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Biom2011
| Question | Answer |
|---|---|
| What are the 5 functions of epithelial cells | Protection, lubrication, sensory, secretory, absorptive |
| what are the 5 extracellular links between epithelial cells | Gap junctions, tight junctions. adherens junctions, desmosones, focal adhesions |
| Describe a gap junction | Link 2 cells. Transmembrane proteins form a tube (ion channels). Cell to cell communcation, electrical signals Connexions line up between cells and allow transfer of ions. Occur on basolateral membrane |
| Describe adhering junctions | Belt like. Provide strong mechanical strength between cells. Actin filaments Occur on basolateral membrane. Hooks on inside attached to actin filaments and hookes on outside (between cells) attached to other cells |
| Describe Tight Junctions | Facilitate selective permeability. Reside under lumen. Forms the weird “band” towards the top of the cell which can sort of separate the apical membrane from the basolateral Occur on the apical side Contain patterns of protein complexes |
| Describe Desmosones | Point-point link. Strength, lots of filaments Occur on basolateral membrane. Keratin hairs sprout into the cell. Hooks on the inside attach cells together. |
| Describe Focal adhesions | They are not between epithelial cells, they link epithelial cells to basement. Communication. Actin binds to vinculin and talin “anchors” which are embedded in the basement membrane and are attached to fibronectin inside the membrane |
| Describe the parts of a neurone | Dendrite - receives the signals. Branches of the soma Soma - contains the nucleus Axon hillock - AP generaged here Axon - conducts signal Synapse - specialised ending of axon that releases neurotransmitter |
| What is the directional flow of information in a neurone | Synapse, dendrite, soma, axon, synapse |
| Describe the parts of a synapse | Pre-synaptic terminal - small swelling at end of axon Mitochondria - Pre-synaptic density - proteins for locating, exocytosis and recycling of synaptic vesicles synaptic cleft post synaptic density - proteins for neurotransmitter response |
| What does the direction and rate of ion transport depend on? | Charge of the ion, chemical gradient across the membrane and electrical charge distribution across the membrane |
| What is ion permeability based on? | Ion channel selectivity based on ion charge and size |
| What is resting membrane potential dependent on and action potential and synaptic potential? | non-voltage gated channels permeable to Na+ and K+. Ap dependent on voltage gated Na+ and K+ channels. SP based on ligand gated Ca, Na, K and cl |
| Define current, potential (voltage), conductance and resistance | Rate of movement (amp) , force acting on charged particles to cause movement, ease with which particles can move, resistance to movement of charged particles |
| What is ohm's law | Rate of movement of a charged particle depends on the force moving it and the ease with which it can move. I = gV |
| What happens when g and V is 0 in Ohm's law | no current can flow through |
| GIga, mega, kilo, milli, micro, nano, pico | 9, 6, 3, -3, -6, -9, -12 |
| Single K+ channel g, single neurone R. How many K+ channels? | Divide 1/g to find R of one K. Divide K of neurone/K of single K+ . 1/value = number of channels |
| How is the membrane like a capacitor | Separation of charges means the membrane can store charge |
| What is the ionic equilibrium potential | electrical potential which exactly counter balances force of ionic concentration gradient. There is no motive force for that ion (voltage). Measured by nernst equation |
| What is resting membrane potential | Potential is negative in comparison to outside. Between -90 and 45mV |
| How does K+ distribution across the membrane control RMP? | K+ permeability is high, ratio of K+ concentration is high, |
| What does increasing and decreasing extracellular K+ concentration do to RMP | Increasing will depolarise it, decreasing will hyper polarise |
| What pumps maintain RMP | Pumps move ions against their concentration gradients. NA/K+ ATPASE move 3 NA= out for every 2K+ in. CA pump also uses ATP to move Ca out of cell cytoplasm into internal stores. K/CI - pumps Ci out and K in |
| What is RMP characterised by | Ion flux and pumping activity. Balance between the two. Ion flux of K, Na and Ci through non-voltage dependent ion channels |
| How can the RMP be calculated | =Goldman Hodgkin Katz equa1on |
| Large change in RMP occurs with how large of an ion concentration change | very small, therefore Eion is static |
| Ions move across membrane at rate dependent on difference between | RMP and Eion. The difference is the driving ionic force |
| why does potential changes move more slowly than ionic current | Membrane capacitance ⇒ poten1al changes more slowly than ionic current as capacitor transiently gains or loses some stored charge. Uneven balance of electrical charge is concentrate at membranes |
| Equation for membrane curren | Membrane I = Ionic I - Capacitative I |
| By convention the direction of current flow refers to what | net distribution of positive charge.+ve ions in cell = inward current, +ve ions out cell - outward current -ve ion in cell - outward current |
| Inward and outward currents are what | Depolarisation and hyperpolarisation |
| Describe neurotransmitter degradation and recovery | Neurotransmitter must be removed to prevent desensitisation of receptor. Diffusion, re-uptake by to nerve terminal by transporters, glial uptake by transporters or enzymatic breakdown in synaptic cleft. |
| What neurotransmitters activate ligand gated ion channels | All amino acids (glutamate, glycine, gaba) and some amines (acetylcholine and serotonin) |
| Which ligand gated channels are excitatory? And provide examples | Those permeable K+, Na+ and Ca+ as they incite depolarisation. Glutamate receptors and nicotonic acetycholine |
| Describe ionotropic glutamate receptors | Main excitory receptor in CNS. Permeable to K+, Na and some Ca. 4 subunits around a central ion pore |
| What are the three different types of inotropic glutamate receptors? | AMPA - fast rising and falling e response, sometimes Ca+ permeable NMDA - slower rising and falling e response, always ca permeable, voltage dependent block of ion pore by Mg Kainate - similar to ampa. |
| Describe the receptors which induce inhibtory postsynaptic potentials and currents | Ligand gated permeable to cl, Hyperpolarisation. Main types are GABA and glycine |
| Describe nicotinic, GABA and clycine receptors | Common structure. 5 subunits, subunit variation confers specificity. GABA and glycine are only permeable to CI-, while nicotinic ach permeable to K+, Na+ and sometimes Ca+. Gaba contains receptors for binding drugs and endogenous factors, which modulate |
| If gaba receptors are mutated | reduce flow through of CI-, reduced ISPS |
| Describe the action of g protein coupled receptors | Known as metabotropic receptors. Cause slow synaptic transmission. Open or close ion channels (usually k proteins) or cause protein phosphorlyation. |
| What are the ligand gated and g coupled receptors for glutamate, GABA and acetylcholine | AMPA, ndma, kainate and metabotropic glutamate. Gaba A Gaba B. Nicotinic and Muscarinic |
| why is summation not linear | Dendritic filtering of synaptic potentials and local interactions between synaptic potentials |
| What is the benefits of placing synaptic inputs at the soma | ESPS and ISPS are not reduced by dendritic flitering and can have a larger influence on whether an AP is generated. Iinhibitory synapses more dense at soma to act as a gatekeeper |
| How do post-synaptic inhibition reduce exitability | Due to opening of Ci channels. Causes hyper polarisation - if RMP is higher than Eci. Shunting inhibition - when MP is lower than Eci, Mp will not change significantly but it shunts other synaptic inputs to the neurone |
| Describe Presynaptic inhibition | controls transmitter release at individual synapses without affecting other synapses on the same neurone. Reduces neurotransmitter release. nt binds ti adjacent synaptic terminal prevents nt release |
| Describe spatial and temporal separation | Simultaneously active synapses at different locations on dendritic tree. Asynchronously active synapes (either same or different synapses) |
| What is short term synaptic plasticity | change in synaptic response from the same synapse |
| Define synaptic facilitation and synaptic depression | F - produces greater than normal summation, enabling excretory inputs to sum and reach AP threshold more quickly. D - opposite |
| What underlies learning | Long lasting changes in synaptic responses |
| What is LTP and LTP | Long term potentiation - persistent increase in synaptic responses induced by high frequency stimulation. LT depression is the opposite |
| LTP involves what type of summation | Temporal and spatial tetannus. Only those neurones stimulated by tetanus undergo LTP. CA1 and Ca3 synapse in the hippocampus |
| How are LTP's induced? | The transmitter is glutamate, which activates AMPA and NDMA receptors. Influx of Ca2+ through NDMA is essential for LTP, however this only occurs the t and s summation depolarises the MP sufficiently. Postsynaptic ca2+ enhances protein kinase activity |
| How are LTP's maintained? | Postsynaptic change in AMPA receptors (phosphorylation of receptors) or recruitment of AMPA receptors into postsynaptic density. Presynaptic increase in amount of transmitter released. Require gene activation. Increase in synapse number |
| What is cardiac output and how would you calculate it? | amount of blood pumped by each ventricle per minute. CO = heart rate (beat/min) * stroke volume (mL/beat) = |
| What is the cardiac output at rest vs exercise | rest = 5L/min exercise 20-30L/min |
| Describe ion channels | voltage dependent memrbane imbedded proteins that pass a particular ion, usually selectively in one direction (depending on chem and e gradients) or can be activated by a ligand |
| Describe pumps | ATP dependent and voltage independent membrane imbedded proteins responsible for the moment of ions against their chemical and possibly electrical gradient. |
| Describe exhangers | voltage independent and ATP independent membrane imbedded proteins that pass two different species of ions uni or bi directionally (affected by chem and e gradients) |
| Name three ion channels | Na+ (one major type), CA+ (L type and T type) and K+ (at least 15 types in the heart) |
| How are sodium channels activated? | S4 region contains highly charged amino acids and physically moves in response to voltage change. Movement of S4 exposes residues to extracellular solution and generates a gating current. |
| How do mutations in S4 that reduce the number of charges affect the activation of sodium channels | Reduces gating current and makes the voltage dependence of NA conduction a less steep function of voltage (reduces the probability of channel opening) |
| What are the special structures of cardiac muscle that are responsible for it's contractile movements | Intercalated discs - interlock adjacent cells together desmosomes - anchor cells together gap junctions - allow ions to move between cells cardiac muscle cells are e coupled and function as one unit (functional synctum) |
| What is autorhythmicity | cardiac cells can generate their own potential |
| What are the different type of cells in myocardium and what is their function | contractile cells (most of cardiac) - mechanical work conduction and auto rhythmic cells - AP (approx 1 percent) |
| What is the nernst potential? | Measured ionic equillibirum. mV = (RT/F)*ln(Kout extra/Kin intra) |
| what is the Goldman-Hodgkin-Katz Equation: | Can calculate RMP. mV = (RT/F)*ln(permability Na * conc. NA out) / (permeability of Na * conc. Na in). + + ca |
| Describe action potentials in cardiac cells | Na channels inactivate rapidly, so fast rising. Na in. At the peak, p of Na decreases and p of Ca increases. Ca channels open during plateau face (essential for initiating contraction), enter slowly. K+ out fast, ca+ inactivate and NA+ reprime (repolarise |
| Are all the action potential in the heart the same? Why or why not? | No! Differences due to different ion subtypes present in each cell |
| Do the contractile and action potential of the cardiac system overlap? | Yes. AP lasts about 250 milliseconds longer |
| How is tetanus prevented (summatino) in the heart | Na inactivate quickly and only reprime 250 milliseconds after it. It needs to relax so blood can refill the heart |
| Why do surges pour potassium in the heart during surgery | Makes the MP 0, every channel is inactivated. Prevents contraction |
| Describe Pacemaker action potential activity (SA node) | Unstable baseline. Funny current. Channels become more active during depolarisation. Slow inward NA+ current. L type calcium channels activated. Unstable baseline - timer in the heart. K+ out. autorhythmicity |
| Describe action potential frequency in ventricular cell | Steady resting phase, so only activated by sudden opening of Na+ channels. Na+ channels open, massive spike, ca+ plateaus, k+ out, resting phase. normal cardiac action potential |
| Describe the sequence of electrical connection and contraction in the heart | SA node generates impulse, atrial excitation and contraction occurs. Impulse is delayed at AV node. Impulse passes to heart apex through branches. Ventricular excitation. Spreads to purkinje fibres. Excitation complete |
| What is an ECG? | ECG is the recording of that part of the electrical activity induced in body fluids by the cardiac impulse that reaches the body surface, not a direct recoding of the electrical activity of the heart. |
| What can't the ECG measure? | Activity of the SA node, AV node, bundle of HIS, bundle fibres and purkinje fibres |
| Does relaxation or contraction occur faster? | Contraction. Depolarisation is slow, depolarisation is fast and synchronous |
| What is the p wave and what has to happen before the wave | SA node induces impulse. P indicates atrial depolarisation. |
| What events happen during the p wave and before the q wave? | AV node, bundle of HIS, bundle fibres, purkinje fibres become excited |
| What is the q wave? | When visible, the Q wave is any initial downward deflection after the P wave. The normal Q wave represents septal depolarisation. |
| What is the R wave? | Early ventricular depolarisation |
| What is the S wave? | Late ventricular depolarisation. |
| What is the T wave? | Repolarisation of the ventricles |
| What is the cardiac cycle? | The period between one heartbeat and the next |
| What is systole and diastole? | S - contraction - ejection of blood D - relaxaation - filling with blood |
| Electrical activity precedes what. Blood flows from blah to blah. Where to values open? | Mechanical. High to low. Where there is the greatest pressure |
| When is ventricular systole and dystole | Ssytole QRS, diastole time between QRS waves |
| How long is the cardiac cycle | 0.8 sec. Systole 0.3, Diastole 0.5 |
| How does the heart fill with blood at such high heart rates? | The critical time for filling blood is the initial stages as the rate is the fastest. The rate slows down so it doesn't matter that the heart rate increases |
| How is cardiac output regulated and by how do the systems affect heart rate | By affecting heart rate and stroke volume. Parasympathetic nervous system decreases heart rate, sympathetic nervous system increases heart rate. |
| How does the parasympathetic nervous system affect cardiac output (mechanism) | Acetycholine slows closing of K, increases resting leakage of K (increases hyperpolation) and opposes normal decrease in K permeability thereby decreasing depolarisation. Slows opening of Ca, slowing depolarisation |
| How does the parasympathetic nervous system affect SA node, AV node and atrial and ventricular contraction | Slows pacemaker activity, therefore decreasing heart beat. Increasses delay at AV node and weakens atrial and ventricular contraction. |
| How does the sympathetic nervous system affect cardiac output (biochemical mechanism) | Noradrenalin decreases K permeability. Accelerates inactivation of K channels, rapid drift to threshold, increases depolarisation rate. Increases CA current |
| How does the sympathetic nervous system affect the SA node, av node and atrial and ventricular contraction | Increases pacemaker activity, increases hear rate. Decreases delay at AV node (increases excitability) and increases atrial and ventricular contraction. |
| What is the proportion of free calcium to total calcium concentration. And what does this mean | Very small. Most bound to protein. Ca bound to protein induces conformational changes |
| Where is the majority of ca2+ bound to | calsequestrin inside the SR, the Ca2+ store of the cell. |
| What is the concentration of extracellular ca2+ at rest and activated | approx 2mM. Nothing changes |
| What is the concentration of cytoplasmic ca2+ at rest and once activated. | At rest - little ca2+ bound to troponin C Activated - lots of ca2+ bound to troponin C |
| What is the concentration of ca2+ in the SR lumen at rest and activated | Lots bound to calsequestrin at rest. Activated - still lots bound to calsequestrin but less than before. |
| What are the steps of excitation-contraction coupling part 1 | Ap propagates membrane. VS in t system membrane is activated. Mechanical activation of SR Ca release channel via VS. Ca is rapidly released into cell increasinc conc. 100 times in few milliseconds. CA binds to contractile proteins causes filament to sli |
| What are the steps of excitation-contraction coupling part 2 | . Ca2+ is pumped from the cytoplasm back into the SR. Ca2+ unbinds from the contractile proteins >> relaxation!! |
| What is DHPR and what does it do in skeletal and cardiac muscle | In skeletal muscle act as voltage sensor - voltage dependent calcium release In cardiac muscle - acts a s a ca channel - calcium induced calcium release |
| Describe how cytoplasmic ca2+ is released in skeletal muscles | Physical interaction between DHPR and RyR. E signal to mechanical signal. Cytoplasmic Ca2+ dependent inactivation “counts” Ca2+ as it is released, for a defined release independent of store load. |
| Describe how lumens ca2+ is released in cardiac muscles | No physical interaction between DHPR and RyR. Lumenal Ca2+ dependent inactivation allows all Ca2+ above a threshold in the internal store to be released.Ca binds to RyR - signal. e - chem signal. No 2nd messenger |
| How is cardiac contraction modulated? | Changes in the cell's ca balance |
| Ca influx during AP must be balanced by a | Ca efflux between APs |
| What are the key players for CA entry | DHPR - l type calcium channel, voltage dependent, receptor - cell membrane RyR - Ryanodine receptor - ca release channel on SR membrane |
| What are the key players for CA exit | SR ATPase surface ATPase surface Na/ca exchanger |
| How does increasing heart rate result in a strong contraction | Increases Ca influx while decreases time between beats (when efflux can occur). Results in more Ca in the SR with increases SR Ca release and thus results in a stronger contraction |
| Describe Autonomic Regulation of Cardiac contractibility | Parasympathetic - acetycholine binds to recetpor, ge protein increases adenyl cyclase, which acts upon DHPR channel and pacemaker channel. Decrease SR pump. Sympathetic - noradrenalin binds to beta receptor - g protein. Increase adenyl cyclase, increase S |
| What is the l type calcium channel responsible for | Keeping the cardiac cell in plateau for 250 milliseconds |
| Describe inactivation of ca in skeletal music | RyR inactivation site counts calcium, ones reaches critical level, it is inactivated. Next action potential opens it again, regulate how much ca released with each AP. Store is not depleted. Directly result in how much force muscle produces. |
| Describe inactivation of ca in cardiac muscle | No side on the outside counting. It comes down, reaches threshold in SR and channel shuts. Increase ca, more calcium has to be released . Changes amount of ca2+ to generate more force from one Ap |
| Why is the valency of the calcium ion important to cell function? | Ca2+ has two positive charges that give it a high affinity for binding to negatively charged proteins. |
| What affects the physiological response to hormones? | Hormone concentration (free biologically active), and receptor sensitivity. |
| What is the hypothalamus comprised of. What are the functional divisions? | Neural tissue and endocrine gland. Neurosecretory cells at the top release hormones at posterior and anterior pituitary. |
| What is the median eminence | Connects the pituitary gland to the me posterior pituitary |
| What function does the hypothalamus serve | Homeostasis, reproductive, feeding and rage behaviour, body temp, metabolism, stress, water balance, reproduction |
| What are the inputs and outputs of the hypothalamus. Where does the hypothalamus receive humour input | Neuronal and humoural. The bloodbrain barrier is imcpomlete at the median eminence. |
| What type of hormones are oxytocin and vasopresssin (ADH) and how many amino acids do each contain? | Both peptide and both contain 9 |
| What is the Parventricular nucleus (PVN) and Supraoptic nucleus (SN) | P - contains large bodied neurons that transport hormones down axon to posterior pityrity for their release. S - small body neutrons transport hormones down axon into primary capillary plexus |
| Where is oxytocin and vasopressin expressed and how many neurons produces them | both in the PVN and SON! Only one expresses these peptides |
| What are the actions of vasopressin and what is it's secretion regulated by. | Decrease water excretion in kidneys and vasoconstriction. IT is regulated by solute concentration in extracellular fluid and blood volume |
| What are the actions of oxytocin | Parturition: stimulates contraction of uterine smooth muscle Lactation - stimulates ejection of during breastfeeding due to contraction of smooth muscle. |
| What stimulates oxytocin secretion and what inhibits its secretion | Stimulated by suckling baby, pressure of baby in birth canal Inhibited by fear and anxiety |
| Describe the milk ejection reflex | Suckling/auditory/visual stimulation/ birth canal pressure stimulates SON and PVN to increase firing rate. Induces oxytocin release from posterior pituitary. Oxytocin myoepithelial breast cells |
| How does the body prepare for breast feeding during pregnancy | Oestrogen upregulates OT expression during pregnancy. OT expression is maintained by suckling stimulus |
| Describe oxytocin signal transudction in epithelial cell | OT binds to OT receptor, which activates G protein which then activates Phospholipase C. It then mediates cleavage of PIP2 into DAG and IP3. IP3 activates IP3 receptor on SR or ER and releases CA2+, attaches to contractile proteins |
| What is the anterior pituitary comprised of | Five different types of endocrine cells which secrete their own different hormone |
| What are the five different hormones and where do they act upon | TSH - thyroid gland ACTH - adrenal cortex GH - liver and other tissues LH and FSH - gonads (ovaries and testes) Prolactin - breast |
| What cells type produces what hormone (anterior pituitary) | somatotrophs - GH Lactotrophs - prolactin gonadotroph - FSH and LH thryrotrophs - TSH corticotrophs - ACTH |
| Why are the anterior pituitary's capillaries fenestrated | The fenestrated structure of capillaries facilitates a rapid exchange between the hypothalamus and the pituitary, with only a small amount of hormones needed to stimulate an accurate effect in the respective target organs in the body. |
| What is a trophic hormone and which anterior pituitary hormones are trophic. Which are the non-trophic | Control activity of another endocrine gland. ACTH, TSH, FSH And LH. Growth hormone and prolactin |
| How is the secretion of anterior pituitary hormones controlled? | Secretion is in response to neurohormones called “releasing hormones or “releasing factors” from the hypothalamus |
| Describe releasing factors | secreted from nerve endings into capillaries (median eminence). Transported in portal circulation to a second capillary bed in AP. Act on target cells to stimulate synthesis and secretion of AP hormone. Often small peptides |
| Is the activity of each cell type in the anterior pituitary independent or dependent on each other | Independent! |
| Which anterior pituitary hormones have a hypothalamus releasing or inhabiting factor | All have releasing factors (so stalk cut, their concentration decrease) except for prolactin. |
| What is the inhibiting factor for protecting, RF and IF for GH, RF for TSH, RF for ACTH and the RF and IF for FSH and LH | Dopamine. GHRH and somatostatin, TRH, CRH, GnRH and GnIH |
| What is the short and long loop of anterior pituitary hormone section | Long: Hypothalamus, anterior pituitary, endocrine gland, hormone, Hormone feeds back into anterior pituitary and hypothalamus. Short loopL hypothalamus, anterior pituitary, hormone, feeds back to hypothalamus. |
| Describe the structure of growth hormone | Glubular protein. 191 amino acids |
| Describe the diurnal variation of GH | The concentration of GH increases while you are asleep |
| Describe the GH pulsatile pattern for females and males. | Smaller amplitude, higher frequency, more consistent - female males - higher amplitude, lower frequency, more pulsatile |
| How does age affect gh level | Decreases in age. Highest point is at puberty |
| Do GHRH and somatostatin come from the same neurone in the hypothalamus | different neurones! |
| How does Somatostatin inhibit GH secretion | Somatostatin has GPCR receptor. Once activated it inhibits the GPCR of GHRF, thus preventing GH secretion |
| Describe the process of GH secretion | Hypothalamus releases GHRH, which acts on anterior pituitary, which releases GH. GH provides negative feedback loop to hypothalamus |
| What are the major actions of GH | Major determinant of growth. Mostly anabolic effects - increase number and size of cells in so tissue i.e. skeletal muscle and increase thickness and length of bones. Metabolic effects |
| Describe GH signalling | Jak/stat pathwaty. Binding of Gh activates Jak, which phosphorylates tyrosine enabling SH2 domains to bind. Stat binds become activated and induces gene transcription |
| What is the somatomedin hypothesis | That Gh acts upon the liver to secrete Somatomedin C (IGF1), which acts on target tissues to cause somatic growth |
| Describe the IGF1 sigalling pathway | Similar to insulin. It's receptor is a tyrosine kinase. PI3kinase/AKT pathway. Causes gene expression resulting in hypertrophy, hyperplasia, cell survival |
| Gh receptors are found in most... Some of the effects are due to.. | tissues. GH (do not require IGF1). Some effects are due to GH-stimulated local release of IGF1 (paracrine IGF1) |
| Why does weight gain alone not equal growth | Involves structural growth of tissues - net synthesis of proteins - lengthening of long bones cell hypertrophy and hyperplasia |
| What are the two main growth spurts and what does it correspond to | Post-natal and pre-pubertal. Corresponds to peak IGF-1 levels |
| why are plasma IGF1 levels so stable from hour to hour when its secretion is stimulated by a pulsatile pattern of GH | Synthesis takes time following GH = lag. Insulin like growth factor binding patterns maintain pool of circulating IGF-1 |
| Is GH or IGF-1 control hypertrophy and proliferation | GH - prolifeation IGF1 - hypertrophy |
| What are the GH actions on muscle | stimulate amino acid uptake decrease glucose uptake inhibits protein breakdown = increase muscle mass |
| What are the GH actions on adipose tissue | decreases glucose uptake increases fat breakdown (lipolysis) = decrease in fat deposits |
| What are the GH actions on liver | increase protein synthesis increase glycogenesis |
| Overall action of GH on blood glucose levels | increase! |
| For optimal growth you also need | Thyroid hormone, sex steriods, insulin, glucorticoids |
| Long loop of GH secretion | Hypothalamus (GHRH), anterior pituiaty, GH, liver (plus other tissues) - IGF1 (feed backs to anterior pituitary and hypothalamus) |
| Pit 1 is necessary for | Pit1 is necessary for pituitary development & GH expression |
| What does a GH deficiency do in adults and children | children - pituitary dwarfism Adults no major symptoms |
| What does a GH hyper secretion do in adults and children | children - gigantism adults - acromegaly |
| What type of hormone is prolactin and what is it inhibited by | Peptide. Dopamine (prolactin inhibiting factor) |
| What causes spontaneous prolactin secretion from lactotrophs | Increase in cAMp induces prolactin expression. AP causes CA influx, results in exocytosis of prolactin |
| What short term and long term (and medium) effects does dopamine have on prolactin in order to reduce its secretion | Short term - reduce its secretion medium - prevent its synthesis Long term - inhibits lactotroph proliferation |
| What type of receptor is Dopamine D2? Where is it expressed. How many pathways does it signal to block dopamine | GPCR. On lactotrophs. Multiple pathways |
| How does dopamine act to prevent secretion of prolactin | Dopamine binds to D24. G protein inhibits the action of ac receptor, thus reducing camp. Thus reducing prolactin expression, It activates another channel, which prevents AP therefore prevents ca influx |
| How does dopamine inhabit prolactin synthesis | Pit 1 is necessary for pituitary development and therefore prolactin development. Dopamine inhibits pit 1 |
| What does prolactin do? | Stimulates alveolar epithelium of mammary gland to synthesise and secrete milk.Immune system behaviour |
| What type of receptor is involved with prolactin signalling | Cytokine receptors (tyrosine kinase associated receptors) |
| Describe prolactin signalling | Prolactin binds to cytokine receptor. Activates jak, phosphorlates tyrosine kinases, enables stat 5 to bind and become activated. stat 5 translates to nucleus and initiates transcription of milk proteins |
| What maintains low prolactin levels in non-lactating individuals | negative feedback! |
| Describe the regulation of prolactin in a non-lactating individual | short negative feedback loop only, prolactin binds to dopaminergic neuron (prolactin receptor). Incites dopamine release, which binds to D2-R receptor on lactotroph and inhibits prolactin synthesis |
| Describe the mechanism of prolactin regulation in a non-lactating individual | So prolactin binds to its receptor on dopaminergic neutron. It is a cytokine receptor. Jak activated, stat 5 binds and results in transcription of tyrosine hydroxylase. TH rate limiting enzyme of prolactin |
| Describe regulation of prolactin in lactating individuals | Sucking stimulus upregulates cis proteins. Interferes with cytokine PRL receptor in dopaminergic neurone. Reduces dompanine |
| What does suckling induce | oxytocin secretion - milk ejection and prolactin secretion - milk synthesis and ejection |
| GnRH stimulates | LH and FSH synthesis and secretion |
| How is GnRH secreted and consequently how are LH and FSH secreted | GnRH - pulsatile, same as LH FSH is secrete continuously. GnRh pulse 5-10 min of intense secretion due to AP, then inactivation for an hour |
| What happens to gonadotroph if GnRH secretion is NOT pulsatile? | If secreted continuously, FSH and LH secretion drops dramatically |
| Describe the long negative feedback of LH and FSH | Hypothalamus releases GnRH (gonadatrophin stimulating homrone) acts on anterior pituitary, LH and FSH acts on gonads, release gonad hormones which feed back onto anterior pituitary and hypothalamus |
| Describe the follicular and luteal stages | F - FSH and LH stimulate oocyte development and follicle growth. Oestrodial production. L - LH bursts triggers ovulation. LH maintains corpus luteum. Progesterone production (some oestrodial) |
| Describe how cholesteroal is converted into oeastrodiol | Cholesterol, pregnenolone - progresterones, androgens (testosterone) - oestrogens (oestradiol). |
| Where does progesterone synthesis take place and describe the process | In the corpus luteum. Cholesteral uptake, intracellular uptake then conversion by enzymes |
| How does LH stimulate progesterone synthesis | Short term - increases availability of cholestoral by phosphyrlation of transport proteins long term - increases gene expression of key transporters and enzymes |
| Describe the secretion pattern of progesterone | Only slightly pulsatile, rathe more continuous secretion |
| How does FSH stimulate oestrodial production | FSH stimulates granulosa in graafian folecule to convert androgens to oestradiol. Stimulates aramotose expressino (the enzyme) |
| Describe the pulsatile pattern of LH secretion during the follicular and luteal phases | frequent, small amp - follicular large amp, less frequent - luteal |
| What does oestrogen and progesterone do to endometrium wall. withdrawal of hormones causes | E - thickens it P - increases number of blood vessels and glands in it withdrawal of hormones causes breakdown of endometrium |
| what are the three parts to the nervous system | CNS - spinal cord and brain Peripheral - efferent and afferent divisions enteric - digestive system |
| what are the two different afferent divisions that send info to the CNS | Somatic - skin, skeletal muscles, touch, sight, hearing, proprioception, olfaction, gustation visceral - interal viscera - smooth muscle, glands, organs, body cavities |
| What are afferent neutrons, interneurons and efferent neutrons | A - sensory neutrons that provide CNS with info about environment I - integrates info and formulates an efferent response E - carry instructions from CNS to organs, muscles and glands |
| what are sensory receptors | specialised peripheral endings of afferent neutrons, Each type responds to a different type of stimuli. Single transduction - translated to electrical signalling |
| Describe receptor potentials | Stimulus causes graded depolarised receptor potential, net na+ entry, if large enough ap generated and will travel along afferent fibre to CNS |
| the strength of the stimulus determines what of action potentials | the frequency! |
| Describe stimulus induce action potential where the receptor is a separate cell | Stimulus sensitive Na+ cases Na influx in receptor cell. Voltage gated ca2+ causes calcium influx. Neurotransmitter release binds to na+ (ligand) on afferent neutron finer. AP induced |
| Describe tonic and phasic adaptors | tonic - do not adapt or adapt slowly to sustained stimulation phasic - adapt rapidly |
| what is the receptive field | area surrounding receptor which detects stimuli |
| what is acuity and what is it influenced by | sharpness or keenness. varies inversely with size of receptor fields. Smaller receptor fields higher acuity. It is influenced by lateral inhibition |
| Describe lateral inhibition | First order afferent neutrons stimulated, but one is stimulated most. Inhibitory interneurons stop transmission of those neutrons next to the one stimulated. |
| what are the two possible pathways of afferent neutrons | reflex arc or brain via ascending pathways |
| what does the frontal lobe, parietal lobe, occipital lobe, temporal lobe deal with | frontal - voluntary movement parietal - reception and perception of somatosensory input (touch, pressure, heat) occipital - vision temperoal lobe - auditory |
| what type of stimuli can receptors detect | solute sensors (molecules dissolved in water, lock and key receptors) Solvent sensors - water, turgor sensors |
| what do chemical receptors do | smell and taste., detect 02 and c02 in blood, detect chemical content in digestive track |
| what do noicicreceptors do | pain receptors that are sensitive to tissue damage or distortion of tissue |
| what are the four types of info that sensory systems convey | modality - what type of sensation is it - type of receptor activated, pathway, area in cerebral cortex location - in receptive field, area in somatosensory cortex, pathway intensity freq. of AP, no of receptors activated Timing - beginning and end of |
| what is the sclera | visible white part of eye. Touch outer layer of connective tissue |
| what is the cornea. What is its function | anterior, transparent portion oft the sclera, light rays pass through this before the interior of the eye. Protection, transmission and refraction |
| what is the choroid | middle layer underneath the sclera, contains blood vessels that nourish the retina. IT forms the ciliary body - controls lens shape and iris- controls amount light entering eye - melanin to prevent scattering |
| what is the pupil | opening which light enters the eye size is adjusted by iris muscles |
| what is the lens | focus light onto retina protection from uv damage little protein turnover (cytosol) occurs in lens fibre cells, so damage accumulates |
| what is the retina | consists of inner nervous tissue layer and outer pigmented area. Contain rods and cones, signals are transmitted via bipolar cells and ganglion to visual areas in the brain. |
| what does the pigmented layer of the retina do | absorbs light after is has passed through rods and cones. IT also removes waste products and delivers nutrients/oxygen from the choroid |
| what are the three parts rods and cones consist of | outer segment - visual pigments that detect light inner segment - contains metabolic structures synaptic terminal - releases neurotransmitter depending on dark or light exposure in the outer segment |
| what are the differences between rods and cones | Rods - high sensitivity, low acuity, night vision, vision in shades of grey, scotopic vision cones - low sensitivity, high acuity, day vision, colour vision, photopic vision, large SA for rapid exchange of visual pigments |
| what are the tree tops of cones and what wavelength do they detect (peak activation)nand rods as well | 3 cones. short wavelength (blue). medium - green. Long - red one rod - peak activation in blue/green |
| Are photoreceptors uniformly distributed in the retina | No! CEntral area of of retina has highest density - fovea. Axon of the ganglion form the optic nerve - blind spot |
| what is the optic disc | point in the retina where the optic nerve leaves. blind spot. No rods or cones |
| what is the fovea | Part of neural retina. Small depression in centre. Only cones, no bipolar or ganglion cells point of most distinct vision (highest resolution) |
| what is the macula luteal | Part of retina. Area immediately surrounding fovea. Has cones, bipolar and ganglion cells. Fairly high acuity |
| what is the distribution of cone types in the fovea like | Most are L cones, then M cones (just over a third). Short cones 7% |
| what are the four factors that influence light | absorption, reflection, refraction, ambient noise |
| describe how reflection and absorption influence light | Absorption - transformation of light energy into heat energy in a medium Reflection - light encounters medium with different optical density. part or all is reflected |
| describe how refraction and ambient noise influence light | refraction - change in propagation direction when passing through media with different optical properties e.g. air and water. Ambient noise - light signals can only be detected if they are bigger than background noise. Large single to noise ratio |
| how do concave and convex surfaces refract light | convex - converge light into a focal point concave - diverge light rays |
| what are the primary refractive structures in the eye a | The cornea and lens. IN land animals it is mostly the cornea |
| How does the lens change its strength in order to focus light | Changes its shape - known as accomidation. Ciliary muscle controls shape of lens. |
| When the ciliary muscle is relaxed the lens is, when the ciliary muscle is contracted the lens is | Flattened weak Rounded, strong lens |
| what is a visual pigment comprised of and what is the rod and cone visual pigments made up | opsin protein + Chromophore Rhodopsin = scoptopsin + 11 cis retinal (vitamin A derivative) cone pigments = photopsin + 11 cis retinal |
| Describe phototransduction part 1 general | Absorption of light - configuration change of retinal cis to trans. Biochemical cascade activated, cell hyper polarises, reducing strength of signal normally relayed to bipolar and horizontal cells (second order cells) |
| Describe phototransduction part 2 general | All trans retinal is transported to pigment epithelium - recycled.Energy and catalysis by retinal isomerase converts back to 11-cis-retinal. Once formed it automatically combines with scotopsin to form rhodopsin until photon is absorbed |
| night blindness = | vitamin A deficiency |
| Is the conformation change of rhodopsin and formation of intermediates fast | Very fast |
| is the reformation of rhodopsin fast or slow | slow, hence why it takes us a minute to adjust to darkness and light etc |
| how many photos can cause a rod receptor potential of 1mV. And what causes this sensitivity | 1! High sensitivity, caused by signalling cascade which amplifies stimulus signal about a millionfold in rods |
| how many times faster is cones than rods | 4! |
| Describe the specific mechanism of photoransduction part 1 | photons isomerise 11-cis-retinal to all trans form. This activates and releases its opsin. Opsin catalyses activation of G-protein transduction. Transduction catalyses activation of PDE. PDE catalyses breakdown of cGMP, loweing [] in cell. |
| Describe the specific mechanism of photoransduction part 2 | Results in loss of cGMP around sodium channels houses in cellular membrane. This causes channels to close and cell hyperpolarises. Rhodopsin kinase inactivates activated rhodopsin and cell potential returns to normal |
| What is the rod receptor potential like in the dark the inner segment | Na/K pump continuously active. K continuously leaks through non=gated K channels typically -70mV |
| Describe rod receptor potential in the dark in the outer segment | Membrane leaky for Na. High cGMP levels - high influx of mostly Na but also CA and mg2+. Neg potential is reduced, -40mV. Constant neurotransmitter release |
| Describe rod receptor potential in the light | activation causes decreased conductance for Na in outer segment. Inner segment continues to pump out NA. More Na leave the cell than back in. Increasingly negative potential. The more light it absorbs the more it hyper polarises |
| How does the retina adapt in light exposure | most visual pigments converted to retinal and opsins. Most of retinal converted to vitamin A. Reduced con of visual pigments, reduced sensitivity |
| How does the retina adapt in dark | retinal and opsin converted back to visual pigments. Vitamin A converted into retinal. limit of sensitivity, amount of opsin |
| white light stimulates what colour cones and in what ratio | S, M and L equally! |
| if l cones are missing or their peak absorbance is shifted | Protonopia |
| if m cones are missing or their peak absorbance is shifted | Deuteranopia |
| if s cones are missing or their peak absorbance is shifted | Tritanopia |
| why are males more affected by colourblindness than females | opsin genes located on x chromosone |
| what are the neurotransmitters associated with the retina | Mostly glutamate but also dopamine and acetylcholine. |
| What type of signal is produced in the retina | Electrical conduction. Graded potentials rather than all in one. Light intensity is encoded by amplitude rather than frequency |
| Describe horizontal cells in the retina | Behind rods and cones.Respond by hyper polarising. Three types HI, HI, HII. Connect laterally between synaptic bodies of rods and cones. Sum over large areas - via gap cjuntions. Are inhibitory - lateral inhibition. Contrast enhancement |
| Describe bipolar cells in retina | Relay signals from photoreceptors to ganglion cells. Behind horizontal cells. Ten typesThey either respond by depolarisation (on centre) or hyper polarisation 9off centre) |
| Describe amacrine cells | Behind bipolar cells. Horizontal integration, modulation and added temporal information to visual message received by ganglion cells. 40+ types. Show an on response only, others only off, during, on and off. Some are directional sensitive |
| Describe ganglion cells | Final AP producing output neutrons following pre-processing by retina. Axons form optic nerve. Fewer ganglion than rods and cones - convergence. Two physiological types with on and off centre receptive field |
| what is an on centre and off centre cell | On centre - outside off - inhibited by light, inside on - stimulated by light Off centre - outside on, inside off |
| light on centre off off centre cell will cause | lateral inhibition |
| What is the visual field | field of view without moving head |
| what does the optic nerve carry information from and where does it lead to | both visual fields, info is separated at optic chiasm. Fibres leaving chiasm are called optic tract. Each optic tract carries info from one visual field to the opposite visual cortex |
| what can the occiptical lobe be partitioned into | 8 visual areas with their own roles and specialities |
| what are the four major cell types in the occiptical lobe in v1 | Simmple - respond to changes in light intensity of a particular orientation complex cells - Bar moving across entire recptive field hypercomplex cells - fire only to moving lines of a particular length blobs - Sensitive to colour/bright not orienta |
| what are the two processing streams in the occipital lobe | Ventral colour processing and form processing and dorsal - motion and disparity |
| what happens when the dorsal stream is damaged | fail to perceive and entire side of an object |
| what happens when the ventral stream is damaged | inability to name or recognise things |
| what do the external and middle portions of the ear do | transmit and amplify airborne soundwaves to the fluid in the ear |
| what does the inner ear do | contains neural receptors for two sensory systems: cochlea for hearing and vestibular apparatus for equilibrium |
| hearing involves what two aspects | identification of the sound (what) localisation of the sounds (where) |
| what are sound waves | mechanical disturbances that displace the molecules of a medium. Cannot ravel through a vacuum. High density regions alternate with low density regions |
| what are the four factors that affect sound transmission | Absorption, reflection, refraction and ambient noise |
| Describe how absorption and reflect affect sound transmission | A - transformation of acoustic energy into heat energy in the medium R - when sound wave encounters a medium with a different impedance e.g. wall, water |
| Describe how refraction and absent noise affect sound transmission | When a sound wave encounters medium with different acoustic impedance, direction of the incident sound will change due to different propagation speeds Noise - background noise |
| what is pitch or tone determined by | Frequency of vibrations higher pitch - higher frequency |
| what does the intensity or loudness of the sound depend on | depends on the amplitude of the wave! |
| what does the timber or quality of the sound depend on | depends on the overtones |
| what happens when the sounwaves entered through the external ear | The tympanic membrane vibrates in unison with sound waves (however the pressure on both sides has to be equal). Middle ear bones convert trympanic vibrations into fluid movements in the cochlea |
| why is sound amplified about 20 times in ear and how | More energy is required to start a pressure wave in a fluid than in ear. Amplification is due to the fact the oval window is smaller than ear drum and the lever action of ear bones |
| Describe the attenuation of sound and why | Loud sounds detected by nervous system - attenuation reflex activated. 2 muscles onctract to pull the malleus inwards and stapes outward. Increases rigidity to protect against damaging vibrations and to increase signal:noise |
| where is the organ of the corti located and and how does it participate in sound transmission | Rests on the basilar membrane in the cochlea. Sense organ for hearing. Movement of fluid in inner ear causes basilar membrane to vibrate |
| oval to round window = shortcut from scala vestibule to scala tympani = | dissipation of energy sound |
| describe in detail the function and components of the organ of court | Trandsduction takes place. Contains hair cells. Nerve cells stimulated by hair cells lead to spiral ganglion of Corti, which project via cochlea to CNS |
| describe the hair cells in the organ of court | specialised receptor cells sensitive to mechanical signals with approx 100 stereocillia each. Differential movement in tectorial and basilar membrane distorts hair cells - mechanical signal leads to opening of mechanically gated cation channels |
| describe signal tranduction mechanism for hearing | Involve the sterocillia. Hair cells bent - open and closes mechanically gated ion channels. Receptor experiences alternating hyper polarisation and depolarisation with same frequency as original sound stimulus |
| what does hyper polarisation do to the frequency of ap | no aps. Less than if there was no stimulation |
| what do the outer hairs do for hearing | Not directly involved in hearing. Stimulation changes length (electromotility). Depolarisation - shortening. Hyper polarisation - lengthening. Length changes properties of basilar membrane. Tunes the stimulation of the inner hair cells |
| pitch discrimination depends on what | the region of the basilar membrane it vibrates. |
| timre discrimintation | highest amplitude wins |
| hearing summary | Vib of tympanic membrane, vib of middle ear, vib of oval window, fluid movement cochlea (vib of round window -dissipation), vib of basilar membrane, bending of organ of corti hairs, graded P in receptor cells, change in APfreq in auditory nerve, |
| what is conductive deafness | sound waves not conducted due to ruptured ear drum, ear wax etc. Hearing aids fix this as they amplify the signal |
| Sensoryneural deafness | sound waves conducted, problem lies with organ of corti. Loss of hair cellscochlear implants |
| what does the vestibular apparatus comprised of | semicircular canals and otolith organs |
| what do the semicircular canals deal with | detect rotaional or angular acceleration or deceleration of the head - rotational equilibrium |
| what do the otolith organs deal with | detect changes in the rate of linear movement and provide info about head position relative to gravity - gravitational equilibrium |
| what is the endolyph, ampulla and cupula | Part of the semicircular canal. E - Fluid filled canals. Ampulla contain the receptors and hair cells. Hairs are embedded in gelatinous material - the cupula |
| Force of the endolyp in the semicircular canals does what | moves cupula and hairs within it |
| describe the transuduction of of rotational equilibrium general | Head turns, endolymph lags behind due to inertia. E in canal in same plan as movement pushes on cupula and hair cells bend in opposite direction of head movement. If head keeps moving, endolymph moves at same speed, no force on c, hc no longer bent. |
| describe the hair cells in the cupula | Separate receptor cells. They have stereocillia and kinocilium. They have mechanically gated ion channels that open/close spending on direction of bending |
| describe the transuduction of of rotational equilibrium (specific mechanism) | Depolarisation in hair cell - neurotransmitter release and increased AP freq. When fluid stops moving, hairs straight, no signal. No signal when head keeps turning at constant speed or head is motionless |
| describe otolith organs | Comprised of utricle and and saccule. Sack like structures in capsule between semiscircular canals and cochlea. Receptors - hair cells. Gelatinous sheet of calcium carbonate crystals lie on hair (otoliths) to increase inertia |
| in an upright position the hairs of the utricle are orientated blah and the hairs of the saccule are orientated | Vertically, horizontally |
| Describe the utriculus | Response if head is tilted so vertical (tilt up or down). Gravity on otoliths cause hair to bend (signal). Depending on tilt, hyper polarise or depolarise. Respond to horizontal linear motion. Heavy otoliths lag behind - no signal if movement is constant |
| Describe the scales | responds if head is tilted away from horizontal position. Getting up from bed. Responds to vertically linear acceleration - jumping up and down. no signals are detected when movement is constant |
| Unlike information from the cochlea - much of the vestibular information does not | reach the level of conscious awareness |
| Axons of afferent neurons form The vestibular nerve combined with the auditory nerve from the cochlea forms | vestibular nerve. the vestibulocochlear nerve |
| Signals from the vestibular apparatus are carried through the vestibulocochlear nerve | to the vestibular nuclei (brain stem) and then to the cerebellum. Cerebellium integrates info from eyes, skin, surface, joints and muscles. Info used to maintain balance, posture eye movement and perceiving motion |
| what is the Vestibulo-Ocular Reflex | Reflex eye movement. when vestibular system detects head movement, eye moves in other direction to stabilise image in the retina |
| efferent copy | Sensory information is heavily filtered and analysed before it reaches level of consciousness and leads to behaviour to save metallic energy, |
| what is the innate immunity comprised of | macrophages, granulocytes, nk cells, complement etc |
| what is adaptive immunity | t and b cells |
| innate vs adaptive | Innate - hours, fixed and limited, response to repeatinfection is identical to primary response adpative - days, highly diverse, improves during the course of the response, response to repeat infection is more rapid |
| first barrier to infection is | epithilial surfaces - mechanical,chemical, microbiological |
| blood cells divide into | erythrocytes - red blood cells leukocytes (white blood cells) - granular: eosinophils, basophils, neutrophils agranular - lymphocytes, monocytes |
| what are the three types of phagocytes and their function | macrohpage - phagocytosis and activation of bacteriicidal mechanisms, antigen presentation dendritic cells - antigen uptake in peripheral sites antigen presentation in lymph nodes. Both p and fixed, long lived neutrophils - short lives, first on site |
| what are the four characteristics of inflammation | Rubor (rednness, vessel dilation), calor (heat, vessel dilation, tumour (swelling) and dolour (pain). |
| what are the three basic steps of inflammation | tissue injury + release of chemical signals, dilation and increased permeability of blood vessels. Phagocytosis of pathogens |
| what are three changes to local blood vessels upon inflammation | dilation of blood vessel - increased blood flow changes in adhesion molecules - allows blood vessels to stick increased permeability - blood cells can move into the tissue |
| how are pathogens recognised by phagocytes | Pathogen associated molecule pattern (PAMP) are bound to receptors and activities secretion of inflammatory mediators e.g. cytokine and lipid mediators |
| What are microglia, alveolar, spleen macrophages, and kuppfer cells, going | all macrohpages! |
| What are microglia, | Macrohpage. They phagocytose dying neurones. Almost inert but but can be reactivated by inflammatory mediators. |
| what are alveolar mediators | respond to local surface attacking stimuli e.g. irritants, asbestos, by cytokine release |
| what are spleen macrophages | immune function. Phagocytosis of naturally dying cells. clearance of particulate agents. e.g. plasmodium |
| what are kuppfer cells | Exposed to gut derived microbial products. cannot mount respiratory burst |
| what are joint macrophages | responsible for cytokines in arthritis |
| what are the four stages of phagocytosis | 1. binding to surface receptors, e.g. PAMP 2. Engulfment into vacuole/phagosome 3. Fusion of phagosome with lysosome 4. Kiling and degradation of bacteria by lysosome, proteases, hydrolyses and free radicals |
| why don't tattoos fade | Long-lived macrophages take up colloidal ink by phagoctyosis and endocytosis in situ. When they die, new macrophages move in to phagocytose the dead cells, resulting in a permanent colouration |
| what does the secretion of cytokine IL-1, TNF alpha and IL-6 induce | IL-1 fever production of il-6 TNF alpha - fever mobilisation of metabolites. Shock Il-6 - induces acute phase protein production and fever |
| what is a neutrophil | Released form bone marrow. Primary function is phagocytosis and killing of pathogens. First cells to bind to inflamed tissue. To do so must gain access to tissues form blood stream - extravasation |
| what are chemotaxis and relate it to neutrophils | the movement of cells up a gradient of attractive molecule, towards its source. Neutrophils chase bacteria and move to site of inflamamation |
| what is the complement system and what is its three main functions | Plasma proteins that defend against pathogens in extracellular spaces. Recruitment of inflammatory cells - c3a c35a killing of pathogens c5b. c6, 7, c8, c9 coats molecules with opsonins that enhances their phagocytosis - c3b |
| what are mast cells and basophils | Cuase type 1 hypersentivity. Certain allergens evoke a IgE response and then bind to mast cells and basophils. Subsequent exposure, results in granulation of mast cell resulting in histamine and other active agent release |
| describe the activation of a mast cell in detail | FceRI are high affinity receptors for IgE on the surface of mast cells. When cross linked with antibody-allergen complexes, mast cells respond my degranulation |
| what are natural killer (NK cells) and what are the activated by | Develop in bone marrow from lymphoid cells. Larger than t cells with distinctive cytoplasmic granules. Recognise infected cells or tumour cell and destroy them. Activated by missing MHC1 (which stimulates inhibitory signal) |
| Describe antibody dependent cell mediated cytoxoicity | Antibody binds antigen on cell surface. FC receptors on NK recognise bound antibody. Cross linkage of FC receptors signals NK to kill cell. Apoptosis occurs |
| in genral what do b cells do and t cells | B = recognise intact antigens directly through antibody molecules T = recognise processed antigen fragments when bound to MHC (major histocompability complex) molecules = antigen presentation |
| the mhc and antigen are specific to the | t cell |
| MHC I AND MHC II BIND PEPTIDES FROM DIFFERENT COMPARTMENTS. What is MHC 1 snd MHC 11 and what evokes them | 1 - peptides are derived from intracellular proteins - short viral proteins. all nucleated proteins 2 - peptides are derived from extracellular or vesicle proteins - long extracellular bacteria. professional pac |
| describe the mechanism of mhc 1 presentation | protein recognised by proteasome, releases peptide fragments which binds to TAP1+2 and MHC1. MHC1 is presented on the cell surface |
| describe mhc11 presentation | Pathogen is engulfed by endocytosis. Forces acidified endosome, then vesivle fusion and is presented on outside |
| What tcells respond to peptide/MHC ? | MHC 1- CD8 t cells MHC 2 - CD4 t cells |
| what is t cell activation (priming) | native t cell - activated effect cell, process in vaccination, modulation of autoimmunity |
| what is costimulation of t cells T require 2 signals to be activated. | 1. antigen-specific,. T receptor interacts with peptide-MHC molecules on the membrane of antigen presenting cells (APC). 2. the co-stimulatory signal, is antigen nonspecific. interaction between co-stimulatory molecules expressed on APC mebrane and T |
| how dp dendritic cells affect signal two of t cell activation | Upon stimulation by “danger signals” (e.g. LPS) DCs stop antigen uptake, Upregulate costimulatory molecules (signal 2) and migrate to the lymph node |
| Once a T cell becomes an effector T cell it requires | only T cell receptor engagement (signal 1) to trigger effector function at the infection site |
| describe t cell development (from bone marrow) | Bone marrow to thymus where they are educated, to blood, to lymphoid organs |
| describe t cell selection | if it has a strong affinity to recognising and killing itself (negative selection) weak affinity (positive selection), very weak affinity - death by neglect |
| what are cd8 t cells | cytoxic l lymphocytes. kill virally infected cells. secrete cytokines |
| what are cd4 cells | helper t cells |
| what do the helper t cells TH1, TH2, TH 17 and treg do | 1 - secrete cytokines which activated macrophages, cellular immunity 2 - provide signals for b cell maturation - antibody 17 - inflammation treg - suppress immune response |
| describe CD8+ T cell killing | primary - tcl triggering leads to release of granules = target cell death secondary MEMBRANE EXPRESSION OF FAS LIGAND CAUSES CROSSLINKING OF FAS ON THE TARGET CELL AND TRIGGERING OF APOPTOSIS |
| TWO MAIN PROTEINS ARE FOUND IN LYTIC GRANULES : PERFORIN - POLYMERIZES TO FORM A PORE IN THE TARGET CELL MEMBRANE | GRANZYMES - AT LEAST THREE SERINE PROTEASES - ACTIVATE APOPTOTIC PATHWAYS IN THE CYTOPLASM OF THE TARGET CELL |
| : Most antibody production is dependent on T help. which t | cd4 |
| antibodies or ig are | • glycoproteins found on surface of B cells (as part of B cell receptor = BCR) and in mammalian serum and tissue fluids • recognise “epitope” of an “antigen” (e.g. on pathogen) • recruit molecules and cells to destroy pathogen. |
| Each B cell produces antibody of | a single specificity |
| wen antigen is recognised by BCR | b cells mature into antibody secreting plasma cells. Antibody has same membrane specificity as bound form |
| describe antibody structure | heavy chain (c terminusa) and light chain (n terminus) connected by disulphide bonds. variable region in the light chain |
| heavy determines what of the antibody and light chain determines | isotype or class of the antibody = heavy light = kappa or lambda |
| what are the main antibody | IgF, IgM, IgD, IgA1, I gE |
| IgA and IgM can form what | multimers! |
| describe b cell development | Generation occurs in bone marrow. negative selection occurs in bone marrow. B cells migrate to lymphoid organs. Antibody secretion and memory cells in bone marrow and lymphoid tissue. |
| describe antibody levels during an immune response | Primarh -lag, IgM Secondary IgG, , IGA, IGE |
| Describe isotype switching | You can switch from iGM production to other isotopes through DNA recombination. The genes are next to each other, so you can simply loop in and loop out |
| what are the 4 mechanisms responsible for antibody diversity | heritable v/d/j segments and somatic recombinatino - Basically, the antibody paratope is polygenic, made up of three genes, V, D, and J. junctional diveristy pairing of different heavy weight and light chains somatic hypermutation |
| describe thymus independent antibody production | Indepenent - antigen lacking peptide componen and therefore cannot be presented by mhc, Release of antibodies, but no formation of immunological memory |
| what is a paratype | antigen binding site |
| and thymus independent antibody production | contain protein component. Signal 2 interaction between b and helper t cells, form immunological memory |
| what are the four antibody effector functions part 1 | neutralisation (fc independent) - bind antigen and block function e.g. prevent entry into cell, block toxicity Opsonisation - promotes phagocytosis compliment activation - recruits/activates phagocytes , kills pathogens, opsonisation. |
| what are the four antibody effector functions part 2 to | ADCC - nk kills anitbody located cells Triggering of mast cells, basophils and neutrophils |
| what is the function of IGM, IGE, I GG, I GA, IGD | M - neutralisation and activates compliment system, opsonisation E - sensitisation of mast cells IGD does M + E + sensation of killing by NKcells A - same as M |
| The earliest isotype is IgM which then switches to | G then A |
| what is primary and secondary immune deficiency | Primary - hereditary or acquired. immune deficiency is cause of the disease Secondary - immune deficiency is the result of another disease or condition |
| what is a mhc class 1 and 2 deficiency | 1 - no cd8 t cels 2 - no cd4 t cels |
| what is type 1, type 2 and type 3 hypersensitivity | Antibody dependent! |
| describe type 1 sensitivity | B cells produce type IGE antibodies. Antibodies bind to mast cell fc receptors and basophils. Later exposure to antigen, cross links IGE on sensitised cells, inciting release of granules (histamine + leukotriene |
| difference between type 1 hypesensitivity and a normal immune response | IGe is the antibody not IgM. iGA etc |
| describe type 4 hypersensitivity (delayed type sensitivity - DH) | antibody dependent! Reactions develop hours or days later. Immune reactant is TH1/TH2 (t cells_) not antibodies |
| what are the three stages of a DTH reaction. | Antigen uptake by APC cells and is presented. TH1 effector cells recognises antigen and releases cytokines, recruitment of phagocytes and plasma to site of antigen injection |
| Examples of organ specificic and systematic autoimmune diseases | diabetes, graves disease, MS - organ arthritis, lupus - systematic disease |
| what is the immune surveillance theory | s that the immune system plays an important role in the regression of established tumours |
| describe immune escape by tumours (low immunogenicity, tumour treated as self antigena | low immunogenicity - no co-stimulatory molecules, no peptide MHC ligand Tumor treat as self antigen - tolerate TC cells. Taken up by APC in absence of co-stimulation. |
| describe immune escape by tumours (antigenic modulation, tumour induced immune supressionand tumour induced privilege site | Antigenic modulation - t cells cannot eliminate tumours that do not have immunogenic antigens. Tumour induced immune suppression - tumour releases factors that suppress t cells. Tumour induced privilege site - factors physical barrier against immune syste |
| Describe tight junction in the kidney | Important in the proximal tubule vs ascending loop of henle in the nephron. TJ are like rivets, which allow ions to avoid cell all together. PT is leaky, while distal tube is tight. not allow ions to permeate through TJ from lumen into interstitial space |
| why does the proximal tube need to be leaky | It is responsible for the reabsorption of the majority of ultrafiltrate. |
| Gap junctions lead to what of type of function | synchrony! |
| Gap junctions are also important for | calcium signalling! |
| Describe gap junctions in relation to cystic fibrosis | Cilia on top of epithelial cells move mucus, which traps and clears bacteria. Cilia need to move via calcium input and to move in sync. CF infection caused by Cl chan defect. Mucus cannot be moved |
| describe simple diffusion and active transport | Simple diffusion (no protein) at pivot points on either end to avoid destroying the gradient o Carrier mediated active transport: moves against the gradient by utilizing ATP |
| what are the two types of passive transport | Channel protein (open and moves through o Carrier mediated (passive) moves with gradient but carries ions through by opening and closing |
| What are the steps of Na/K ATP ase and relate it to tight junction. How does it create a net negative charge in the lumen compared to interstitial space | ATP binds. 3 Na enter protein. ATP is hydrolised. Na enters extracellular space. 2 k enter protein. Pi unbinds and channel closes. ATP binds and K enter cytosol. Ci diffuse out of cell via tight junctions. By pass the cell. NA pumped in apical, out baso |
| How are cl and Na reaborped proximal tubule | Na enters through apical membrane and into lumen (downhill) via tight junctions. But exit of na out of basolateral membrane is uphill, therefore you need the NA ATPASE |
| What is the nerst equation and how do you calculate i | Emv = 61.5 log [Co]/[Ci] - 37 Emv = -58 log [Ci]/[Co] - room temp alculation of the electrical potential reached by charged ions separated by a permeable “membrane”. |
| Remember that epithelial cells are not excitable so there won’t be very huge | influxes or effluxes of ions in or out of the cell |
| what happens to potential when k and na channels open | Na eq potential is + 50mV, K+ = -80mV. RMP is between the values, therefore when doors open ions want o move towards eq. K moves out of cell, becomes more neg, na channels open eq becomes more positive as it moves into the cell |
| what is the proximal tube unimportant for | Na+, Cl- recovery, water recovery, protein recovery, secretion of renin. Impermeable to blood cells |
| Describe proximal tubule ionic movements of NA and K+ | NA/KATPAse on basal side as always to move K+ into cell. K + channels let k out freely, high apical NA+ and low in cell. Enac channel lets NA+ into cell through apical side, recovered by NA/K TPASE |
| Describe proximal ionic movements of H+ and HC03 | Created via c02 + H20. H+ channel to remove on apical side HC03- exits on basal side |
| Describe proximal ionic movements of glucose | Recovered by SGLT (sodium, glucose linked transporters). Mechanism is saturable, since only through specific pathway. If blood glucose is too high (diabetes) it cannot be recovered and glucose is lost in urine |
| The net ion movement in the proximal tubule creates an osmotic gradient to what side | basal side |
| describe water movement in the proximal tubule | leaky so water can move freely intercellular (tight junctions) or intracellular (AQP1 on basal and apical membranes) |
| Describe water movement in the collecting duct | utilises AQP2 on basal side to recover water. AQP2 can be exocytosed into the membrane to be used. AQP4 is on the basal side and lets water out into the blood . ADH binds to receptor, ge coupled then incites exoctyosis of aquaporin |
| Aborption in the gut is dependent on | apical microvilli! |
| Describe acid secretion in the stomach | HCl is produced outside as Cl and H+ are moved into the lumen. A H/K/ATPase transporter is on the apical membrane in to push H+ ions out. Cl' is pushed in through basal membrane via a HC03-/Cl- transporter than out into lumen |
| Describe chloride movement in the lungs | NA/K/2Cl- sympporter pushes ions into cell via basal membrane. Na/K ATPase and K" channels also present on basal membrane. Ci channel on apical membrane to allow Cl to flow into lumen |
| describe cystic fibrosis in more detail | enac channels are inhibited (by blocking of CTFR receptor which stimulates ENAC). Lack of h20 movement due to low osmotic gradient. Water cannot be moved, sticky mucus, infections, cystic fibrosis |
| how does the pancreas work | eat, body produces CCK. CCk binds to receptors on acinar cells. Acinar cells release digestive enzymes through pancreatic ducts. CKK - peptide hormomne |
| what are the two type of cells in the pancreas and how are they linked | acinar cells and duct cells. Linked via tight and gap jucntions |
| what is the function of acinar cells | secrete digestive eynzmes, cck more enzyme release, thought to secrete water as well to wash enzymes out |
| what is the function of duct cells | Monolayer. Lumen inside of duct (with cilia pointing inside the duct - apical) Water secretion to wash enzymes into vessel. Has a CFTR (cystic fibrosis transmembrane regulator) ci' channel similar to the lungs. In the pancreas leads to a CA2+ rise |
| Describe protein secretoin in acinar cells | CCk and ACh signal through GPCR second messengers to signal release of calcium from the ER. Ca allows protein to fuse to granule and trigger exoytosis |
| describe the pathway to release ca in protein secretion in acinar cells | CCK ->GPCR-> alpha subunit confomrational change ->Pip2 -> IP3 + DAG - ca2+ release on the ER |
| why can yo measure CKK conc but not ACh | Ckk we know where it is. ACh is everywhere |
| how much ckk when hungry and when full. How much ACh | 4pM when hungry, 10pM when full, 8pM average. |
| would a sustained concentration of the ckk agonist result in continuous CK+ release until ER is emptied? | no! Ca conc actually oscillates.These are called puffs |
Created by:
Lui24