Physiology Flash Cards

This Is For The Final In Physiology 502 At The University Of Michigan
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What is homeostasis?
the maintanence of relatively stable conditions of the internal environment
What is the internal environment?
the extracellular fluid = plasma + interstitial fluid
What are homeostatic reflex arcs?
-stimulus response sequences involving negative feedback
-responds to changes in variable
What are some variables regulated by the homeostatic reflex arc?
-body temp.
-arterial PO2 and PCO2
-arterial pH
-plasma glucose
-plasma Na+, K+, Ca2+
What are the four functions of membranes?
1. form selective barrier
2. detect chemical messengers at cell surface
3. link adjacent cells together
4. anchor cells to extracellular matrix
What are two types of passive movement across membranes?
-diffusion - solute driven by concentration gradient
-osmosis - water driven by osmolarity
What are the forms of mediated transport systems for movement across membranes?
-faciliated diffusion - movement requiring binding of molecule to transport protein, movement is passive
-active - against concentration gradient
-primary: transport protein directly utilizes ATP (Na/K
-secondary: uses electrochemical gradient of an ion to
move a molecule uphill (Na/K, Na/glucose)
What is membrane potential?
-separation of charge across the plasma membrane
-resting membrane potential: -70 mV
-determined by ion permeabilities
What is the equilibrium potential?
-for any ion
-the membrane potential at which the net flux of the ion is 0
-Nernst: E(ion) = (60/z) * log[ion]o/[ion]i
E(K) = -90 mV, E(Na) = +60 mV
How is the resting membrane potential determined?
-Goldman's equation, based on equilibrium potentials and their relative permeabilities
-Vm = [(ENa * gNa) + (EK * gK) + (ECl * gCl)/] (gNa + gK + gCl)
What are action potentials?
-all-or-none depolarization used to send signals over long distances
-threshold (must depolarize to threshold potential)
-refractory period (when another AP cannot occur or requires a stronger stimulus)
-conducted without decrement (does not decrease with distance)
-neurons, muscles cells; also endocrine, immune, reproductive
What are synapses?
-sites of interaction between two neurons or a neuron and a target cells
-ex: gland cell or muscle cell
What are some types of synapses?
-electrical: direct connections between cells via gap junctions (direct ion flow)
-chemical - indirect connections; AP depolarizes and opens Ca2+ channels, vesicles released by exocytosis
-in postsynaptic cell: K, Cl = hyperpolarization and IPSPs, Na, Ca = depolarization, EPSPs
What is the importance of the medulla oblongata?
cardiovascular, respiratory, swallowing and vomiting centers
What are some features of the autonomic nervous system?
-innervates smooth muscle, cardiac muscle and endocrine glands
-sympathetic (NT = norepinephrine), parasympathetic (NT = ACh), enteric (local nervous system of GI tract)
-principle dual innervation
-adrenal medulla: releases EPI:NE (80:20), modified sympathetic ganglion
What are teh four elementary attributes to any stimulus?
-type of stimulus (thermoreceptors, mechanoreceptors, photoreceptors, osmoreceptors, chemoreceptors)
-intensity of stimulus (coded by AP frequency)
-location of stimulus (coded by site of stimulus and pathway into CNS, enhanced by lateral inhibition)
-duration of stimulus
What are properties of light waves?
-visible light: wavelengths = 350-750 nm
-reflection: light waves bounce off surface
-refraction: bending of light waves as they pass through transparent materials; concave (light scatters, divergence of waves) and convex (light waves converge to a point, lens)
What is the anatomy of the eye?
-3 concentric layers
-outermost: sclera (white of eye), cornea (transparent)
-middle: choroid (dark pigmented layer that absorbs light), ciliary muscle (controls shape of lens via zonular fibers, changes shape to focus), iris (controls size of pupil)
-innermost: retina, photoreceptors, fovea (central point), optic disc ("blind spot")
-fluids: aqueous humor in anterior cavity (nutrients), vitreous humor in back chamber (maintains shape)
How is light focused on the retina?
-waves pass through cornea and lens and bend
-those striking perpendicular to surface will pass straight without bending
-projected upside down due to bending
How do we focus light on different distances onto our retina?
-by changing the shape of the lens
-zonular fibers are attached to the lens and ciliary muscle
-ciliary muscle is under parasympathetic control, circular - contracting = smaller, relaxing = larger
-no PS activity - ciliary muscle relaxed - lens becomes flatter - light bends less
-PS activity - ciliary muscle contracted - zonular fibers are slack - lens becomes more convex - light bends more
What is accommodation?
-start with distant object, ciliary muscle relaxed, lens is flat, light is focused on retina
-closer - ciliary muscle contracts and zonular fibers slacken, lens domes up into rounded shape, light is bent more and focused forward onto retina
What is near-sightedness?
-cannot see objects far away
-eyeball is too long for ability of lens to accommodate
-object focuses in front of retina because fully flattened lens still bends light too much and focus in front of retina
-to fix: concave lens in front of eye to scatter light
What is far-sightedness?
-cannot see near objects
-eyeball is too short for ability of lens to accommodate
-object focuses behind retina because cannot bend light enough to focus on retina
-to fix: convex lens in front of retina to bend light
What are features of the retina?
-where photons of light are absorbed and converted to graded potentials and APs
-two photoreceptors: in back, rods (dim light vision), cones (bright light vision, color)
-bipolar cells: middle layer, relay info from photoreceptors to ganglion cells
-ganglion cells: front, axons form optic nerve, signals brain, first cells in retina fire APs, others have graded potential changes
Where are the rods and cones located?
-cones: primarily in center, fovea has highest density, greatest acuity
-rods: in periphery, object in center more difficult to see at night
-optic disc has neither rods or cones
What are the important molecules for phototransduction?
-photopigment: cones (red, blue and green opsin), rods (rhodopsin)
-retinal: light absorbing portion located within the pigment, same in all opsins, made from vitamin A
-transducin: G-protein
-phosphodiesterase: an enzyme that breaks down cGMP
-cation channel: gated by cGMP (open in cGMP is present)
How does phototransduction occur in the dark?
-GTP to cGMP by guanylyl cyclase
-cGMP binds channel and it opens
-Na/Ca influx depolarizes cells; voltage-gated Ca channel opens due to depolarization causing NT release
How does phototransduction occur in the light?
-photon absorbed by retinal/opsin, causes opsin to change shape and dissociate ("bleached")
-activates transducin, which activates phosphodiesterase
-phosphodiesterase breaks down cGMP, cation channels close, cell "repolarizes"/hyperpolarizes, NT release decreases
How do the cells of the retina communicate?
-rods and cones generate graded potentials (light - less glutamate is released onto bipolar cells)
-bipolar cells: receptors for glutamate and generate graded potentials ("On" cells hyperpolarize in presence of glutamate, "Off" cells depolarize in presence of glutamate)
-ganglion cells: generate APs (connected to "on", release of more NT causes increased AP firing in light, connected to "off", release of less NT causes decreased AP firing)
How does color vision work?
-three sets of cones absorb along different parts of spectrum, overlap is color vision
-perception of color determined by comparing proportion of red, blue and green cones activated
What are some of the effects of cortisol?
-steroid hormone, secreted by adrenal cortex, controlled by CRH and ACTH
-anti-inflammatory, anti-immune functions
-important for fetal and neonatal life
What are some of the effects of thyroid homrone?
-under control of TRH and TSH
-iodine is required, T4 and T3 secreted by hyorid gland, some tissues converted from T4 to T3 (higher affinity)
-major determinant of basal metabolic rate
-increases number of beta-adrenergic receptors on heart and nervous system (increases responsiveness to EPI/NE)
-required for normal GH secretion, important for fetal and infant NS development
What are some of the factors affecting growth?
-environmental: adequate nutrition for substrates, adequate calorie intake, sickness and disease
-hormones: insulin, GH, IGF-1, testosterone/estrogen, cortisol (inhibitory - blocks mitosis and inhibits protein synthesis)
-growth factors (paracrines): mitogens (stimulate cell division and proliferation), growth inhibiting factors
What is the role of growth hormone?
-secreted from anterior pituitary; stimulates liver to release IGF-1, mediates growth effects (proliferation/mitosis and differentiations into cartilage producing cells - chondrocytes)
-osteoblasts - lay down matrix for hydroxyapatite to bind and form hard bone
-dwarfism (deficiency in children), gigantism (excess in children), acromegaly (excess in adults)
What are the three types of muscle?
-skeletal: attached to bone via tendons, make up system of mechanical layers that develop force via contraction to move skeleton
-cardiac: muscle of the heart
-smooth: muscle surrounding tubes and hollow cavities
What are the proteins of skeletal and cardiac muscle?
-thin filament (actin - binding sites for troponin and myosin; tropomyosin - blocks myosin binding to actin, troponin - Ca2+ binding subunit, tropomyosin and actin binding subunits)
-thick filament: myosin - heads contain actin binding site and ATP binding site and ATPase
What is the functional unit of skeletal and cardiac muscle?
-sarcomere - repeating unit that shortens and/or generates force
-Z line demarcates the sarcomere, thin filaments attached to Z-lines, thick attached to M-line in center of sarcomere, interact with titin
-A band is length of myosin and contains actin and myosin
-H zone is region in center of sarcomere, only contains myosin filament
-I band overlaps two sarcomeres with Z-line in center, only contains actin
What is an isotonic contraction?
-fiber shortens while load on muscle remains constant
-load-velocity relationships - velocity of shortening is greater at lighter loads, slower at heavier loads
What is an isometric contraction?
-fiber generates tension but does not shorten (or lengthen)
-force-frequency relationship (increased AP frequency can increase tension)
-length-tension relationship: maximum tension generation occurs at optimal sarcomere length, lengths past optimal - fiber tension generation decreases
What is a eccentric contraction?
-fiber generates tension but load is too great to shorten or isometrically contract, so fiber is pulled to a longer length
How is skeletal muscle energy metabolized?
-creatine phosphate - available for a few seconds, provides time for glycolysis and oxidative phosphorylation enzymes to increase activity
-oxidative phosphorylatino: moderate intensity, longer duration exercise where O2 supply is not limiting, utilizes glycogen (first 5-10 min), blood glucose and fatty acids (next 30 mins), and then fatty acids exclusively after 35-40 min
-glycolysis: high intensity exercise, produces ATP in absence of O2, uses glycogen and blood glucose
What is fatigue?
-not due to ATP depletion
-contributing factors: decreased pH (increased acidity), build up of inorganic phosphate, reduced troponin sensitivity to Ca2+, build-up of K+ in T-tubules causing excitation-contraction coupling failure, glycogen depletion, dehydration
What are the three skeletal muscle types?
1. slow oxidative fibers (hydrolyze ATP slower than fast fibers, most resistant to fatigue, lowest force contraction)
2. fast oxidative fibers (hydrolyze ATP at faster rate than slow fibers, intermediate resistance to fatigue and force generation)
3. fast glycolytic fibers (hydrolyze ATP at faster rate than slow fibers, fatigue quickly, greatest force generation)
Does skeletal muscle undergo hyperplasia (increased fiber mitosis and increased number of fibers)?
-strength training leads to hypertrophy (increased sarcomeres in parallel)
-endurance training leads to increased capillaries per muscle fiber
What are the differences in smooth muscle?
-fibers smaller than skeletal and cardiac
-maximum tension per cross-sectional area is same
-smooth muscle can generate tension over wider range of muscle lengths
-very fatigue resistant
-has calmodulin instead of troponin for contraction regulation
What is the cross-bridge cycling for smooth muscle?
-inputs = nerves from PS/SNS, hormones, stretch, pacemaker cells (spontaneous APs)
-intracellular Ca2+ rises, binds to calmodulin, activates myosin light chain kinase (MLCK), phosphorylates myosin regulatory light chain, changes position of myosin head so it can bind to actin
-relaxation - when Ca2+ levels falls, MLC phosphatase dephosphorylates MLC and moves myosin head
What are the functions of the cardiovascular system?
-delivers nutrients to tissues (O2, glucose, fatty acids, aa's)
-removes waste products (CO2, metabolic end products)
-inter-organ communication (hormones)
-thermal regulation (alterations in skin blood flow can increase/decrease heat loss)
-immune system (white blood cells)
What is the flow of blood in the CV system?
-blood returns to right atrium via superior/inferior vena cava
-right atrium to right ventricle through AV (tricuspid) valve
-right ventricle to pulmonary artery via pulmonary valve
-pulmonary vein to left atrium, left atrium through AV (mitral) valve into left ventricle
-left ventricle to aorta through aortic valve
-aorta to systemic circulation (large arteries - arterioles - capillaries - venules)
What is cardiac output?
-volume of blood pumped by one ventricle per minute (about 5L/min); left = right under normal conditions
-SV = stroke volume (volume of blood pumped by one ventricle per beat), HR = heart rate (beats/min)
-CO = SV x HR
-CO = MAP/TPR (MAP = mean arterial pressure, TPR = resistance), MAP = SV x HR x TPR
What are the different types of blood vessels?
-arteries: pressure reservoir, stretch as blood is pumped into them during systole, recoil to maintain pressure and drive flow during diastole
-arterioles: resistance vessels, contribute to total peripheral resistance (TPR), regulate flow distribution & arterial pressure
-capillaries: exchange vessels (gases, nutrients, wastes and fluid)
-venules: post capillary resistance vessels
-veins: capacitance vessels, low resistance vessels, very expandable without as much recoil, can hold large volumes of blood w/o major effects on R and arterial pressure
What is the equation for flow?
flow = pressure/resistance
-major determinant of R is radius (R = 1/r^4)

What are the pacemaker cells of the heart?
-located in SA node, AV node, and bundle of His
-under tonic control of Sym and PS systems (basal level = 70 beats per minute), Sym increases, PS decreases
-the SA node is the normal pacemaker of the heart
What is an electrocardiogram?
-ECG; used to measure electrical currents through the heart
-P wave = atrial depolarization, QRS complex = ventricular depolarization, T wave = ventricular repolarization
-P-Q interval = AV ndoe conduction time
-Q-T interval = ventricular contraction time (systole)
-T-Q segment = ventricular relaxation time (diastole)
-R-R interval = used to determine HR
What is the cross-bridge cycling in cardiac muscle?
-regulated by Ca2+ binding to troponin
-Ca2+ levels rise due to "calcium-induced calcium release"
-membrane depolarization due to AP propagation, opens Ca2+ channels
-Ca2+ influx occurs, Ca2+ interacts with ryanodine receptors, causes Ca2+ release from SR, Ca2+ binds to troponin -- cross-bridge cycling
How does the sympathetic nervous system innervate cardiac muscle?
-SA/AV node - increase HR
-ventricular muscle cells - increase contractility
-arterioles - vasoconstriction, affects TPR
-venules/veins - increase peripheral venous pressure and venous return; increases end diastolic and stroke volumes
How does the parasympathetic nervous system innervate cardiac muscle?
-SA/AV node - decreases HR
What is the Starling's Law of the heart?
-SV increases as EDV (end diastolic volume) increases
-an increase in venous return will increase EDV, SV and CO
-length-tension relationship (force generation can increase if fibers are stretched to a longer length)
How can venous return be increased?
-sympathetic-mediated constriction
-increased blood volume
-skeletal muscle pump - contractions of skeletal muscle compress veins and drive blood flow toward the heart
-respiratory pump - increase depth of respiration, increases pressure difference between periphery and central veins to increase flow to heart
What are the periods of the cardiac cycle?
-systole: period of ventricular contraction
-diastole: period of ventricular relaxation
What are the events of systole?
-atrium is relaxed, ventricle begins to contract
-isovolumetric contraction occurs (pressure in atrium is greater than ventricle initially, AV valve opens, pressure in aorta is greater than ventricle, aortic valve closed)
-at start - contraction of ventricle increases ventricular pressure, all valves closed (first heart sound)
-ventricular pressure surpasses aortic pressure, aortic valve opens, blood is ejected into the aorta
What are the events of diastole?
-ventricle begins to relax, aortic pressure greater than ventricular pressure, aortic valve closes (2nd heart sound)
-isovolumetric relaxation occurs (all valves closed, ventricular pressure is falling)
-ventricular pressure drops below atrial pressure and AV valve opens, blood flow into ventricle from atrium
-return to systole
What are some regulators of arteriolar diameter?
-local metabolites play a role
-sympathetic activity
-circulating EPI
-circulating angiotensin II, ADH, ANP
-paracrine factors (nitric oxide)
How does arteriolar constriction and dilation affect bloodflow?
-constriction: increase pressure upstream and decrease pressure downstream
-dilation: decrease pressure downstream and increase pressure upstream
What are some properties of capillary exchange?
-diffusion: major mechanism for exchange of nutrients, solutes and gases
-bulk flow: shifts plasma-like fluid between capillaries and interstitial fluid, driven by pressure gradient
-filtration (reabsorption of water and solute from ISF)
-at arterial end, net pressure is in favor of filtration and fluid/solutes move into ISF from plasma
-at venous end, net pressure is in favor of reabsorption
What is the baroreceptor reflex?
-senors that detect changes in arteriol BP, located in aortic arch and two carotid arteries
-respond to increases/decreases in pressure (increased MAP increases AP frequency to CV center in medulla oblongata, decreased MAP decreases frequency)
-effectors: heart, arterioles, veins
-decreased MAP due to hemorrhage -- decreased baroreceptor firing rate, CV center mediates (increase Sym output to heart, arterioles, veins, decrease PS output)
-increase HR (above normal), increase TPR (above normal), increase VR and SV (toward normal)
-CO and MAP return toward normal
What is heostasis?
-blood clotting, involves platelets and clotting factors that circulate in blood in inactive form (activated by damage)
-damage exposes blood to underlying collagen, activates platelets (adhere to collagen, becomes activated and secrete thromboxane A2 to enhance platelet aggregation)
-blood vessels constriction to decrease blood flow/loss
-platelet plug forms
How are clots formed?
-activation of clotting factors is a chain reaction (one factor activates the next), leading to activation of factor X (with co-factor Factor V), cleaving prothrombin to thrombin
-thrombin cleaves firinogen to fibrin which forms clot, activates factor XII which cleaves loose fibrin to make stablized fibrin, positively feeds-back to activate other factors, leading to more thrombin
-plasmin breaks down fibrin to dissolve clots
What are the functions of the respiratory system?
-ventilation (movement of air between atmosphere and lungs)
-gas exchange (transfer of O2 and CO2 between lungs and circulatory system)
-acid-base balance (H2O + CO2 -- H2CO3 -- H + HCO3)
-phonation (airflow across vocal cords for speech)
-biotransformation (metabolism of bioactive molecules)
-pulmonary defense (lung macrophages)
How are pressures involved in inspiration and expiration?
-at rest between breaths, Patm = Palv = 0
-during inspiration, Palv < Patm, during expiration, Palv > Patm
-transpulmonary pressure and chest wall pressure are equal and opposite elastic recoil at rest, stabilizes resting lung volume
What is active expiration?
-contraction of abdominal muscles and expiratory intercostals to push diaphragm up and pull chest downward
-increases pressure in thoracic cavity and increases interpleural pressure towards 0, allows elastic recoil
-this increases Palv and forces air out
What is compliance?
-expandability of lung, determined by amount of elastic tissue and surface tension
-compliance = volume change/pressure change
-high compliance = lungs expand easily
-determined by elastic tissue (emphysema destroys lung tissue making lungs more expandable, fibrosis stiffens fiber making lungs less expandable) and surface tension (surfactant secreted by Type II alveolar cells, reduce water molecules attraction to each other, decrease force against expansion at surface)
What is tidal volume?
-amount of air entering lungs during resting inspiration and passive expiration
-functional residual capacity (FRC) - volume of air remaining in lungs after a resting (passive) expiration
-residual volume: amount of air remaining in lungs after maximal forced expiration
-vital capacity: maximal volume of air that can be expired after maximal inspiration
What is anatomic dead space?
-volume of the conducting zone in which no gas exchange takes place
-some inspired air remains in conducting zone and is unavailable for gas exchange
What are the two ventilation equations?
-minute ventilation = TV x frequency
-alveolar ventilation = (TV - VD) x frequency (more accurate indicator of amount of air entering alveoli)
What is the airway resistance?
-not limiting to airflow
-factors that affect airway resistance: lateral traction (resistance less during inspiration than expiration), PS activity and inflammatory mediators increases mucus secretion and causes airway constriction, EPI is bronchodilator
What diseases affect airway resistance?
-asthma - chronic inflammation reduces airway diameter, amking smooth muscle hypersenitive and prone to bronchospasm, incrases airway R, expiration affected more
-COPD - bronchitis (viral infection, excessive mucus, constriction of airways), emphysema (destruction of alveolar and airway walls, decrease elastic tissue, small airways collapse during expiration, decreased expiratory volume, increased residual volume)
How does gas exchange work?
-diffusion of gases occurs down a partial pressure gradient
-at lungs, O2 moves from atmosphere into alveoli into blood, CO2 moves from blood into alveoli into atmosphere
-at tissues, O2 moves from plasma and RBCs to ISF into tissue cells, CO2 moves from cells into ISF into plasma and RBCs
-CO2 is 24x more soluble than O2 and diffuses more easily across membranes
What is hyperventilation? What is hypoventiliation?
-hyper: indicates a state in which ventiliation is elevated compared to metabolism, arterial PO2 levels rise and arterial PCO2 levels fall
-hypo: indicates a state in which ventilation is decreased compared to metabolism, arterial PO2 levels fall and arterial PCO2 levels rise
How is oxygen transported?
-bound to Hb, binds to iron atom in heme portion
-22% is unloaded into the tissues
-if O2 delivery to kidneys decreases, kidneys secrete erythropoietin (EPO) which stimulates RBC production by bone marrow
-factors that increase O2 unloading in tissues (right-shift) - decreased pH, increased temp, PCO2 and 2,3 DPG
-factors that decrease O2 unloading in tissues (left-shift)- opposite as right shift
How is carbon dioxide transported?
-10% dissolved in plasma, 30% bound to globin portion of Hb, 60% as bicarbonate ions (carbonic anhydrase)
-acid-base balance (ventilation can alter arterial pH - hyperventilation: increase pH, hypoventilation: decrease pH)
What is rhythmic breathing?
-pacemaker cells in medulla oblongata send output to motor neurons of inspiratory muscles; inspiration occurs with each burst of APs (ceasation = expiration)
-strength of contraction is determined by AP frequency and duration of burst
-frequency of breathing determined by interval between bursts
What inputs into the respiratory system of the medulla oblongata?
-inputs from higher center (cortex, pons)
-receptors in lungs and airways (stretch receptors, irritant receptors, J receptors in pulmonary vasculature)
-receptors in muscles and joints
-pain receptors
-chemoreceptors (most important) - peripheral located in aortic arch and carotid bodies, sense changes in arterial PO2, PCO2 and pH; central located in medulla oblongata, sense changes in arterial PCO2 by detecting changes in brain ISF pH
How does exercise affect breathing?
-moderate exercise - chemoreceptor input not involved with increased ventiation (ventilation is increased to match metabolic demand, no changes in PO2, PCO2, pH), input from motor cortex, receptors in joints & muscle and increased EPI
-strenuous exercise - peripheral chemoreceptors mediate hyperventilation in response to metabolic acidosis
What are some functions of the kidney?
-maintain salt and water balance
-eliminate metabolic wastes and foreign substances
-regulate pH of internal environment
-secrete hormones - renin, erythropoietin, calcitriol
What are the two regions of the kidney? What is the functional unit?
-renal cortex (outer region), location of all renal corpuscles (glomeruli, Bowman's capsules)
-renal medulla (inner region), juxatamedullary nephron loops of Henle and collecting ducts
-nephron = functional unit, begins at renal corpuscle, proxial tubule, loop of Henle, distal tubule, collecting ducts)
-blood vessels: afferent arteriole, glomerular capillaries, efferent arteriole, peritubular capillaries, vasa recta capillaries
What are the four basic renal processes?
-filtration (bulk flow movement from glomerular capillaries to Bowman's space)
-reabsorption (movement of substance from nephron lumen into ISF, must be lipid soluble or have channel)
-secretion (movement of substance from ISF to lumen, must be lipid soluble or have channel)
-excretion (bulk flow of final urine from bladder through urethra and out to exterior)
How is glomerular filtration rate determined?
-if filtered load > amount excreted = net reabsorption
-if filtered load < amount excreted = net secretion
-if equal, neither reabsorbed nor secreted
How is glucose handled in the kidneys?
-gluose transporters on apical and basolateral membranes in proximal tubule
-co-transported with Na+ across apical membrane, down gradient by facilitated diffusion on basolateral membrane
-if plasma glucos > 300 mg/dL all glucose cannot be reabsorbed
-glucose in tubule becomes osmotically active, cannot be reabsorbed, inhbits reabsorption of water, increases water secretion
How is sodium handled in the kidneys?
-reabsorbed by proximal tubule, asecnding limb of loop of Henle, distal tubule and collecting duct
-apical: proximal - Na/glucose cotransporter, Na/aa cotransporter, Na/lactate transporter, Na/H exchanger; ascending- Na/K/2Cl cotransporter; distance - Na/Cl cotransporter, collecting duct - Na channel
-basolateral - Na/K ATPase
How is water reabsorbed in the kidneys?
-by proximal tubule, descending loop of Henle and collecting duct
-passive, downhill through aquaproins
-in proximal tubule, reabsorption of Na+ directly provides osmolarity gradient
-in descending, reabsorption is indirectly coupled to Na+ in the ascending (countercurrent multiplication)
-in collecting duct, water reabsorption can occur without direct couping to Na+ because ISF is hypertonic
How are sodium and water reabsorption of the kidneys regulated? **(study this section of notes)
-water: hormones (ADH), sensors - osmoreceptors in hypothalamus, volume receptors in large veins and atria, baroreceptors in aortic arch and carotid arteries; thirst mechanism
-Na+: renin, angiotensin II, aldosterone, ANP
How is the excretion of potassium by the kidneys regulated?
-effect of aldosterone (increases K+ secretion)
-increased plasma [K+] directly stimulates aldosterone release
-effect of flow rate (high flow stimulates K+ secretion)
-direct effect of high ECF to stimulate K+ secretion
How does the kidney play a role in acid-base balance?
-reabsorbs filtered bicarbonate
-adds new bicarbonate and secretes H+ and excretes H2PO4-
-adds new bicarbonate and secretes and excretes bound to NH4+
-compensations for respiratory acidosis/alkalosis and metabolic acidosis/alkalosis
How does renal failure develop and how is it treated?
-hyperkalemia, acidosis, proteinuria, anemia, wate product build up in blood, high BP, problems with water regulation
-treatment: hemodialysis, peritoneal dialysis, transplant
What are the four layers of the GI tract wall?
1. mucosa (layer of polarized epithelial cells in contact with luminal contents, secretory and absorptive cells, receptors)
2. submucosa and submucosal plexus
3. muscle layer (circular and longitudinal muscle layers (responsible for contractions and motility, myenteric plexus)
4. serosa (outer layer)
What are some secretions made by the stomach?
-neck cells (mucus)
-cheif cells (pepsinogen and gastric lipase)
-parietal cells (HCl and intrinsic factor)
-enteroendocrine cells (gastrin to stimulate acid secretion)
-ECL cells (histamine, stimulates acid secretion)
-D cells (somatostatin, inhibits acid secretion)
How are stomach secretions regulated?
-stimulated by cephalic phase and gastric phase stimuli (stomach distension, chyme pH, chyme osmolarity, presence of protein in stomach) via gastrin, histamine and ACh
-inhibited by intestinal phase stimuli (change in duodenum - distension, pH, osmolarity, presence of aa's, peptides and fatty acids) via CCk, secretin, somatostatin and ACh
What is the motility of the stomach?
-basic electrical rhythm (set by pacemaker smooth muscle cells in stomach wall)
-force of contraction - stimulated by cephalic phase and gastric phase stimuli, inhibited by intestinal phase stimuli
What are some of the secretions of the SI?
-CCK and secretin
-regulated by pH, distension, osmolarity, peptides and fats in duodenum
How does digestion and absoprtion occur in the SI?
-digestion: brush border enzymes for protein and carbs, enzymes secreted from pancreas for protein, carb and lipid, bile secreted by liver for fat digestion
-absorption: brush border transporters for sugars and aas, huge surface area
What is the motility of the SI?
-segmentation: mixing contractions, slow movement of chyme toward ileum
-migrating myoelectric complex: peristalsis, but each contraction only travels about 2 feet before stopping, subsequent contractions start a bit lower down and travel two feet, etc; eventually reaches LI, stimulated by motilin
What are the secretions of the LI?
How does absorption occur in the LI?
What is the motility of the LI?
-some segmentation
-mass movement (peristalsis)
-gastrocolic reflex (food/chyme in stomach and duodenum stimulate contractions of colon)
What are the secretions of the pancreas and how are they regulated?
-enzymes: stimulated by CCK, potentiated by secretin
-trypsinogen, chymotrypsinogen, procarboxypeptidase, amylase, lipase and colipase
-HCO3-: stimulated by secretin, potentiated by CCK
What are the secretions of the liver and how are they regulated?
-bile and HCO3-
-hepatic portal blood bile salt concentration regulates liver production of bile
-CCK - gall bladder contraction, Spincter of Oddi relaxation
-secretin - bicarbonate secretion
What is the digestive process of carbs?
-begins in mouth with salivary amylase
-stops in stomach (salivary amylase inactivated by acid)
-completed in SI (pancreatic amylase to maltose and dextrins)
-brush border enzymes (dextrinase and glucoamylase - dextrins to maltose, lactose and sucrose; maltase, lactase and sucrase (disaccharides into monosaccharides)
What is the absorption process of carbs?
-glucose and galactose by active transport coupled to Na+ absorption across apical membrane
-fructose by faciltated diffusion across apical membrane
-glucose, galactose and fructose by facilitated diffusion across basolateral membrane
What is the digestive process of protein?
-none in mouth
-begins in stomach with pepsinogen secretion - activatedto pepsin by acid - breaks down into proteins
-completed in SI (trysinogen activated to trypsin by enterokinase, trypsin activates other pancreatic proteases, brush border enzyme - aminopeptidases)
What is the absorptive process of protein?
-aa's absorbed by active transport coupled to Na+ across apical membrane and facilitated diffusion across the basolateral membrane
-short peptides can also be absorbed
What is the digestive process of lipids?
-none in mouth or stomach
-occurs in SI: emulsfication (motility mixes and breaks up big fat droplets, bile salts from liver and gallbladder interact with smaller droplets to keep them from reaggregating) and digestion (lipase and colipase secreted by pancreas, triglycerides broken down to fatty acids and monoglycerides, equilibrium between some free fatty acids/monoglycerdies and some form micelles)
What is the absorptive process of lipids?
-free fatty acids and monoglycerides diffuse across apical membrane and are taken up by ER
-more fatty acids and monoglycerides are released from micelles and diffuse across the apical membrane
-in ER, triglycerides reformed and shuttled to Golgi for packaging in chylomicrons, which exit across basolateral membrane by exocytosis and are taken up by lacteals
What are some features of the absorptive state?
-food in GI tract and being absorbed
-glucose and aa's levels high, triglyceride levels high, fatty acid levels low
-insulin is being secreted (increase plasma glucose and aas, increase PS activity, decrease Sym activity and EPI, increased GIP from SI)
How does insulin stimulate liver during absorptive state?
-liver: glucose to ATP, glycogen, fatty acids, alpha-glycerol-phosphate
-aas to protein or alpha-ketoacids
-production of triglycerides (fatty acids come from glucose/aa's, alpha-glycerol phosphate comes from glucose)
How does insulin stimulate adipocytes during absorptive state?
-stimulation of glucose uptake and triglyceride production
-increased numbers of glut-4 transporters on membrane
-increased activity of enzymes to convert glucose to alpha-glycerol phsophate and fatty acids
-lipoprotein lipase releases fatty acids from circulating chylomicrons to diffuse into adipocytes
-increase production of triglyercides within cell
-aa uptake and protein production increases
How does insulin stimulate skeletal muscle during absorptive state?
-stimulation of glucose uptake
-increased number of glut-4 transporters on membrane
-increased activity of enzymes, convert glucose to glycogen and to breakdown glucose by glycolysis
-increased aa uptake and protein synthesis
What are some features of the postabsorptive state?
-no food in Gi tract
-plasma glucose falling, aa's initally fall then remain stable as released from protein, triglyceride levels low, fatty acid levels high
-insulin low, low PS, high Sym; glucagon high due to low plasma glucose and insulin, increased EPI/Sym activity
-acts mainly on liver to increase glycogenolysis, gluconeogenesis and ketone production (small effect on lipolysis, no effect on skeletal muscle)
How do various hormones affect the postabsorptive state?
-EPI levels increase - increased glycogenolysis and gluconeogenesis by liver, increased glycogenolysis by skeletal muscle, increased lipolysis by adipose tissue
-cortisol remains constant - maintains liver enzymes for glycogenolysis and gluconeogenesis
What catabolic activities occur in liver in postabsorptive state?
-glycogenolysis and gluconeogenesis and release of glucose to plasma - substrates = lactate and pyruvate from skeletal muscle, aa's released mostly from skeletal muscle, glycerol from adipose tissue
-decreased production of triglycerides
-increased production of ketone bodies from fatty acids
-decreased production of protein from aa's
What catabolic activities occur in adipocytes in postabsorptive state?
-breakdown of triglycerides to fatty acids and glycerol
-fatty acids released to circulation and taken up by most cells (not CNS) to undergo beta-oxidation for production of ATP
What catabolic activities occur in skeletal muscle in postabsorptive state?
-glycogenolysis and release of pryuvate and lactate to travel to liver
-protein breakdown to release aa's to liver
-increased use of fatty acids and ketone bodies for energy (glucose-sparing)
What catabolic activites occur in brain cells in postabsorptive state?
-continued uptake of glucose for energy
-if ketone levels build up enough in blood (prolonged fast or diabetes) begin using ketone bodies for energy
What catabolic activites occur in all cells except CNS in postabsorptive state?
-decreased uptake of glucose and aas
-increased uptake and utilization of fatty acids for energy (glucose-sparing)
-increased utilization of ketone bodies for energy (glucose-sparing)
What are the two types of diabetes mellitus? What is the treatment for diabetes?
-type 1: insulin deficient, requires insulin
-type 2: insulin resistant, treatment involves weight loss/control, exercise, dietary modification, insulin stimulatory drugs and sometimes insulin

What is diabetic ketoacidosis?
-develops when blood ketone body levels are highly elevated becomes ketone bodies are acidic
How are the basal metabolic rate and metabolic rate regulated?
-TH is major determinant, starvation decreased TH secretion which decreases BMR and decreases breakdown rate of energy stores
-another determinant is skeletal muscle mass
-metabolic rate is increased by EPI, food induced thermogenesis, skeletal muscle activity, leptin
How do hypothyroidism and hyperthyroidism affect BMR?
-hypo: decrease BMR (sometimes results in weight gain), cold intolerance due to decreased heat production, lethargy
-hyper: increased BMR (usually associated with weight loss), heat intolerance due to increased heat production, increased physical and nervous activity, increased hunger and food intake
What are inhibitors of hunger/signals for satiety?
-distension of stomach and duodenum
-neural feedback from stomach
-CCK from SI
-neural feedback from liver
-PYY for LI
-high plasma glucose
-insulin from pancreas
-leptin from fat (long term regulator)
What are stimulators of hunger?
-low plasma glucose
-Ghrelin from stomach
What are some characteristics of leptin?
-secreted by fat cells (adipocytes)
-decreases hunger by decreasing neuropeptide Y (NPY) in brain hunger center
-increases Sym activity and metabolic rate
-increases reproductive function
What is obesity?
-multifactorial disorder (sedentary lifestyle, abnormal feeding behavior, neurogenic abnormalities, genetic factors)
-BMI > 30
-results in significant impairment of health
-must treat by changing input and output (decrease calorie intake, change both calorie intake and exercise)

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