative feedback |
influence of anterior pituitary hormone on hypothalamus |
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posterior pituitary gland |
neurohypophysis Axons of neurons (supraoptic and paraventricularnuclei) end in posterior pituitary (from hypothalamus Release hormones directly into capillaries forcirculation Return through circulation to heart and then towhole body (can have widespread effects) |
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oxytocin |
Stimulates contraction of smooth muscle inbreasts- milk ejection- lactation Stimulation: sensory cells in nipples-hypothalamic cells make oxytocin Stretch receptors in cervix triggers release ofoxytocin- stimulates contraction of uterus until baby born Possibly involved with memory and behavior inmales and females (love, maternal behavior, pair bonding) |
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2 hormones secreted by the posterior pituitary |
oxytocin vasopressin |
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vasopressin |
Acts on smooth muscle around blood vessels tocause contraction (constriction), increases BP Stimulation: loss of blood In kidneys to decrease water excretion in urine-maintaining blood volume Stimulation: dehydration Antidiuretic hormone (ADH) |
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deiodinases |
convert T4 to T3 |
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what does thyroid hormone produce |
Throxin (T4) and triiodothyronine (T3) |
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follicles |
enclosedsphere of epithelial cells surrounding a core containing protein rich material |
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synthesis of Thyroid hormone |
Step 1: Iodide trapping- Circulating iodideactively cotransported w/ Na across basolateral membranes of epithelial cells Step 2: Pendrin (integral membrane protein)transports iodide into colloid Step 3: Iodide is oxidized at luminal surface toiodine and then attached to phenolic rings of tyrosine residues within thyroglobulin Step 4: phenolic ring of MIT or DIT is removedfrom remainder of tyrosine and coupled to another DIT on thyroglobulin (2 DIT= T4; MIT + DIT = T3) Step 5: extensions of colloid facing membranesof follicular epithelial cells engulf portions of colloid by endocytosis Step 6: thyroglobulin (contains T3 an T4)contact with lysosomes Step 7: proteolysis of thyroglobulin releases T4and T3- diffuse out of follicular epithelial cell into interstitial fluid-blood |
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thyroglobulin |
1. synthesized by follicular epithelial cells andsecreted by exocytosis into colloid |
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thyroid peroxidase |
enzymethat oxidizes iodide and attaches to tyrosines on thyroglobulin |
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monoiodotyrosine |
MIT tyrosine with 1 iodine |
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diiodotyrosine |
DIT tyrosine with 2 iodines |
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goiter |
enlarged thyroid gland |
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metabolic actions of thyroid hormone |
T3 stimulates carb absorption from smallintestine and increases fatty acid release from adipocytes Supports activity of Na/K- ATPases (providesATP) Decrease in ATP concentration triggers anincrease in glycolysis Byproduct is heat- most of body heat produced |
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permissive actions of thyroid hormone |
T3 up-regulates beta-adrenergic receptors (heartand nervous system especially) Potentiates actions of catecholamines eventhough they are in normal concentrations |
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congenital hypothyroidism |
Absence of T3- poorly developed nervous systemand severely compromised intellectual function Treat with T4 at birth to prevent long-termeffects Cause: dietary iodine deficiency in mother- nota common problem b/c of iodized salt |
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hypothyroidism |
plasma concentrations of thyroid hormoneschronically below normal Most are primary (damage to/loss of functionalthyroid tissue; inadequate iodine consumption) |
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iodine deficiency |
decrease in thyroid hormone- no negativefeedback inhibition Increase in TRH concentration in portalcirculation Increase in plasma TSH concentration |
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autoimmune thyroiditis |
autoimmunedisruption of normal function of thyroid gland- most common cause ofhypothyroidism in US\ |
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hashimotos disease |
hypothyroidism cells of immune system attack thyroid hormone More common in women, processes with age Thyroid hormone decreases b/c inflammation, TSHincreases (lack of negative feedback)- cellular hypertrophy |
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secondary hypothyroidism |
releaseof TSH from from ant pituitary is inadequate |
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symptoms of hypothyroidism |
Cold intolerance, tendency toward weight gain Decreased calorigenic actions normally producedby thyroid hormone Fatigue, changes in skin tone, hair, appetite,GI function, neurological function Myxedema- |
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myxedema |
puffinessof face and other regions- hydrophilic molecules accumulate and water tends tobe trapped with them |
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hyperthyroidism |
thyrotoxicosis Hormone secreting tumors of thyroid gland |
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graves disease |
autoimmunedisease- production of antibodies that bind to and activate the TSH receptorson thyroid gland cells- chronic overstimulation of growth and activity ofthyroid |
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symptoms and treatment of hyperthyroidism |
Symptoms: heat intolerance, weight loss,increased appetite, increased sympathetic nervous system activity Treatment- inhibition of thyroid hormonesynthesis, surgical removal of thyroid, destroying a portion of thyroid usingradioactive iodine (ingested) |
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stress |
real/perceived threat to homeostasis |
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cortisol's function in the body during non-stress situations |
helps maintain normal blood pressure (permissiveactions on epinephrine and norepinephrine Maintains cellular concentrations of enzymesinvolved in metabolic homeostasis Anti-inflammatory and anti-immune functions Inhibits production of leukotrienes andprostaglandins (involved in inflammation) Decreases capillary permeability in injuredareas (less fluid leakage) Suppresses growth and function of lymphocytes Fetal and neonatal- differentiation-parts ofbrain, adrenal medulla, intestine, lungsSurfactant production for lungs |
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functions of cortisol in stress |
organic metabolism Increasesability of smooth muscle to contract in response to norepinephrine Large amounts of cortisol reduce inflammatoryresponse to injury/infection |
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organic metabolsim |
mobilizeenergy sources to increase plasma concentrations of amino acids, glucose, glycerol,free fatty acids |
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effects of long term stress- increased cortisol |
Decrease activity of immune system significantly Worsen symptoms of diabetes (effects on bloodglucose) Increased death rate of neurons in brain Decreased reproductive fertility, delayedpuberty, suppressed growth through childhood/adolescence |
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adrenal insufficiency |
any situation in which plasma concentrations ofcortisol are chronically lower than normal Weakness,fatigue, loss of appetite/weight; low blood pressure, low blood sugar |
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addison's disease |
primary adrenal insufficiency loss of adrenocortical function autoimmune attack diagnosis: lowplasma concentration of cortisol, high ACTH concentrationbody treatment: lowplasma concentration of cortisol, high ACTH concentrationbody |
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tuberculosis |
infection that infiltrates and destroys the adrenal glands |
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pituitary disease |
secondary adrenal insufficiency inadequate ACTH secretion |
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Cushings syndrome |
excess cortisol in blood Increased blood concentration of cortisol- uncontrolled catabolism bone, muscle, skin, other organs immunosuppression obesity hypertension |
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cushings disease |
secondary cause ACTH secreting tumor of anterior pituitary Increased blood concentration of cortisol-uncontrolled catabolism bone, muscle, skin, other organs immunosuppression obesity hypertension Treatment: remove tumor |
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osteoporosis |
loss of bone mass |
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hormones released during stress |
cortisol Aldosterone, vasopressin: Retain water and Na growth hormone, glucagon; Insulin secretiondecreases:mobilize energy stores, increase plasma glucose beta-endorphin (coreleased with ACTH): pain killing? Sympathetic Nervous System activated: Secretion of epinephrine |
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epiphyseal growth plate |
plateof actively proliferating cartilage at the portion of the epiphysis in contactwith the shaft |
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osteoblasts |
boneforming cells at shaft edge of epiphyseal growth plate convert cartilaginoustissue to bone |
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chondrocytes |
lay down new cartilage in the interior of theplate |
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epiphyseal closure |
-Linear growth ceases when growth plates themselves are converted to bone(hormonal influences at end of puberty) |
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when do growth spurts occur |
1: first 2 years of life 2: puberty |
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environmental factors influencing growth |
malnutrition illness catch-up growth- growth spurt after illness/malnutrition |
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IGF-1 |
released by liver mediated by growth hormone autocrine/paracrinesubstance to stimulate differentiating chondrocytes to undergo cell division secreted by cells |
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what is short stature a result of |
decreasedgrowth hormone secretion, decreased production of IGF-1, failure of tissues torespond to IGF-1 |
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growth hormone insensitivity syndrome |
genetic mutation that causes a change in growthhormone receptor so that it fails to respond to growth hormone |
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control of growth hormone (stimulatory, inhibitory, daily rhythm)
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Stimulatory- Growth hormone-releasing hormone(GHRH) Inhibitory- Somatostatin (SST) Daily rhythm- generally growth hormone notreleases unless certain stimuli (exercise) 1-2 hours after going to sleep, prolongedsecretion Highest secretion during adolescence, thenchildren, then adults |
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IGF-2 |
independent secretion from growth hormone |
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thyroid hormone involvement in growth |
facilitates synthesis of growth hormone T3 stimulates chondrocyte differentiation,growth of new blood vessels, responsiveness of bone cells |
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sex steroid involvement in growth |
Secretion increases between ages 8-10 (plateauover next 5-10 years) Stimulates secretion of growth hormone and IGF-1 Stop growth by inducing epiphyseal closureTestosterone- effect on protein synthesis |
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cortisol effect on growth |
Antigrowth effects in high concentrations Inhibits DNA synthesis and stimulates proteincatabolism, inhibits bone growth Breaks down bone Inhibits secretion of growth hormone and IGF-1 |
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osteoid |
collagen matrix of bone contains hydroxyapatite |
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mineralizations |
when matrix becomes calcified |
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osteoclasts |
breakdown previously formed bone by secreting H+, dissolving crystals, and hydrolytic enzymes, digesting osteoid |
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parathyroid hormone |
Produced by parathyroid glands (in the neck,back side of thyroid) Decreased Ca concentration stimulates secretion Increases resorption of bone by osteoclasts (Cato move from bone to extracellular fluid) Stimulates formation of 1,250dihydroxyvitamin D-increases intestinal absorption of Ca Increases Ca reabsorption in kidneysDecreases reabsorption of phosphate ions inkidneys- keeps plasma phosphate concentration steady |
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1,25-Dihydroxyvitamin D |
Vitamin D3 (cholecalciferol)- formed by actionof UV radiation from sunlight on cholesterol derivative in skin Vitamin D2 (ergocalciferol)- derived from plants Vitamin D metabolized by addition of hydroxylgroups (liver, then kidneys) End result: 1,25-dihydroxyvitamin D- active formof vitamin D Stimulates intestinal absorption of CaPTH stimulates enzyme in kidney to form1,25-(OH)2D |
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calcitonin |
peptide hormone secreted by parafollicular cellsin the thyroid gland Decreases plasma Ca concentration by inhibitingosteoclasts, reducing bone resorption Stimulated by increased plasma Ca concentration |
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Rickets/ osteomalacia definition and cause |
rickets-children; osteomalacia- adults mineralization of bone matrix is deficientcausing soft, easily fractured bones Cause: Vitamin D deficiency |
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osteoporosis- definition, symptoms |
matrix and minerals lost as a result ofimbalance between bone resorption and formation Decreased bone mass, strength leads to increased fragility,fractures |
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cause of osteoporosis |
Immobilization (disuse osteoporosis) Excessive plasma concentration of hormone thatfavors bone resorption Old women especially because loss of estrogen Deficient plasma concentration of hormonefavoring bone formation |
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treatment of osteoporosis |
Estrogen replacement- long term consequences Weight-bearing exercise program Adequate Ca and vitamin D intake Bisphosphonates- interfere w/ resorption of boneby osteoclasts Selective estrogen receptor modulators (SERMs)-interact and activate estrogen receptors, compensating for low estrogen |
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primary hyperparathyroidism |
hypercalcemia Cause: tumor of one of parathyroid glands-secretes PTH in excess, increase in Ca resorption and reabsorption, increasedproduction of 1,25-(OH)2D in kidney Increased Ca reabsorption from SI |
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humoral hypercalcemia of malignancy |
Release of PTH-related peptide (PTHrp) withsimilar effects to PTH from cancerous cells Authentic PTH release is decreased because ofhypercalcemia caused by PTHrp Treatment: treat the cancer causing it,bisphosphonates |
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3 causes of hypercalcemia |
primary hyperparathyroidism humoral hypercalcemia of malignancy excessive ingestion of Vitamin D |
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primary hypoprarthyroidism |
Loss of parathyroid gland function 1,25-(OH)2D production in kidney decreased, PTHdecreased Decreases in bone resorption, kidney CAreabsorption, intestinal Ca reabsorption |
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pseudohypoparathyroidism |
resistance to the effects of PTH in target tissue |
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secondary hyperparathyroidism |
Failure to absorb Vit D or decreased kidney1,25-(OH)2D production Decreased absorption of Ca in intestine Increased release of PTH Plasma Ca concentration same because Ca pulledfrom bone |
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hypertension |
sustained abnormal elevation of the arterial blood pressure |
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what is HTN a risk factor for |
coronary artery disease, congestive heart failure, stroke, renal failure |
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risk factors for hypertension |
age, obesity ,sedentary lifestyle, family history, smoking, alcohol, high sodium intake, low potassium/magnesium intake |
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diagnosing hypertension |
BP on 2 separate occasions, averaging 2 readings at least minutes apart |
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definition of type 2 diabetes |
carbohydrate intolerance characterized by insulin resistance, relative (rather than absolute) insulin deficiency, excessive hepatic glucose production, and hyperglycemia |
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beta cell dysfunction |
inability of the pancreatic islet cells to respond appropriately to a rise in blood sugar |
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symptoms of diabetes/ hyperglycemia |
fatigue, polyuria, polydipsia, nocturia, subtle losses of visual acuity, delayed wound healing, numbness or tingling sensations, decreased sensory perception of the feet |
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values of HDL and tiglycerides for dyslipidemia |
HDL <35 triglyceride >250 |
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diagnosis of diabetes |
any one of the following: fasting plasma glucose level >7 mmol/L (126 mg/dL) Any casual plsama glucose concentration >11.1 mmol/L (200 mg/dL) a 2 hour plasma glucose level of >11.1 mmol/L during an oral glucose tolerance test glycosylated hemoglobin level >6% identification of characteristic diabetic retinopathy |
