208 Review Question

TOPIC 1: Neurophysiology
1.1 Describe the changes that occur in membrane permeability to Na+ and K+ ions when a neuron generates an action potential. When a neuron generates an action potential, muscle cells become more permeable to Na+ and K+; Na+ enters the cell (membrane potential becomes less negative) and K+ leaves the cell (K+ main ion species contributing to the negative charge on the inside of the membrane). K+ movement across membrane has more impact on resting membrane potential than Na+

*Purple Font = extra info Muscle Contraction 1 - Calcium released from sarcoplasmic reticulum 2 - Myosin head energized via myosin-ATPase activity which converts the bound ATP to ADP + Pi 3 - Calcium binds to troponin 4 - Tropomyosin translocates to uncover the cross-bridge binding sites 5 - The energized myosin binding sites approach the binding sites 6 - The first myosin head binds to actin 7 - The bound myosin head releases ADP + Pi, flips and the muscle shortens 8 - The second myosin head binds to actin 9 - The first myosin head binds ATP to allow the actin and myosin to unbind 10 - The second myosin head releases its ADP + Pi, flips & the muscle shortens further 11 - The second myosin head binds to ATP to allow the actin and myosin to unbind 12 - The second myosin head unbinds from the actin, flips back and is ready for the next cycle 13 - The cross-bridge cycle is terminated by the loss of calcium from the troponin 14 - Tropomyosin translocates to cover the cross-bridge binding sites 15 - The calcium returns to the sarcoplasmic reticulum, the muscle relaxes & returns to the resting state

Action Potential/Excitation Coupling/Muscle Contraction

Nerve impulse reaches neuromuscular junction Action potential from motor neuron causes the release of acetylcholine (neurotransmitter) into the synaptic cleft Acetylcholine binds to receptors on the motor end plate, creating an end-plate potential, that leads to depolarization (excitation) of the muscle cell. Sodium enters muscle cells through ion channels Excitation is conducted down the transverse tubules deep into muscle fibre 1

Action potential reaches sarcoplasmic reticulum, calcium is released Calcium diffuses into muscle and binds to troponin, which causes a positional change in tropomyosin, unblocking active sites on actin, allowing myosin heads to form strong attachments The strong binding of actin-myosin cross bridges initiates the release of energy stored within myosin molecule, producing an angular movement of each cross bridge causing the muscle to shorten

Ending Contraction cycle: Nerve impulses to contracting muscle cease Ca2+ pump moves Ca2+ back into sarcoplasmic reticulum Absence of Ca2+ causes tropomyosin to re-cover active sites of actin, therefore strong binding of cross bridges is ceased and muscle no longer contracts 1.2 List the main structures of a neuron and state their primary function.

Dendrites: highly branched, receives information from other neurons thru dendrites Cell Body: contains nucleus, mitochondria, golgi apparatus, neurofilaments & neurotubules Nucleus: same as other cells: control centre of the cell. Axon Hillock: initial region of the axon, Axon: propagates electrical impulse (action potential) Myelin sheath: made of Schwann Cells, insulates axon, allowing faster signal transduction Nodes of Ranvier: gaps btw the Schwann Cells, electrical impulse jumps btw nodes Axon/ Synaptic Terminals (Telodenria): ends of axon, branched, were the synaptic terminals are, start of neuromuscular junction. Neuromuscular Junction: site of action potential transferring from one neuron to the next / from neuron to receptor cell.

1.3 List the main structures of a synapse and state their primary function. Telodendrion: (axon terminal) last bit of axon, leading into synptic knob; Synaptic knob; Mitochondria; Synaptic vesicles; Presynaptic membrane; Post synaptic membrane; Synaptic cleft; Endoplasmic reticulum;

1.4 Describe the main differences in structure and function between the sympathetic and parasympathetic divisions of the autonomic nervous system.

Functions:
Sympathetic: fight or flight response incr HR incr SV incr RR stimulates vasoconstriction (to areas that are not involved in exercise) incr [adrenaline] decr digestive activity

Parasympathetic: returns body to homeostasis (i.e. normal resting state) decr HR little effect on SV little effect on blood vessels incr digestive activity causes release of actylecoline

Structures:
Sympathetic: SNS fibres leave the CNS via the thoracic & lumbar region of the spinal cord. Parasympathetic: PNS fibres leave CNS via the brainstem & sacral portion of the spinal cord.

Sound Transmission:
Step 1: Sound waves enter external auditory canal (EAC) The pinna/auricle and the EAC help amplify & direct sound Sound waves reverberate from sides and end of EAC, filling it with continuous vibrations of pressure waves Tympanic Membrane (T membrane) /eardrum is stretched across the end of the EAC As air molecules push against T membrane, they cause it to vibrate at the same frequency as the sound wave Under high pressure (zone of compression) the T membrane bows inwards (how far relates to loudness/force of air molecules hitting T mem) During subsequent zone of refraction T membrane bows outwards When sound ceases it returns to midpoint T membrane separates the EAC from the middle ear Middle ear: air filled cavity in the temporal bone of the skull Pressure in EAC and middle ear normally same as atmospheric pressure Eustachian tube: connects middle ear to pharynx (normally closed; swallowing/yawning/sneezing opens it) When sudden change in atmosph pressure occurs (i.e. sudden change in altitude), a pressure diff btw middle ear and atmosph pressure results in T membrane being stretched causing discomfort This problem is relieved by swallowing or yawning; which opens the Eustachian tube and allows pressure to equilibrate with new atmosph press

The entire system described thus far involves the transmission of sound energy into the cochlea

Step 2: Transmission of sound energy from T membrane through middle ear cavity, to the inner ear (cochlea): spiral shaped, fluid-filled space in the temporal bone. Because liquid is more difficult to move than air, the sound pressure transmitted to the inner ear must be amplified This is achieved by a moveable chain of three small bones; the malleus, incus and stapes These bones act as a piston and couple vibrations of the T membrane to the oval window Oval window: membrane covered opening separating middle ear from inner ear Force of sound wave transferred from T membrane to oval window, However coz the oval window is much smaller than the T mem, the force per unit area (i.e. pressure) is increased 15 to 20 times. The amount of energy transferred to the inner ear can be lessened by contraction of two small muscles in the inner ear (tensor tympani muscle & stapedius muscle)

Cochlea duct: membranous tube that divides cochlea lengthwise. Contains sensory receptors of the auditory system. Cochlea duct is filled with fluid (endolymph) On either side of cochlea duct are compartments filled with fluid (perilymph) Scala vestibuli: is above the cochlea duct and begins at the oval window Scala tympani: is below the cochlea duct and connects middle ear at a 2nd membrane covered opening (the round window). The scala vestibuli and scala typani are continous at the far end of the cochlea duct at the helicotrema.

Components of the Auditory System:

Pinna: Auditory: Tympanic membrane Middle ear bones (malleus, incus, stapes): Cochlea Oval window

1.6 Describe in detail the role of the muscle spindle organ in monitoring muscle length, and briefly contrast its function with that of the Golgi tendon organ. Muscle spindles detect changes in muscle length, when the muscle reaches the point of being over stretched the muscle spindles send messages to the brain to stop the muscle from becoming any more stretched, to protect them from injuries. Golgi tendon organs detect the amount of tension being produced by a muscle, they ensure antagonist muscle work to prevent damage to agonist muscle that are overloaded.

1.7 Discuss neuro-chemical links with depression in the context of drug treatments for the disorder. Clinical depression is thought to be caused by low levels of amine neurotransmitters (serotonin, noradrenalin/norepinephrine, dopamine) at synapses that use serotonin as a neurotransmitter. Antidepressants increase the amount of serotonin at synapses that use it as a neurotransmitter. There are many different types of antidepressants and they affect serotonin levels in different ways. There are four main categories of antidepressants: serotonin-specific re-uptake inhibitors, dual reuptake inhibitors, monoamine oxidative inhibitors, and tricyclics. The most commonly prescribed antidepressants fall into the category of serotonin-specific re-uptake inhibitors, this means that they inhibit the reuptake of serotonin, therefore increasing the amount of serotonin at the synapses. Dual reuptake inhibitors inhibit serotonin and noradrenalin re-uptake, tricyclics inhibit the re-uptake of dopamine, serotonin and noradrenalin. REM sleep: deep sleep, high brain activity Storing memories in LTM Important for development (especially in infants) Dreams Incr HR Incr respiration Paradoxical sleep

TOPIC 2: Endocrine System

2.1 What are the 3 main hormone categories? 1. Steroid hormones: a. Glucocorticoids: b. Mineralocorticoids: c. Androgens: d. Estrogens: e. Progestagens: 2. Peptide hormones: pituitary hormones, insulin, follicle-stimulating hormone (FSH) 3. Amine hormones: norepinephrine, epinephrine, dopamine, thyroid hormones

2.2 Intracellular signal transduction pathways used by lipid-soluble messengers (steroids). Steroid soluble hormones diffuse into target cells and then attach to a receptor in the cytoplasm. When the steroid hormone needs to be released from the cell and enter the blood stream, it detaches from receptor, diffuses through cell membrane, travels thru intercellular fluid and diffuses through capillary wall into the blood stream, where it can be transported around the body. the lipid soluble hormones diffuse through the cell membrane and into the nucleus where they bind to a receptor. Then, the hormone-receptor complex binds to the DNA to activate specific genes.

2.3 Give examples of intracellular signal transduction pathway/s that are activated by plasma-membrane receptors. Steroid hormones - Phosphorylation of tyrosine kinase pathway - G-protein coupled receptor - Second messenger cAMP through activation of adenylate cyclise and in addition to cAMP, other second messengers that can be activated by G-proteins include: Inositol triphosphate (IP3) Diacylglycerol (DAG) Calcium (Ca2+ or PKC) Nitric oxide (NO) And, yes, ion channels can be activated as a result of G-protein activation.

2.4 What are the inputs to endocrine glands that control hormone secretion? Hormone Secretion is stimulated by: neural signals, other circulating hormones or both.

2.5 Describe the anatomical and functional differences between the hypothalamus, and the posterior and anterior pituitary. Hypothalamus: Function secretion of: CRH (corticotrophin-releasing hormone): secretion of ACTH TRH (thyrotropin-releasing hormone): secretion of TSH GHRH (growth hormone-releasing hormone): secretion of GH SS (somatostatin): secretion of GH GnRH (gonadotropin-releasing hormone): secretion of LH & FSH DA (Dopamine): secretion of PRL

*contains important control & integration centres, in addition to those associated with the limbic system. Structure: located at the top of the brainstem, the hypothalamus is a brain structure composed of distinct nuclei and less anatomically distinct areas. Anterior Pituitary: Function secretion of: FST (follicle stimulating hormone): gamete production (males); ovarian follicle growth (females) LH (luteinizing hormone): testicular production of testosterone (males); ovarian production of estradiol & stimulates ovulation (females) GH (growth hormone): growth, mainly via IGF-1 production; protein, CHO & lipid metabolism TSH (thyroid stimulating hormone): thyroid activity & growth PRL (Prolactin): milk production in breast ACTH (adrenocorticotropic hormone): adrenal cortex activity & growth

Beta-lipotropin & Beta-endotropin: possibly fat mobilisation & analgesia during stress

Structure: Pituitary gland is a pea-shaped structure located below the hypothalamus

Posterior Pituitary: Function secretion of: Oxytocins: milk secretion, uterine motility Vasopressin (anti-diuretic hormone, ADH): blood pressure, water excretion by kidneys

Structure: Pituitary gland is a pea-shaped structure located below the hypothalamus 2.6 List the six major anterior pituitary hormones, their functions and the hypothalamic hormones that control their release. Anterior Pituitary Hormones: FSH (follicle stimulating hormone): o Function: ovarian follicle growth (females); gamete production (males) o Secretion stimulated by - GnRH (gonadtropin-releasing hormone). GH (growth hormone): o Function: growth, mainly via production of IGF-1, peotein, CHO & lipid metabolism o Secretion stimulated by- GHRH (growth hormone releasing hormone) & SS (somatostatin) LH (luteinizing hormone): o Function: testicular production of testosterone (males); ovarian production of estradiol & stimulation of ovulation (females) o Secretion stimulated by GnRH (gonad-releasing hormone) TSH (thyroid-stimulating hormone): o Function: thyroid activity & growth o Secretion stimulated by TRH (thyrotropin-releasing hormone) PRL (prolactin): o Function: breast milk secretion o Secretion stimulated by DA (dopamine) ACTH (adrenocorticotropic hormone): o Function: adrenal cortex activity & growth o Secretion stimulated by CRH (corticotrophin-releasing hormone)

HYPOTHALAMUS HORMONES Hormone CRH (corticotrophin-releasing h.) TRH (thyrotropin-releasing h.) GHRH (growth hormone-realising h.) SS (somatostatin) GnRH (gonadotropin-releasing h.) DA (dopamine) Function Secretion of ACTH Secretion of TSH Secretion GH Secretion GH Secretion of FSH & LH Secretion of PRL

ANTERIOR PITUITARY HORMONES Hormone (all peptide hormones) Function Secretion Stimulated by which hypothalamic hormone GnRH GnRH DA GHRH CRH TRH -

FSH (follicle stimulating h.) LH (luteinizing h.) PRL (prolactin) GH (growth h.) ACTH (Adrencorticotropic h.) TSH (thyroid stimulating h.) Beta-lipotropin Beta-endotropin

Gamete production (males); ovarian follicle growth (females) Testosterone secretion (males); ovulation & estradiol secretion (females) Breast milk secretion Growth, via production of IGF-1, protein, CHO & lipid metabolism Adrenal cortex activity & growth Thyroid activity & growth Possibly fat mobilization & analgesia during stress Possibly fat mobilization & analgesia during stress

POSTERIOR PITUITARY HORMONES Hormone Oxytocin Vasopressin (anti diuretic hormone) Function Breast milk secretion & uterine mobility BP regulation, H2O excretion by the kidenys

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2.7 What are the major hormones produced by the adrenal gland and their functions? Structure: Adrenal gland is a small, conical organs on top of the kidneys 2 adrenal glands in the body (1 on top of each kidney) Each composed of: o Adrenal medulla, which secretes: amine hormones o Adrenal cortex, which secretes: steroid hormones Amine hormones: Epinephrine (adrenal medulla): stimulates increase in HR, blood glucose, blood pressure, and redistribution of blood flow via vasoconstriction. Norepinephrine (adrenal medulla): stimulates increased HR, BP, and blood flow redistribution. Smaller effect on BG and HR than epinephrine.

Steroid Hormones: Cortisol (adrenal cortex) Aldesterone (adrenal cortex) 2.8 Describe how the hypothalamicpituitary adrenal axis functions. The hypothalamic-pituitary adrenal axis (HPAA) regulates cortisol secretion from the adrenal cortex. The hypothalamic-pituitary-adrenal axis (HPA or HTPA axis), also known as the limbic-hypothalamicpituitary-adrenal axis (LHPA axis) and, occasionally, as the hypothalamic-pituitary-adrenalgonadotropic axis, is a complex set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal (or suprarenal) glands (small, conical organs on top of the kidneys). The key elements of the HPA axis are: The paraventricular nucleus of the hypothalamus, which contains neuroendocrine neurons that synthesize and secrete vasopressin and corticotropin-releasing hormone (CRH). These two peptides regulate: The anterior lobe of the pituitary gland. In particular, CRH and vasopressin stimulate the secretion of adrenocorticotropic hormone (ACTH), once known as corticotropin. ACTH in turn acts on: the adrenal cortices, which produce glucocorticoid hormones (mainly cortisol in humans) in response to stimulation by ACTH. Glucocorticoids in turn act back on the hypothalamus and pituitary (to suppress CRH and ACTH production) in a negative feedback cycle.

Functions Release of CRH from the hypothalamus is influenced by stress, by blood levels of cortisol and by the sleep/wake cycle. In healthy individuals, cortisol rises rapidly after wakening, reaching a peak within 3045 minutes. It then gradually falls over the day, rising again in late afternoon. Cortisol levels then fall in late evening, reaching a trough during the middle of the night. An abnormally flattened circadian cortisol cycle has been linked with chronic fatigue syndrome,[2] insomnia[3] and burnout.[4]

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Anatomical connections between brain areas such as the amygdala, hippocampus, and hypothalamus facilitate activation of the HPA axis. Sensory information arriving at the lateral aspect of the amygdala is processed and conveyed to the central nucleus, which projects to several parts of the brain involved in responses to fear. At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis. Increased production of cortisol mediates alarm reactions to stress, facilitating an adaptive phase of a general adaptation syndrome in which alarm reactions including the immune response are suppressed, allowing the body to attempt countermeasures. Glucocorticoids have many important functions, including modulation of stress reactions, but in excess they can be damaging. Atrophy of the hippocampus in humans and animals exposed to severe stress is believed to be caused by prolonged exposure to high concentrations of glucocorticoids. Deficiencies of the hippocampus may reduce the memory resources available to help a body formulate appropriate reactions to stress. 2.9 Identify the cells that make up the endocrine portion of the pancreas. Alpha and beta cells 2.10 List the factors that control insulin secretion. Insulin is secreted from the beta cells of the islets of Langerhans (pancreas) in response to high [blood glucose]. It causes BG to decrease. Glucagon is secreted from the alpha cells of the islets of Langerhans (pancreas) in response to low [blood glucose]. It causes BG to increase. 2.11 What effects do the pancreatic hormones have on carbohydrate, lipid and protein metabolism? Glucagon causes an increase in CHO metabolism Insulin causes a decrease in CHO metabolism

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TOPIC 3: Cardiovascular
3.1 List the structures through which blood passes from systemic veins to systemic arteries. Veins, venioles, capilliaries, arteriols, arteries ??? 3.2 Name a vein that carries oxygenated blood. Pulmonary Vein 3.3 Name the major factor regulating resistance to blood flow and the blood vessels that contribute most to the regulation of resistance. 1.The diameter of blood vessels. Posted on DSO 2. ? 3. ? Blood vessels that contribute most to resistance regulaton: Capillaries ??? 3.4 What causes AV valves to shut? Atrioventricular (AV) Valves: There are 2 AV (cuspid) Valves: o Mitral Valve o Tricuspid Valve. o They close due to pressure changes on either side of the valve. When the pressure is greater in the atrium than the ventricle: the AV valves are open. When the pressure is greater in the ventricle than the atrium: the AV valves are closed. The Mitral (bicuspid) valve is btw the left atrium and left ventricle. The Tricuspid valve is btw the right atrium and the right ventricle. Semilunar Valves: Aortic valve: within the aortic artery Pulmonary valve: within the pulmonary artery 3.5 What causes the second heart sound? First heart sound: AV valves closing Second heart sound: semilunar valves closing

3.6 Describe (in sequence) the structures through which the wave of depolarisation travels in the heart. Atrium to ventricles ???

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3.7 Draw a cardiac muscle cell action potential and explain its ionic bases. ????

3.8 Explain what is meant by the term pacemaker potential. What causes this phenomenon and how can it be regulated? Sinoatrial (SA) node - hearts natural pacemaker

3.9 Draw and label a normal ECG. Relate the waves to electrical events occurring in the heart. ???

3.10 Compare and contrast the sequence of events occurring during EC coupling in cardiac and skeletal muscle. ???

3.11 Explain why summation of contractions cannot occur in cardiac muscle. ??? check TB Cardiac muscle acts as a syncitial unit; when one cell contracts, they all contract in turn. Thus the force of contraction of the heart is not affected by recruitment of motor units, temporal or spatial summation, or tetany as is seen in skeletal muscle. ??? 3.12 Draw a diagram of the pressure changes in the left atrium, left ventricle, and aorta throughout the cardiac cycle. Show when the valves open and close, when the heart sounds occur, and the pattern of ventricular filling and ejection.

3.13 Are both sets of valves ever opened or closed at the same time during a cardiac cycle? No ??? 14

3.14 Calculate the stroke volume when each cardiac cycle takes 0.5 sec and the cardiac output is 7.2 l/min. Cardiac cycle takes 0.5 sec = HR: 120 bpm Cardiac Output: 7.21 l/min = 7210 ml/min Q = SV x HR 7210 ml/min = SV x 120 SV = 60.08 ml

3.15 What are the two major factors influencing force of ventricular contraction? Size of ventricle wall i.e. heart muscle strength ??? From web. Check TB Force of contraction of the heart can be varied to meet demand in various ways: The factors that affect the force of cardiac contraction can be grouped into three categories of mechanisms; Preload effects, Afterload effects, and Contractility (or Inotropic) effects.

A. Effect of Cardiac Filling: Preload Effect As with skeletal muscle, the force (tension) developed by contracting cardiac muscle is proportional to the length of the muscle (preload) at the moment contraction is initiated. For cardiac muscle, the ventricular end-diastolic volume reflects the resting length (preload), and the pressure developed in the ventricle is a measure of force. With greater end-diastolic volume producing stronger contraction, stroke volume and ejection fraction should also increase. This phenomenon was described separately by persons named Frank and Starling. It is commonly known as the Starling Effect or the Frank-Starling Effect. B. Effect of Aortic (Pulmonary Artery) Pressure: Afterload Effect

In order for blood to flow from left ventricle into the aorta, intraventricular pressure must be raised by contraction of the ventricle until it exceeds aortic pressure. Part of the contractile ability of the ventricular muscle must be employed to raise intraventricular pressure to this level. With a low aortic pressure, intraventricular pressure easily exceeds aortic pressure and continued contraction of the ventricle ejects a large proportion of the blood. In the face of elevated arterial pressure, a greater proportion of the contractile effort of the ventricular muscle is employed to raise pressure to exceed the higher aortic pressure and less contractile ability remains to eject blood. Therefore, just as in any isotonic contraction, the greater the afterload, the smaller will be the resulting contraction in terms of extent and velocity of shortening of the ventricular muscle.

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Elevated arterial pressure reduces ejection fraction, stroke volume, and cardiac output. Lower arterial pressure results in lower afterload on the ventricle. C. Effect of Changes in Cardiac Muscle Function: Contractility or Inotropy

As described above, the sympathetic nervous system stimulation of the cardiac muscle ensures that the subsequent contractions of the cardiac muscle generate greater force, even in the absence of any change in preload or afterload, because of the changes in calcium handling of the cardiac muscle. Therefore, sympathetic stimulation provokes a change in force of contraction that is not related to any change in preload (end diastolic volume) or afterload (arterial pressure). Such a change in force of contraction, in the absence of changes in preload or afterload, is known as a change in "Contractility" of the muscle. Under these conditions, an increase in contractility is also known as a 'positive inotropic' effect.

A variety of agents can cause an increase in contractility. Among those agents having a positive inotropic effect are the following:

1. Sympathetic nerve stimulation - as described above. 2. Humor agents with beta-one adrenergic activity, including norepinephrine and epinephrine released from the adrenal medulla 3. Pharmacological agonists with 1 adrenergic activity, including isoproterenol 4. Cardiac glycosides increase cardiac contractility via a non-adrenergic mechanism.

3.16 Calculate mean arterial pressure and pulse pressure if systolic and diastolic blood pressure are 140 and 80 mmHg, respectively. MAP = CO x TPR (total peripheral resistance) TPR = systolic diastolic / CO Pulse Pressure = systolic - diastolic 3.17 Describe the intrinsic and extrinsic mechanisms regulating arteriolar radius. Exterinsic: SNS stimulates vasoconstriction Intrinsic: 3.18 Discuss the factors involved in regulating net fluid movement across the capillaries. Concentration gradient of solute

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3.19 List three factors which increase venous return. 1. Skeletal Muscle Pump 2. Respiratory Activity 3. BP ??? 3.20 Describe the mechanisms involved with the short and long-term regulation of blood pressure. Short Term: Exercise Posture i.e. sitting, standing, lying flat

Long Term: Cholesterol Stress Fitness Weight (& area which weight is concentrated) Blood volume (controlled by re-absorption rate of H2O in the Kidneys)

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TOPIC 4: Respiratory system

(Kat + Tenille) 4.1 Summarise the processes involved in moving O2 from the atmosphere to the peripheral tissues. VE: exchange air between atmosphere and aveoli via bulk flow Exchange between o2 and Co2 between the capillary lungs and aveoli via diffusion Transport of o2 and CO2 through the pul and systemic system via bulk flow Exchange of o2 and CO2 between the blood in the capillaries and cells utilization of o2 and production of Co2 4.2 Describe the structural characteristics of the airways that are essential for their function in gas exchange and in body defence. Gas exchange occurs in: -respiratory zone in the aveoli -contains bronchi, bronchioles and trachea -This increases surface area and increases diffusion Defence is in the upper respiratory tract -ciliated columnar endothelium cells protect against germs and bacteria - one layer of flat endothelium cells that secrete surfactant which decreases the surface tension -smooth muscles also manages the radius. 4.3 What are the static and dynamic resistances that must be overcome in order to fill the lungs with air and enable gas exchange? Static and dynamic resistance to fill the lung with air are: -Tissue resistance (lung compliance) lung compliance depends on 1. Collagen and elastin 2.surface tension Alveoli stability via the pull of adjacent one = alveoli interdependence -airway resistance depends on the radius which is effected by: 1.lung volume 2.density and viscosity of gas 3.smooth muscles 4.4 Why is surfactant such an important molecule? Surfactant is important because: -reduces the surface tension so it increase lung stretchability = lung compliance

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4.5 Describe the sequence of events and pressure changes during a normal inspiratory expiratory cycle. Inspiratory expiratory cycle Inspiratory -activation of the phenic nerve contracts the diaphragm -the intercostal muscles also contract which increases the thorax volume -aveoli pressure drops greater than the atmosphere pressure = inspiration neck muscles aid when exercising Expiration -at rest it is passive so the lung recoils on its own. Atmosphere pressure greater than aveoli pressure -intercostal muscles and ab muscles and contract which decreases chest size 4.6 Summarise the structural and functional determinants of gas exchange in the lungs and peripheral tissues. Gas exchange is determined by: 1. Aveoli VE 2.Diffusion capabilities 3. Perfusion 4.Perfusion: diffusion ratio -PP moves from high to low 4.7 How are O2 and CO2 transported in the bloodstream? Transportation of o2 and CO2 O2 2% with physical solution 98% in haemoglobin CO2 10% physical solution 20-30% carbaminohaemoglobin 60-70% bicarbonate 4.8 Using a diagram, describe the relationship between haemoglobin saturation and PO2 and discuss the physiological significance of the shape of this relationship. HE saturation curve effected by: -temp -2,3 DPG -Bohr effect rapid increase (Sao2 the fastest here) then plateau(altitude or disease) -Right shift = tissue unloading -left shift = loading the lung

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4.9 You decide to stop breathing, but after ~4 min you have to take a breath. What mechanisms are involved in the control of breathing in these circumstances? Cannot hold your breath for long because aveoli pressure greater than the atmospheric pressure. There is an increase in H+ and PCo2 in the aterial blood and brain extracellular fluid which activates the chemoreceptors which causes expiration. 4.10 How does ventilation increase during exercise? During exercise VE increases because: -increase in metabolism -respiratory neurons -temp -K+ -adrenaline

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TOPIC 5: Fluid & Electroyletes

5.1 What are the main receptors that monitor fluid volume and electrolytes in the body? Fluid volume: Baroreceptors Electrolytes: Osmoreceptors (regulate fluid absorption) 5.2 List the sources of water and sodium gain/loss in the body. Urine Sweat Chemical processes within the body that require H2O 5.3 Describe the cellular mechanism of sodium re-absorption, and how it is coupled to the re-absorption of other solutes. Loop Helene (Kidney) Osmolality of body fluid 5.4 Which hormones mediate major physiological adjustments that affect fluid and electrolyte balance? Describe the primary effects of each hormone. ADH encourages water resorption at the kidneys and creates a desire to drink. Aldosterone increases the rates of sodium resorption at the kidneys. ANF opposes these actions and promotes fluid and electrolyte losses in the urine.

5.5 Why does drinking a large volume of water lead to excretion of a large volume of osmotically dilute urine? Because ingesting a large amount of H2O results in the body fluid becoming hypotonic (low solute), to rectify this, the body has to excrete H20, whilst holding on to as much sodium as possible.

5.6 Discuss the counter regulatory mechanisms that occur after ingesting a large amount of salt. Excrete urine with a high salt content

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TOPIC 6: Acid base balance

6.1 List the three important chemical buffer systems in the body. How does each system work? Phosphate buffer system -intracellular -bind H+ and remove depending on Ph levels -maintain Ph to 4-4.5 -loose 1 H+ and HP04 and gain 1 HCO3 -lowest buffer Protein buffer system -H+ binds to He and amino acids -extracellular buffer -loose 1 NH4 = loose 1 H+ -gain 1 HCO3 Bicarbonate Co2 system -H+ buffered by HCO3 -extracellular fluid -maintains CO2 levels at 40mmHg -loose 1 H+ 6.2 How do respiratory and renal mechanisms support the buffer systems? Respiratory system -buffers H+ by removing CO2 by increasing VE -peripheral and central chemoreceptors 6.3 Describe the respiratory process that regulates plasma pH. pH is regulated via: -H+ removal -change HCo2 absorption /reabsorption 6.4 Describe the renal mechanisms that maintain acid-base balance by regulating the plasma bicarbonate concentration. Renal system -removes H+ and adds HCO3 -slow and complex and long term -B.C reabsorped when H+ generated and then combines with filtered B.C -excreted when H+ binds with phosphate 6.5 What are the differences between respiratory and metabolic disorders that disturb acid-base balance? For each condition, describe the compensatory mechanisms that return acid-base levels to normal. Respiratory acidosis -increase CO2 22

-decrease Ph and increase H+ -ph= 7.1 -excrete urine to remove H+ and add more HCO3 to get the blood back to normal ph levels -all the respiratory values increase besides the carbonic acid formation which decreases Metabolic acidosis -decrease PCO2 which will lower the acid Respiratory alkolisis -decrease in CO2 -increase in Ph and decrease in H+ -ph = 7.7 -excrete HCO3 to get ph back to norm -all R valiables decrease bar the carbonic acid formation which increases Metabolic alkolisis -increase PCO2

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TOPIC 7: Heat Loss

7.1 Discuss the processes that are activated to increase heat production during a period of cooling. Non voluntary thermogenesis: shivering Voluntary thermogenesis: voluntary skeletal muscle contraction 7.2 Summarise the internal and external processes that facilitate heat loss. Internal: Blood flow distribution: vasodilating peripheral blood vessels to allow more blood flow to the skin, allows the blood to cool and then travel back into the bodys core, causing a drop in body core temp. On the other hand vasoconstriction of peripheral blood vessels occurs when the body is trying to conserve heat, and needs to reduce the amount of heat lost to the environment. External: Conduction is the process of losing heat through physical contact with another object or body. Convection is the process of losing heat through the movement of air or water molecules across the skin e.g. a fan blowing air on the body Radiation is a form of heat loss through infrared rays. This involves the transfer of heat from one object to another, with no physical contact involved. Evaporation is the process of losing heat through the conversion of water to gas (evaporation of sweat). 7.3 Discuss the cardio respiratory responses that facilitate oxygen delivery to contracting skeletal muscle during exercise of increasing intensity. Incr HR Incr SV Incr Q Redistribution of blood flow: Vasodilationof blood vessels that supply working skeletal muscle. Vaso constriction to less active areas i.e. digestive tract, reproductive organs Increased SaO2% (increased percentage of Hb saturated with O2 within the blood)

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Tenilles Answers Intercostal Muscles: external, parasternal and levator costae Islets of langerhan: endocrine portion of the pancreas...secretes insulin and glucagon how is carbon dioxide transprted in the blood? (there are 3 ways):

1. Dissolved in plasma (10%) 2. carbaminohaemoglobin is the protein thing... (30%) 3. bicarbonate (60%)
What increases respiratory work: (a) decreased lung compliance, (b) increased airways resistance, (c) decreased elastic recoil (increases expiratory work) and (d) increased ventilation (e.g. exercise).

so exercise is one.. lun compliancy is another biggie airway resistance wold be like an ashma attack

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DSO Notes
Topic 1: Neurophysiology Selected Attention / Directed Attention = same thing Topic 3: Cardiovascular Blood Pressure & Resistance: In the case of exercise, BP rises due to an increase in CO, not due to an increase in resistance. Resistance is created by constriction of arterioles and in exercise you get dilation of resistance vessels in and around muscles to increase the blood supply to and from working muscles. During exercise some vascular beds dilate and others constrict. This is due to the effects of sympathetic nervous system stimulation. If you can't remember which beds think about which areas of the body are likely to be required most during exercise, obviously the working muscles need more blood when they are working harder, but other parts of the body that aren't essential for exercise don't need as much flow during exercise (eg digestive or reproductive organs). So resistance is increased in these vascular beds to redirect blood flow to where it is needed most. You need to start thinking about what is going on and why. If you think about the why, then it will be much easier to remember.

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