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Physio 2130 Review .docx

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Physiology 2130
Kim Luton

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MIDTERM 1  Hypothalamus functions Body temperature regulation Body energy balance and exchange Water balance and exchange Sodium balance and exchange Control of autonomic system Neuroendocrine control (posterior pituitary, catecholamine released from adrenal medulla) – interaction between nervous system and endocrine glands Drives and emotions (ex feeding, attack) Circadian rhythms Reproduction (behavior and pituitary function) Parasympathetic (fast + specific) Sympathetic (slow, low specificity) Saliva secretion – watery (parasympathetic), mucus, thick (sympathetic) Bladder contraction – contraction (direct), vasoconstriction cause urine to squeeze out of bladder Pupil constrict Pupil dilation Bronchiole constrict Bronchiole dilate Stimulate peristalsis, secretion, and Inhibition of peristalsis, secretion release of bile Conversion of glycogen to glucose Secretion of adrenaline and noradrenaline  Hypothalamic control of pituitary gland Anterior pituitary  Hormone secreted by basomedial hypothalamus through circulatory system  hypophyseal portal system Posterior pituitary  Supraoptic (SON) and paraventricular nuclei (PVH) (both part of hypothalamus) have AVP neurons that produce ADH (vasopressin - VP) and oxytocin and are directly released to posterior pituitary through their axons connection (hypothalamic hypophyseal tract) where they are temporarily stored in neurohypophysis  ADH and oxytocin are both made in the hypothalamus and released into circulation  Neural-endocrine reflex – a stimulation to sensory neuron sends signal to the brain, which then respond through endocrine system – release of hormone  (ex. Oxytocin release- stimulate mammary gland – hypothalamus – posterior pituitary – release oxytocin back to mammary gland  allow milk letdown)  Positive feedbacks More sucking on breast, more oxytocin is produced to create milk letdown More pressure exerted in uterus, the more oxytocin is produced  Negative feedback – response to salt ingestion Hypothalamus produce ADH to increase water reabsorption in the kidney (conserve water) Cause thirst (to drink and obtain more water)  Ways hypothalamus is stimulated to release ADH (VP) Hypothalamic osmoreceptor – osmolarity greater than 280 mOsM Atrial stretch receptor – low blood volume Cartotid and aortic baroreceptor – decreased blood pressure  60% men obese, 38% female obese in Canada  Why do we eat – (environment and lifestyle) Taste and smell palatability Cost/reward optimization Internal clock Availability Cues and social habits  Individual predisposition for obesity (Genetics) Genetics Epigenetics Imprinted Early life events  High fat and sugar diets contribute to development of obesity  Adipose tissues release leptin – hormone that provides satiety signal (high leptin = high fat = satiation, low leptin = low fat = hunger)  Oxrexin (peptide) – formed in lateral hypothalamus neurons – helps induce feeding  Interferences with Satiety Centre Chronic secretion of leptin (too much leptin release)  increase leptin resistance  no longer have satiety signal  SNS (sympathetic nervous system) hypertension Ablation (lesion) of Arcuate/VMH hypothalamic nuclei  damage satiety center  never feel full  GAIN WEIGHT (ex. Obesity)  Interference with Hunger Center Ablation of lateral hypothalamic nucleus  LOSS WEIGHT (ex. Anorexia)  Metabolic syndrome- collection of signs and symptoms that are associated with metabolic disorder and cardiovascular disease  Anorexia & obesity involves genetic, neurochemical, psycho-developmental, and socio-cultural factors  ALL involve hypothalamus  Melatonin (produced in pineal gland) is suppressed in the presence of light  Circadian rhythm – 24 hr cycle in which biological rhythm is found – (ex. Corticosterone, LH, melatonin release all follow 24 hr pattern)  Suprachiasmatic nucleus (SCN) – biological clock – control the following circadian rhythms Sleep (melatonin) Food and water intake Urine production Blood pressure (spike in the morning) Platelet aggregation White blood cell production Body temperature change Hormone release (corticosterone, luteinizing hormone, melatonin) Menstrual cycle  Heat is produced through Radiation (sun) Conduction Metabolism Muscle contraction (skeletal)– most heat produced and highest efficiency * blue indicates external heat inputs  Heat is lost through Convection Radiation Evaporation Conduction  At low temperature – activate posterior hypothalamus  Sympathetic adrenergic muscle contraction (somatic neurons stimulate skeletal muscle)+ vessel constriction (increase blood pressure)+ sweat gland inactive  RAISE temp  At high temperature – activate anterior hypothalamus  Sympathetic cholinergic vessel dilation + inhibit heat conserving mechanism + sweat gland activate  LOWER temperature  Brown fat produce heat through chemical process  Exogenous pyrogens (fever producing) – Bacteria + virus produce endotoxins  activate phagocytic cell  produce interleukin 1 (endogenous pyrogen)  activate hypothalamus to produce prostaglandin derivatives that raise temperature (fever) = kill off pathogens with high temp  Babies can have higher temperature (>41 C) because they have high [surface are]/[volume] can dissipate a lot more heat  also need more fluid b/c they thermoregulate so efficiently.  Symptoms (Heat Exhaustion) Symptoms (Heat Stroke) Heat loss mechanism working over time Body fails to regulate temperature (working TOO WELL) effectively Normal/Subnormal body High body temperature temperature Moist clammy skin Dry hot skin Low blood volume and pressure Treatment: Give Fluid Treatment: Bring Body Temperature Down  Most of olfactory (smell) smell is DIRECTLY passed into the limbic system  very unusual  All receptors OTHER THAN olfactory receptors have a thalamic relay nucleus  Hypothalamic-Limbic system – limbic system act as relay between external and internal environments  regulate endocrine system, ANS (autonomic nervous system), emotion and motivated behaviors  Limbic system: Amygdala (emotion) + hippocampus (memory)  Substance must have the following characteristics to be detected as smell Volatile Water soluble OR Liquid soluble  Richard Axel and Linda B. Buck discovered odor receptors and organization of olfactory system  Due to irritants, smell sensory receptors (olfactory epithelium/nasal mucous) undergo neurogenesis (regenerate its cells) – 1% lost per year  only place where neuron/receptor regenerates.  1000 different type of smell receptors (total 5 million receptors)  all receptors of each type go to one specific neuron  Glomeruli is the synapse cleft region between olfactory neuron axon and dendrite of mitral cell  Olfactory receptor is only excitable at the cilia end (and not at soma), like receptors converge at glomeruli. Mitral cell has a lot of dendrites  can have summation (spatial) from different sources of olfactory neurons. Olfactory neurons are unmyelinated and very fragile. Both glomeruli and mitral cells are located in olfactory bulb  Olfactory pathway: odorant bind to receptors  olfactory specialized receptors are activated and send electric signal  signal relayed to glomeruli  signal transmit to higher region of brain (LIMBIC SYSTEM)  Anosmia- lost of smell (may impair taste too)  1 order neurons – respond to stimuli  RECEPTOR CELLS  2 order neurons – MITRAL CELLS  Retronasal route – when odorant reach olfactory mucosa through nasal pharynx  Jacobson’s organ – “sexual nose”  detects pheromones (ex. Androsterone), input directly to limbic system, involved in emotional + socio-sexual behaviors, genetic link for odor perception, never conscious awareness.  Parts of central nervous system (CNS) Cerebrum – contralateral (opposite side) sensation and movement Cerebellum – has two hemispheres  ipsilateral (same side) motor control Brain stem – life functions – respiration, body temperature  most primitive Spinal cord – conduit for information to and from the brain  sensory and motor losses following sections  Brain divisions Forebrain o Telencephalon – cerebrum o Diencephalon – thalamus + retina Midbrain o Tectum – superior and inferior colliculus o Tegmentum Hindbrain (rhombencephalon) o Metencephalon – cerebellum and pons o Myelencephalon – medulla  Gray matter (cell bodies) are outside, white matter (axon) are inside of cerebrum cortex  Gray matter are inside, white matter outside of spinal segment  Each spinal nerve consist of dorsal root (sensory – afferent (incoming)) and ventral root (motor – efferent (exiting))  Total 31 pairs of spinal nerves and 12 pairs of cranial nerves  Five regions of spinal cords (total 31 segments) – each segment receive and direct signal to 1 region of body (ex. Dermatome – sensory region for skin) Cervical- 8 Thoracic – 12 Lumbar – 5 Sacral - 5 Coccygeal – 1  No spinal cord in lumbar region- can take spinal fluid without damage any nerves  Brain does not need spinal cord control, have their own cranial nerves (12 pairs)  Face does not need dermatomes because there are controlled by cranial nerves  Cerebrospinal fluid (CSF) – found between arachnoid and pia mater layer (in subarachnoid space) – produced by choroid plexus (usually in the ventricular system in the BRAIN)  produce 500 mL of CSF/day  Ventricular system – series of ventricles and canals that move CSF within brain and transport in and out of subarachnoid space.  Central sulcus – divide lines between frontal and parietal lobes . Humans have the biggest frontal lobes.  Most important role for touch is to protect from injury  Somatosensory system – concerned with conscious perception such as touch, pain, temperature position movement  unique in that receptors are NOT concentrated in one location (unless cochlea or retina)  Located EVERYWHERE Cutaneous sensations (originates from skin) o Proprioception – sense of limb position o Kinesthesis – sense of limb movement  Peripheral nerve terminates in either spinal cord (spinal nerves) or brain stem (cranial nerve)  Skin types Hairy – arm or leg Glabrous (hairless) – palm  Skin is composed of two layers  epidermis and dermis  Mechanoreceptor- sensitive physical distortion to the skin (ex. Stretch, bend)  Thermoreceptors – respond to specific temperatures and to more importantly change in temperature  Tactile acuity Two point discrimination – smallest separation between two points on the skin that is perceived as two points rather than one. Smaller separation/distance = greater tactile acuity = smaller receptive field  Dorsal column-medial lemniscal pathway (touch, vibration)  crossover occurs at brainstem. Spinothalamic pathway (temp, pain)  crossover occurs at base of spinal cord  Somatotopy – point to point correspondence of an area of body and specific point in somatosensory cortex  some body regions (ex. Hands and face) are overrepresented in the brain (magnification factor) MIDTERM 2 Sensory Physiology III – Vision (Eye+Retina)  Where to visual signal go after exiting retina Lateral geniculate nucleus (LGN) – DOMINANT pathway Superior Colliculus (SC) – in tectum in midbrain Pretectum – Edinger-Westphal nucleus  controls pupillary constriction (depending on amount of light)  BOTH eyes must constrict at the same time Hypothalamus – suprachiasmatic nucleus (SCN)- synchronize diurnal rhythm with day-night cycle  Visual pathway synapse at LGN  Visual acuity – capacity to resolve fine spatial detail, affected by Stimulus Eye Central visual pathways  Stimulation for vision is LIGHT  electromagnetic energy produced by electric charges that are radiated as waves. Human perceive light from 400- 700 nm  Snellen Acuity – how well you see at 20 ft (6 m) At 20 ft – can detect 1 deg critical features (20/20) At 20 ft- can see as clear as a normal person 40 ft away (20/40) – poor acuity *poorer acuity as one age  Legal blindness – when a person’s best-corrected vision (ex. even after contact lens) is 20/200 or worse Rods Cones Light sensitive Color sensitive Dim light – scoptopic vision Daylight – photopic vision 120 million / retina (eye) 5 million / retina (eye)  Phototransduction – convert light into electricity  outer segment of photoreceptor  Three types of cones- red, green, blue  having ALL three types of cones make me trichomat  Color blindness  total 8% men have some color blindness (impairement) 2% men lack red or green pigment  red-green color blind  dichromats 6% men have red and green pigment but their peaks shifted (absorb different wavelengths)  Input from both eyes come together in primary visual cortex Sensory Physiology VI – Vision (Pathways and Brain)  Primary visual cortex (V1, or Striated Cortex) – locate on far side of back of the brain Neurons in V1 (known as feature detectors b/c help breakdown complex stimulus into simpler features) are specialized for specific aspect of stimuli such as orientation, movement, and size – do not get stimulated by light only - experiment of Hubel and Wiesel o Orientation – change orientation cause greater firing o Direction- movement in one direction is more favored (greater firing of neuron)  Further away we move from retina, the neurons will respond to more complex stimuli Sensory Physiology V – Audition  Human hearing frequency range – 20 – 20,000 Hz  Audibility curve – plot threshold for fearing vs. frequency  most sensitive between 2,000 and 4,000 Hz  lower the threshold = more sensitive  Variables in sound Frequency (pitch) – measured in Hz Intensity (loudness or volume) – amplitude (amount of pressure) – measured in dB (logarithmic)  Speed of sound – air = 767 mph (340 m/s), water = 1500 m/s  Deafness Unlike visual system, destructing auditory cortex in one hemisphere does not result in loss of hearing on one side  can still hear fine, but the ability to localize sound in opposite hemifield is impaired Most hearing loss is due to death (from aging) or destruction (due to loud noise) of hair cells  hair cells cannot regenerate  Auditory canal enhance intensity of sound by resonance  resonance frequency (allow highest intensification) is from 2,000-5,000 Hz in human  Ossicles (malleus, Incus, Stapes) amply force exerted against oval window by converting air pressure changes into mechanical pressure, which is more effective in vibrating perilymph (fluid) in cochlea  Unlike visual pathway (which information of two eyes converge at primary visual cortex), information from two ears converge at brain stem (ventral cochlear nucleus)  Hair cell synapse with spiral ganglion cells  axons of spiral ganglion cells form the auditory portion of Vestibulocochlear Nerve (Cranial Nerve VIII) Motor System  Motor unit – 1 motor neuron (alpha motor neuron) and all muscle fibers it innervates  basic unit needed to perform any movement  Somatic motor neuron – excitatory ONLY  no such thing as inhibitory alpha motor neuron  alpha motor neuron activate muscle muscle spindle Muscle Spindles Golgi Tendon Organ (GTO) Tell you about length and change in Tell you about tension in the muscle length of muscles  1a – Muscle spindle (intrafusal fiber), Alpha motor neuron – Muscle fiber, 1b – Golgi tendon organ (GTO)  Reflex/reflex arc Can involve skeletal, cardiac, or smooth muscle Involves 1) receptor 2) afferent neuron 3) synapse 4) motor neuron 5) effector Have reflex latency (time lag between stimulus and reginning of response)  depends on 1) latency of receptors to respond, 2) length of nerve pathway, 3) conduction time along the pathway, 4)number of synapses Influenced by CNS (inhibitory OR facillitary). Motor neuron = final common pathway (several neurons converge on it (ex. sensory, interneuron, excitatory…) Spinal shock – followed by spinal cord transection (cutting) – all reflexes below section are lost for a period of time  soon reflex return, but reflex action is often exaggerated – hypertonic Reciprocal innervation – contraction of a muscle is accompanied by inhibition of an antagonist muscle. Reciprocal inhibition – cause the opposing muscle group to relax  Power-lift – weight too heavy  to prevent muscle ripping off, Golgi Tendon Reflex is activated to relax muscles and drop weight  Golgi tendon reflex (Inverse stretch reflex) – relax the muscle – protective method vs. Stretch reflex (by muscle spindles) – accommodate more load by contraction  Motor movement important areas Motor cortex (frontal lobe on precentral gyrus)  origin for command/execution of movement o Somatotopic organization  arranged according to body parts. Factors that determine how much motor cortex is devoted to a part of a body  Density of motor unit  increase density = greater representation  Size of motor unit  smaller size (ex. 1 motor unit/ muscle fiber)  greater representation Cerebellum functions o Balance o Coordination of movement o Timing of movement o Programs of movement o Maintain muscle tone Basal nuclei (ganglia) Substantial Nigra o Inhibits basal ganglia o Associated with Parkinson’s disease  Babinski sign – test if there is damage to lateral corticospinal spinal tract Normal Adults  Babinski negative  toes curl inwards Abnormal adults + baby (haven’t fully developed corticospinal)  Babinski positive  toes curl outwards  Treatment for Parkinson disease 1. Lesions of Basal Ganglia. 2. L-Dopa (in combination with Ach inhibitor).
 3. Transplant of non- differentiated embryonicß adrenal medulla tissues.
 4. Thalamic nucleus stimulation Cardiac Vascular Physiology II Conduction speed Rate of spontaneous depolarization of conducting cells Speed of propagation of AP The speed for reaching threshold (self- depolarization) SA node – 0.05 m/sec – not the fastest SA node – FASTEST Atrial muscle – 1 AV node – 0.03 – 0.05 m/sec (SLOWEST) Bundle of His – 1 m/sec Purkinje fibres – 5 m/sec (FASTEST) Ventricular muscle – 1 m/sec  Repolarization of atrial contracting cells is TOO SMALL to be seen by ECG  hid by QRS complex.  What can ECG tell Extent and type of disturbances of rhythm or conduction Extent and location of myocardial damage Effect of drug Heart rate (pick up as # of QRS complex per minute)  Cardiac cycle shows mechanical and electric event of single contraction (1 contraction-relaxation phase) of LEFT heart at REST. Include Pressure change Volume change ECG Valve open and closing  Atria contract from TOP-DOWN. Ventricle contract from BOTTOM-UP, but relax from TOP-DOWN  End diastolic volume (EDV) – 160 mL  amount of volume at end of diastole (max volume for left ventricle)  End systolic volume (ESV) – 90 mL  amount of volume at end of systole (minimum blood volume for left ventricle)  Stroke volume = EDV – ESV (roughly)  around 160-90  70 mL (about 30% is from ventricular filling (from contraction of atrium – phase 1), and 70% filled when ventricle is relaxed (phase 5))  Systole – contraction vs. diastole – relaxation Cardiovascular Physiology III  Maximum Heart rate = 220 – age of the person  Cardiac output can be changed through changing heart rate (beats/min) or stroke volume (mL) Heart rate (beats/min – bpm) o < 100 bpm (parasympathetic – vagal tone) , = 100 bpm (intrinsic rate (set by SA node) - no autonomic stimulation), > 100 (sympathetic) o Autonomic nervous system change heart rate by changing the slope of pacemaker potential  Parasympathetic (PNS) - SLOW heart rate  Distribute to SA, AV node, and lesser extent atrial and ventricular muscle through vagus nerve  Release Acetylcholine  slow heart rate by  Close some Ca 2+ channels  decrease slope of pacemaker potential  takes longer to reach threshold potential  Open K+ channel  hyperpolarization – increase the “resting” membrane potential to -70 mV from -60 mV  Sympathetic (CNS)  Distribute to SA node, AV node, strong representation to ventricular muscle  Release neurotransmitter norepinephrine and indirectly hormone epinephrine + 2+  Open Na and Ca channels  increase slope of pacemaker potential (and nothing else) Stroke volume (SV) control – amount of blood pumped by each ventricle in one contraction (SV = EDV – ESV) o At rest, EDV = 160 mL, ESV= 90 mL  SV about 70 mL During exercise EDV and decrease to as low as 10-30 mL and EDV as high as 200-250 mL 1. SV affected by autonomic nervous system (Δ the ESV part) – regulate amount of Ca2+change force of muscle contraction and ESV (high contraction = lower ESV)  Parasympathetic – increase ACh = close Ca channel = decrease Ca 2+= decrease force of muscle contraction = lower ESV (hence SV) 2+  Sympathetic – increase NE + Epinephrine = open Ca channel = more Ca = increase force of muscle contraction = higher ESV (hence SV) 2. SV affected by preload – pressure on cardiac muscle before contraction (depend on the EDV part)  higher EDV = greater preload = greater stretch in myocardial cells  greater force of contraction of cells  greater amount of blood ejected  greater SV  Frank-Starling Law of heart – an increase in EDV will cause an increase in stroke volume Physiology IV  In order to increase EDV  increase venous return to the heart  ex. during dynamic exercise, following mechanisms help increase venuous return Muscle pump – skeletal muscle squeeze veins  more blood pushed back to the heart Respiratory pump – when breathing  diaphragm contracts  decrease chest cavity pressure and increase peripheral pressure  increase venous return Sympathetic nervous system (SNS) – venoconstriction  small constriction of veins  squeeze blood toward the heart  increase venous return  Diastolic pressure (80mmHg  during relaxation of heart) vs. systolic pressure (120 mmHg  during contraction of the heart) that’s the ARTERIAL PRESSURE (ex. pressure reaches near ZERO by the time vena cava reaches the right atrium). Capillaries (40 mmHg), venules (10-15 mmHg)  Pressure gradient drives movement of blood. Greatest pressure drop (drop about 55 mmHg) takes place in ARTERIOLES caused by HIGH RESISTANCE of vessels (50% of resistance in entire systematic system).  Change in one unit of radius has a greater affect on blood flow than change in pressure  when vessels are constricted (smaller radius) although pressure is increased, blood flow is still reduced b/c smaller radius has greater effect Mean blood velocity (cm/s) Blood flow (L/s) Speed which blood is moving through Volume flow rate of blood blood vessel Mean blood velocity can vary depends on Total blood flow is constant (5L/min) the total cross-section area of vessel. Physiology V  Types of exchange in capillaries Diffusion o Water and dissolved substance (polar) – diffuse through slits (cleft) in capillary walls  degree of leakiness varies for capillaries in different cells o Lipid-soluble substance – diffuse through entire length of capillary wall Filtration and reabsorption (4 Starling forces) o Filtration – movement of fluid OUT of capillary o Reabsorption – movement of fluid INTO capillary o 4 Starling forces – Hydrostatic pressure Osmotic pressure  Capillary hydrostatic pressure of plasma (Pc) – pressure from blood in capillary  cause filtration  arterial end 25 mmHg, venuous end 10 mmHg  Interstitial Fluid Hydrostatic Pressure (IF)- pressure on the fluid in interstitial space (can be +ve (cause reabsorption) or –ve (cause filtration))  Intersitial Osmotic Pressure (TT IF– pressure caused by osmosis of protein in interstitial fluid (5mmHg)  Plasma Osmotic Pressure (TT ) P pressure caused by osmosis due to proteins in the plasma (28mmHg)  The protein in plasmid is 6 times as much as the protein in interstitial fluid Midterm 3 Renal  Major functions of kidney Regulation of extracellular fluid volume and blood pressure Osmolality and ion balance and pH and Hormone and gluconeogenesis Excretion of waste as urine  Kidney located posteriorly to abdomen at level 11 and 12 rib. Two layers Medulla (inner layer) – striated (contain tubules) and triangular structure (calyces – used to collect urine before converge in pelvis and then ureter) Cortex (outer layer) – granular (all renal corpuscles contain here)  Filtrate is called URINE only after leaving the kidney. Multiple nephrons per collecting duct.  Nephron- functional unit  1million/kidney. Consist of: Renal corpuscle (glomerulus (capillary - endothelium)+ bowman’s capsule (hollow, fluid filled visceral epithelium)) – FILTER blood Tubules – single layer of EPITHELIAL cells  process filtrate Cortical nephron (80% of nephron) Juxtamedullary nephron (20% of nephron) Renal corpuscle at upper/mid CORTEX Renal corpuscle lower CORTEX (just above medulla) Shorter loop of Henle Longer loop of Henle  can concentrate urine better Peritubular capillaries – wrap ALL the Vasa Recta  wrap around tubules, but way around tubules + loop less on loop  help concentrate urine through countercurrent flow  Bowman’s capsule (epithelium) is fused with glomerulus (endothelium) through basal lamina. Blood flow from afferent arteriole  capillary bed  efferent arteriole.  Three barriers to filtration 1. Endothelial cells + pores (fenestrae) of “leaky, fenstrated” capillaries in glomerulus  exclude RBC, WBC 2. Basal lamina (basement membrane) – collagen and NEGATIVELY charged protein  NON-CELLULAR (extracellular component)  oppose most protein (through –ve charge repel) 3. Podocytes – foot-like pertrusions around glomerular capillaries  TIGHTNESS can be adjusted by the body to regulate how much filtrate is leaked in *Ions (both + and -), glucose, amino acids, and water, CO ,2O 2 H , HCO 3 Creatinine, Urea (waste) allowed in. Red Blood Cell, WBC, and protein not allowed.  Blood consists of plasma (Ions (both + and -), glucose, amino acids, and water, CO 2 O 2 H , HCO 3 hormones) and RBC, WBC  Only PLASMA is filtrated into bowman’s capsule. Arterioles (w/smooth muscle) constrict/dilate  regulate blood flow st  Kidney blood flow contains 2 capillary beds (glomerulus (1 ) and Peritubular/Vasa recti (2 ) and 2 arterioles (afferent + efferent). Kidney filters 180 L plasma/day, but only 1.5-2 L urine produced. 20% cardiac output to kidney, about 20% of that gets filtrated (amount depends on net filtration pressure). Glucose must be 100% reabsorbed (no glucose can be found in urine)  Processes in nephron Filtration – movement of plasma into bowman’s space (in renal corpuscle ONLY) Reabsorption – Substance from filtrate  back to blood (Peritubular or vasa recta) o THROUGH epithelial cell (transcellular reabsorption)  Diffusion – small nonpolar molecules (O2, CO2)  Channels + Pores – charged, hydrophilic, or large molecules (ions, water, glucose) o IN BETWEEN epithelial cell (paracellular reabsorption) Secretion (rare) – blood (Peritubular or vasa recta)  back to filtrate in nephron  very SELECTIVE  need channels or transporters that pass basolateral and luminal membrane (ex. drugs) * Excretion (as urine) = Filtration – Reabsorption + Secretion  Net filtration pressure  (+ve) – FILTRATION (-ve) – NO FILTRATION  affected by 4 pressures seen in next picture drawing  NORMAL PERSON (10 mmHg)  >10 mmHg = more filtration. <10 mmHg = less filtration  14% filtrate is reabsorbed after passing through collecting duct. Hormones control all channels/pumps in collecting duct except for Aquaporin III and IV  Glomerular Filtration Rate (GFR) – amount solute/fluid filtered per unit time (ex. day) into Bowman’s space. Affected by: Net filtration pressure  Hydrostatic Pressure of Glomerular Capillaries (PGC is the main contributor. Affected by AUTOREGULATORY mechanisms o Renal blood flow. o Blood pressure. Can be adjusted to normal by: 1. Myogenic Response – response to Δ blood pressure – through vasoconstriction/dilation of arteriole (efferent/afferent) by stretch-sensitive ion channels  High pressure (high GFR)– smooth muscle in afferent arteriole stretch  activate stretch sensitive ion channel  muscle cell depolarize  VG Ca2+ channel open  smooth muscle CONTRACT (VASOCONSTRICTION)  DECREASE BLOOD FLOW = DECREASE GFR 2. Tubuloglomerular Feedback – response to [NaCl] – through vasoconstriction/dilation of arteriole (afferent/efferent) by local chemical signal by macula densa cells (distal tubules)  High [NaCl] (High GFR)  macula densa cells produce local chemical signals  afferent arterioles constrict  DECREASE BLOOD FLOW (DECREASE GFR) *Afferent arteriole constrict (Hydrostatic pressure DECREASE, GFR DECREASE). Efferent arteriole constrict (hydrostatic pressure INCREASE, GFR INCREASE)  Increase GFR = decrease reabsorption = increase excretion Filtration coefficient. Affected by: o Surface area o Permeability of capillary (adjusted by podocytes and basal lamina)  Measure GFR by measuring rate of excretion (urine) of a substance that 1) gets filtrated into Bowman’s space 2) not reabsorbed or secreted so that rate of excretion (urine output) = rate of filtration Creatine (waste) is used  Clearance rate of creatine = excretion rate of creating (mg/day) / [creatinine] in plasma (mg/L)= GFR * Normal 180 L/day GFR  Tubules along nephron made of epithelia cells attached to basement membrane and linked via tight junctions  but vary in properties b/c have different channels present.  Symport and Antiport are all SECONDARY ACTIVE TRANSPORT  1 molecule is down the [ ] gradient (Na ) while the other is against the [ ] gradient  Diabetes Mellitus – when nephron can’t reabsorb ALL glucose in filtrate Type I – deficiency in insulin production Type II – decreased cellular response to insulin  both types cause MORE GLUCOSE filtrated into Bowman’s capsule  and since glucose transporters in proximal tubules have LIMITED CAPACITY  can’t reabsorb ALL glucose  cause o Glucosuria – Glucose found in urine o Osmotic diuresis – Increased urine volume (because increased amount of glucose cause more water retention)  Channels and transporters can be Regulated – respond to hormone, which causes regulation at 1. Gene expression level 2. Cellular location (allocate to right place) 3. Level of activity Non-regulated – constitutively expressed  Regulation of water and salt excretion occur INDEPENDENTLY in human. Input of water occurs from 1) food + beverage (MOST) 2) metabolically produced (byproduct of cellular respiration). Output of water 1) urine (MOST) 2) Skin and Lungs (SOME) 3) Sweat, Feces . Higher ECF = Higher blood pressure . Urine output (due to regulation) can vary from 0.4 L/day (dehydration environment) to 25L/day (over hydration) – normal 1.5 L/day. ADH=vasopressin  Action of ADH: binding of ADH (peptide hormone) to cell receptor at basolateral membrane  INCREASE cAMP (secondary messenger)  transduction cascade  Insertion of INCREASE Aquaporin II at luminal membrane  INCREASE water reabsorption (SEE DRAWING FOR MECHANISM)  Diuresis – increased production of urine  result DEHYDRATION. Causes Diabetes Insipidus – defect in ADH system o Posterior Pituitary can’t release ADH o Kidney can’t respond to ADH Alcohol – easily cross blood-brain-barrier  inhibit ADH +  Recommend 2.5g Na /day. Sodium input 1) food. Sodium output 1) Urine (MOST) 2) Sweat + feces Angiotensin II (peptide) ADH (peptide) Aldosterone (steroid) Luminal membrane Basolateral Diffuse through receptor binding membrane receptor basolateral membrane * b/c small size  enter binding as filtrate into nephron INCREASE cAMP DECREASE cAMP No cAMP INCREASE Na /H+ + INCREASE Aquaporin INCREASE Na channel exchanger and Na /K + II at COLLECTING DUCT and Na /K ATPase at ATPase at PROXIMAL COLLECTING DUCT TUBULE VASCOCONSTRICTOR N/A N/A Respiration  Respiratory system – include both lungs and blood vessels  functions: Gas exchange – O a2d CO , 2H regulation Speech, microbial defense Arterial concentration of chemical messengers, break down small blood clots  Air is brought through ventilation2(O ) and pulmonary circulation 2CO ). Pleurisy – infection in intrapleural space (painful breathing). Left lung – 2 lobes (superior, inferior), Right lung – 3 lobes (superior, middle, inferior)  left lung 1 less lobe because of cardiac notch (space to accommodate heart – b/c it lays to the left side). Parietal (outer- fused with rib) and visceral (fused with lungs) pleura are continuous (connected).  Intrapleural space (between visceral and parietal) – 0.5 mm wide and contain 1-5 mL intrapleural FLUID. Diaphragm (skeletal muscle) separates thoracic cavity (lung here) and abdominal cavity Conducting Zone Respiratory Zone primary bronchi  secondary bronchi  respiratory bronchioles (w/ alveoli)  tertiary bronchi  bronchioles  alveolar ducts  alveoli sac  alveolus terminal bronchioles 1. Conduct air (low resistance to air) 1. Gas exchange 2. Microbial defence (via cilia 2. Alveoli (epithelial cell) present  (macrophage, mucus) provide surface for gas exchange 3. Warm + moisten air macrophage  Air Pathway: trachea  primary bronchi  secondary bronchi  tertiary bronchi  bronchioles  terminal bronchioles  respiratory bronchioles (w/ alveoli)  alveolar ducts  alveoli sac  alveolus  Blood pathway: RIGHT HEART  pulmonary artery  pulmonary arteriole  pulmonary capillaries (wrap around each alveolus)  pulmonary venules  pulmonary vein (oxygenated) LEFT HEART  Inside alveolus: Air, Blood-gas barrier (BGB – 0.3-0.5 um wide), macrophage Alveolar cell  1) Type I – thin – wall of alveolus – good for gas exchange 2) Type II – produce surfactant  Fick’s law –  Factors that maximize simple diffusion that across blood gas barrier Lipophilic gas (CO 2 O 2, low blood speed (allow more time for diffusion) Thin membrane, high surface area, high pressure gradient  Pressure is inversely related to Volume (Boyle’s law). Breathing is facilitated by pressure gradient (by changing volume in thoracic cavity (lung) only) Inhalation Exhalation ACTIVE process (CONTRACTION) PASSIVE process- RELAXTION (QUIET 1) External intercoastal muscle EXPIRATION) contract (outwards and upwards) - (25% 1) External intercoastal muscle relax contribution) (inwards and downwards) 2) Diaphragm (skeletal muscle) relax 2) Diaphragm (skeletal muscle) (upwards) contract (downwards) -75% contribution) ACTIVE process (in exercise only) (FORCED EXPIRATION) CONTRACTION of 1) Internal intercostal muscle (in and down) 2) Oblique muscle 3) Rectus Abdominus (abs) *2 and 3 force push visceral organ up against diaphragm. Are both ADBOMINAL MUSCLE  At rest  atomospheric pressure = intrapulmonary (aveolar) pressure = 760 mmHg  Peneumothorax – when alveolar (intrapulmonary) pressure = intrapleural pressure  transpulmonary pressure = 0  will result LUNG COLLAPSE  Lung compliance – “stretchiness” of lung – ΔVolume = Compliance * Δ Pressure  more compliant = easier to change volume (stretch) with a given pressure unit. Compliant = can stretch OUTWARDS. Collapse/Elastic (strech INWARDS)  more compliant = less likely to collapse  following can DECREASE compliance (1/3 contribution) Elastic tissue in the lung  elastin and collagen generate recoil/collapse force o INCREASED elastic tissue (elastin+collagen) = DECREASED compliance = INCREASE % of lung collapse (2/3 contribution) Surface tension (force due to attraction between water molecules)  promotes elasticity  DECREASED compliance = INCREASE % of lung collapse o Surfactant (phospholipid protein w/hydrophobic and hydrophilic moieties) can 1) reduce surface tension (INCREASE compliance) and 2) microbial defence  Neonatal Respiratory Distress Syndrome (nRDS) – premature surfactant system Premature in infants, poor lung functioning, alveolar collapse, and hypoxemia Treatment: Surfactant injection (LECTURE RECORDING HERE) FEV-1  NORMAL (80% FVC) Obstructive disease Restrictive disease Obstruction in air flow  DECREASE - Decreased compliance FEV-1/FVC (<80%) - Decreased total lung capacity - Lower FVC (FEV1 same)  >80% FEV1/FVC Asthma Pulmonary Fibrosis Airway inflammation  airway Fibrous scar tissue form  increase hyperresponsiveness  airway smooth collagen (make inelastic)  decrease muscle contract (spasm) airway compliance narrowing Triggered by exercise, air pollution, allergies Chronic Bronchitis (smoking main cause) Inflammation, enlarged mucus glands  enlarged mucus gland  excess mucus in air way Emphysema (smoking main cause) Alveolar wall destruction  loss of elastin  reduce elastic recoil + surface area  Increase elastin = increased compliance. Increase collagen = decreased compliance  Partial pressure = total pressure (760 mmHg (atmospheric)) X Fraction concentration of one gas (O2= 21%, Nitrogen= 78%, CO =20.04%) pO 2 pCO 2 No Breathing DECREASE INCREASE (low pH) Hyperventilation INCREASE DECREASE (high pH) Increase metabolic DECREASE INCREASE (low pH) activit
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