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Physiology of cells and systems > Physiology > Flashcards

Physiology Flashcards

1
Q

What is the meaning of a gated ion channel?

A

Part of the membrane can block or undergo an conformational change to block the pore

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2
Q

Describe the Kv structural ion channel family

A

-6 transmembrane spanning domains
-The 4th transmembrane domain is the voltage sensor. Voltage dependent ion channels are sensitive to the membrane potential which is mediated by amino acids in the 4th transmembrane domain.
-Pore region is where amino acids which construct the pore are located.
-4 subunits must come together to create a functioning potassium channel.

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3
Q

Describe the structure of Kir ion channels

A

-2 transmembrane spanning domains
-4 subunits must come together to create a functioning potassium channel.

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4
Q

Describe the structure of Nav or Cav ion channels

A

-24 transmembrane spanning domains
-4 pore regions
-Come together to make one channel
-Beta subunit

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5
Q

Describe the structure of the CFTR Cl- ion channels

A

-12 transmembrane spanning domains
-Regulatory domains

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6
Q

Describe the structure of Ach receptors

A

-Ligand gated ion channel
-Binding of Ach opens the channel and depolarises the membrane potential.

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7
Q

What is the function of the patch clamp technique and how is it performed?

A

-Allows us to evaluate ion channel physiology
-When there are mutations we can look at ion channel pathophysiology
-Glass pipette is filled with salt solution
-A reference electrode is used
-Glass pipette touches cell membrane
-Suck on the end of the pipette. Membrane of cell seals onto pipette
-You can look at single ion channels moving across membrane, current can be measured
-Ripping away part of the membrane allows you to record currents from the whole membrane of the cell

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8
Q

What is the function of ion channels?

A

When open, they drive the membrane potential towards the Nernst potential for the channel

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9
Q

What is FHEIG?

A

Disease which cases Bi-temporal narrowing, hypertrichosis (hair), thin upper lip, bushy long eyebrows.
Also causes delayed development of intellectual ability and motor skills.
Seizures and Egg anomalies
Mutants have larger currents in potassium channels
This impacts the interstitial space, more potassium is lost which goes into interstitial space and potassium accumulates. Depolarises Nernst potential for potassium. Membrane potential in other neurons set by Nernst potential for potassium. They then have more positive resting membrane potential and more likely to fire action potentials.

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10
Q

What is Vm measurement and how is it collected?

A

-The voltage across the plasma membrane
-Reference electrode in extracellular solution
-Sharp glass electrode inserted through cell membrane into extracellular fluid
-Majority of cells measure -70mV

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11
Q

Describe sodium potassium ATPase’s role in setting the membrane potential

A

-Hydrolyses ATP to move 3 sodium ions out of the cell in exchange for 2 potassium ions.
-Electrogenic (net charge movement)
-Loss of positive charge

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12
Q

Describe the Nernst potential for potassium

A

-Potassium channels in cell membrane
-High intracellular potassium, low extracellular concentration
-Large anionic proteins which are not membrane permeable
-Concentration gradient for potassium to leave the cell
-Potassium carries positive charge leaving behind a negative charge
-Generates a potential gradient which works in opposite gradient, moving potassium ions in
-Number of ions leaving balances ions coming in so there is no net movement of potassium.
the potential at which there is no net movement is the Nernst potential for potassium

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13
Q

Describe the nernst potential for cells with sodium channels

A

-High extracellular sodium and low intracellular sodium
-Concentration gradient moves sodium down conc gradient into cell
-Movement of sodium carries charge
-Positive sodium moves in, positive potential.
-Sodium then passed out due to potential gradient
-At the point where potential and concentration channels are equal and opposite, this is the Nernst potential

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14
Q

Describe the movement at the membrane potential

A

-Sodium potassium ATPase (3 Na+ out and 2 K+ in) sets low intracellular sodium concentration
-K+ channels drive membrane potential in negative direction
-At rest cells around the body have negative resting membrane potentials
-If sodium channels are opened, sodium will move in down the electrochemical gradient. This moves the balance of selectivity

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15
Q

Describe the action at the sodium amino acid co-transporter

A

-Sodium shifts the membrane potential towards the Nernst potential for sodium
-Activation of potassium leads to repolarisation
-Sodium is still being transported, the balance just shifts

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16
Q

What are normal conditions of intra and extracellular Na+?

A

-Extracellular; high 145mM
-Intracellular; low 15mM

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17
Q

What is the function of the thick ascending limb of the loop of Henle?

A

-Reabsorption of NaCl in preference to H2O
-Apical membrane is impermeable to water, so NaCl is absorbed
-Creates transepithelial osmotic gradient responsible for counter current multiplication

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18
Q

Describe action at the thick ascending limb of the loop of Henle

A

On the basolateral membrane:
-Sodium potassium ATPase pumps sodium out and potassium in. This keeps intracellular sodium low
On the apical membrane:
-NKCC2, sodium at this transporter uses sodium gradient to drive uptake of one sodium, one potassium and 2 chloride ions into cell.
-Sodium leaves via pump, chloride leaves down electrochemical gradient via basolateral chloride conductance (CICKB)
-Potassium recycled over membrane
-Activity of NKCC depends on inward Na+ gradient
-If sodium inside cell increases too high, this reduces NKCC driving force so its function impaired. Leads to diuresis.

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19
Q

What are the normal conditions of intra and extra cellular Ca2+?

A

Extracellular; high 1,000,000nM
Intracellular; low 100nM

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20
Q

What is the role of Ca2+ in acinar cells?

A

Under control of different second messengers or hormones leads to stimulation of pancreatic acinar cells leading to increase in calcium, aiding binding of secretory vesicles to apical membrane and no enzymes are released.

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21
Q

What keeps in intracellular calcium low?

A

There are 2 mechanisms involves; Na+/Ca2+ exchanger and Ca2+ ATPase

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22
Q

If inwards Na+ gradient is 10 fold and Ca2+ gradient is 10,000 fold, how can the Na+/Ca2+ exchanger keep Ca so low?

A

-Normally exchanges extracellular Na+ for ca2+
-Na+/Ca2+ exchanger is electrogenic
-Stoichiometry is 3Na+:1Ca2+
-This means the effect of Na+ gradient is magnified
-The effect of the 10 fold gradient is cubed.

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23
Q

Describe the role of PMCA

A

-Virtually inactive at physiological Ca2+
-Increases Ca2+ which activates calmodulin
-Removal of auto inhibition and activation of PMCA
-At resting levels is the major mechanism for controlling Ca2+

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24
Q

Describe role of the Na+/Ca2+ exchanger

A

-Major role when Ca2+ rises above resting levels
-Important when there are large influxes of Ca2+

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25
Q

Describe the relationship between Ca2+ release from stores and store operated calcium channels

A

-Store operated calcium channels are involved in the filling of stores
-Agonist binds to GPCR stimulating PLC, breaking PIP2 into DAG and IP3
-IP3 will activate IP3 receptors in store membrane
-Ca2+ rushes out of store into cytoplasm
-Ca2+ must be replenished inside store
-Mechanisms linked to SOCC, SOCC are activated, calcium moved in and selectively refills stores.

-SOCC located in plasma membrane are inactive at rest.
-In membrane there is STIM1 protein.
-Starts with high levels in store, when store is depleted, calcium binding to STIM is removed, leading to activation of STIM.
-Complexes are formed. conformational change allowing STIM to interact with plasma membrane.
-Can activate SOCC, Ca2+ can move from extracellular domain to store.
-PMCA pumps are slightly inhibited, SERCA pumps are stimulated. Entry of Ca2+ is favoured into cytoplasmic space. Exit pathway is inhibited, movement of calcium across plasma membrane. Stocks are replenished.

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26
Q

What happens if the calcium balance goes wrong?

A

-Chronically de myelinated axons on MS
-Decrease in expression of Na+/K+ ATPase
-The impact is; inefficient transmission of action potentials. Impacts on function of NCX, rise in Ca2+ leading to Ca2+ mediated axon degeneration

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27
Q

Why is it important to control intracellular pH?

A

-pH is a logarithmic scale
-A small change in pH reflects a large change in protein concentration
-Proteins act to buffer changes in pH
-Change in pH changes protein charge which changes protein conformation and changes protein function.

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28
Q

What are the 3 factors involved in control of intracellular pH?

A

-Buffering
-Acid extrusion
-Acid loading

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29
Q

How does buffering control intracellular pH?

A

-pH buffer is any system that moderates the effects of an acid or alkali load by reversibly consuming or releasing protons.
-Buffering systems act to minimise pH changes and help protect the cell from damage.
-A buffer cannot reverse the changes in pH caused by an acid or alkali load, any recovery is due to the presence of acid loading/ extrusion mechanisms.
BUFFERS CANNOT PREVENT CHANGE IN PH, THEY MERELY MINIMISE THE MAGNITUDE OF THE CHANGE.

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30
Q

What is the buffering power?

A

The amount of strong base (or acid) that must be added to a solution in order to raise (or lower) the pH by a given amount.

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31
Q

Describe acid extrusion

A

-Na/H exchanger:
-Under normal physiological conditions, the sodium proton exchanger moves sodium into cell and protons out.
-The action of the Na/H exchanger relies upon sodium potassium ATPase.

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32
Q

What is the role of NHE1?

A

Housekeeping function; primary roles in regulation of pH and in control of cell volume.
Inhibited by ‘low’ concentrations of amiloride and its analogue EIPA. Found in basolateral membrane of epithelial cells.

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33
Q

Describe the acid loading system

A

-Cl/HCO3 exchanger- anion exchanger family
-Under normal conditions, direction of transport is inward movement of Cl for exchange of HCO3
-Removal of bicarbonate, leaves proton behind leading to acidification
-Like the Na/H exchanger, the activity of the Cl-/HCO3- is modulated by pH
-low activity at acid pH which increases as pH becomes alkaline

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34
Q

what are the three types of airflow?

A

Laminar
Unstable
Turbulent

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35
Q

How is the flow type determined?

A

It is governed by the Reynolds number which is influenced by the viscosity and density of the gas
Re < 2000 is laminar flow
Re = 2000-3000 is unstable flow
Re > 3000 is turbulent flow

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36
Q

Describe laminar flow

A

Steady flow down a tube in a uniform direction and speed. Flow rate is maximal in the centre of the tube and reduces towards the edges

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37
Q

Describe turbulent flow

A

If flow rate is beyond a critical value, irregular currents lead to vortices developing. The rate of gas movement is proportional to square root of the pressure difference. A greater pressure gradient is needed to obtain the same flow rate seen under laminar conditions.

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38
Q

What is COPD?

A

A group of progressive obstructive lung diseases characterised by increase in airway resistance and decreased airflow
It includes; chronic bronchitis and emphysema

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39
Q

How is COPD treated?

A

A progressive disease and so there is no cure, only the symptoms can be controlled
-Bronchodilators; anticholinergics or B2 adrenoreceptor agonists
-Glucocorticosteroids

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40
Q

What is poiseuille’s law?

A

-Airway resistance is proportional to gas viscosity and the length of the tube is inversely proportional to the fourth power of the radius
-This means that small changes in the airway diameter have big impacts on the resistance and hence the flow rate

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41
Q

What is the difference in airway resistance in someone with COPD?

A

In a normal individual, airway resistance is 1.5cm H2O.s.litres-1
In an individual with COPD, airway resistance is 5.0cm H2O.s.litres-1

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42
Q

Describe the effect of inspiration on resistance

A

The lungs and chest wall expand and intrapleural pressure becomes more negative. Large pressure gradient in alveoli allowing air to rush into lungs. The airways expand during inspiration which decreases resistance

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43
Q

What is the effect of emphysema on the airways?

A

Airway compression is exaggerated. There is loss of elastic tissue and breakdown of alveolar walls. Tethering between the walls of adjoining airspaces is reduced. The airways are flimsy and doing forced expiration are less Abel to resist collapse.

44
Q

How can individuals with emphysema overcome the problem of airway collapse?

A

-Slow exhalation
-Breathing takes place at a higher lung volume
-Exhaling through pursed lips

45
Q

What is total ventilation?

A

The volume of air moved out of lungs per unit of time

46
Q

What is alveolar ventilation?

A

During each breath, not all air reaching the alveoli is ‘fresh’ air. The first portion of air entering the respiratory zone is ‘stale’ air that was in the conducting zone. Alveolar ventilation is the volume of ‘fresh’ air entering the respiratory zone. So alveolar ventilation is total ventilation- dead space ventilation

47
Q

Describe ventilation în the lung dependant on position

A

Ventilation is greater at the base compared to the apex, linked to starting volume of the alveoli. At the apex, larger starting volume means lower compliance, but at the base, a smaller starting volume leads to higher compliance

48
Q

Describe the process of recruitment

A

-Some vessels are collapsed, some are open but aren’t conducting blood and some are open and conducting blood.
-In the first stage of recruitment, previously collapsed vessels become patent but don’t conduct blood, previously open but non-conducting vessels now conduct blood and previously open and conducting vessels are distended.
-All vessels dilate and now conduct blood.

49
Q

What is PPA in relation to respiration?

A

Pressure in pulmonary arterioles, a mean of about 15mmHg

50
Q

What is PPV in relation to respiration?

A

Pressure in pulmonary venules, a mean of about 8mmHg

51
Q

What is the ventilation to perfusion ratio and why is it important?

A

-Ratio of the rate of alveolar ventilation and pulmonary blood flow
-Variations in ventilation and perfusion influence blood gas composition

52
Q

What happens if a tumour or foreign body is in the airways?

A

-Local reduction in ventilation
-Gas can’t be removed from the area, the composition therefore becomes the same as mixed venous blood. The ventilation:perfusion ration becomes 0.
-Air is redirected to other areas of the lungs

53
Q

Describe the contraction of airway smooth muscle

A

-Increase in intracellular calcium
-Calcium binds to calmodulin
-Activated calcium calmodulin complex will stimulate MLCK which then phosphorylates myosin light chain leading to muscle contraction.
-Smooth muscle remains contracted whilst myosin light chain is phosphorylated.

54
Q

Describe the Gq control of airway smooth muscle

A

-Receptor in membrane, agonist binds and GPCR activated
-Stimulation of phospholipase c breaks down PIP 2 into IP3 and diacyglycerol
-Short term; IP3 to IP3 receptors which leads to calcium release and muscle contraction, increasing resistance to airflow and more effort needed for breathing
-Longer term; diacyglycerol stimulates protein kinase C which has longer term effects on muscle cells, leading to remodelling of airway smooth muscle

55
Q

Describe the Gs control of airway smooth muscle

A

-Receptor activated
-Stimulation of adenylate cyclase leads to cAMP formation
-Activation of protein kinase a
-Stimulation of potassium channels, potassium influx, hyperpolarizing membrane
-Less likely for there to be a calcium influx
-Downstream inhibits MLCK and promotion of muscle relaxation.
-Longer term stimulates reduction of inflammation of airway smooth muscle.
-Decrease in resistance to airflow therefore easier to breathe.

56
Q

Describe the Gi control of airway smooth muscle

A

Activation of Gi receptors leads to inhibition of adenylate cyclase
-Knock on effects of this counteract the stimulatory effect of Gs activation
-Opposes the relaxation of smooth muscle
-Also inhibits the BK potassium channel and there is more likely to be membrane depolarization
-Receptors acting through Gi pathway; M2 muscarinic

57
Q

What happens to airways when M3 receptors are activated?

A

-Negative feedback mechanism
-ACh released at nerve terminal
-Some interacts with M2 receptors and their activation leads to inhibition of ACh release
-Prevents over contraction of airway smooth muscle

58
Q

What happens when B2 adrenoreceptors on airway smooth muscle are activated?

A

-B2 agonist (salbutamol) acts on B2 receptor to stimulate adenylate cyclase
-Production of cyclic AMP reduces inflammation
-Stimulates potassium channel, hyper polarising membrane and reducing calcium influx leading to relaxation.

59
Q

What is the link between M2 receptors and asthma?

A

-in case of antigen challenge, the change in M2 function was linked to eosinophils
-Eosinophils cluster around the nerve fibres
-Activated eosinophils release major basic protein (MBP)
-MBP inhibits M2 receptors

60
Q

How is asthma treated?

A

-Anticholinergics; block the effects of endogenous ACh. Short and long lasting.
-Competitive inhibitors of M1, 2 and 3 receptors.
-Dissociate more slowly from M3 receptors compared to M2
-Exert effects to help reverse bronchoconstriction, mucus secretion and airway remodelling
-Short lasting; ipratropium; used in combination with B2 receptor agonists as add on therapy

61
Q

What are the symptoms of cystic fibrosis?

A

-Clogging and infection of the airways
-Blockage of the small bile ducts and problems with liver function
-Blockage of the ducts of the pancreas which prevents secretion of digestive enzymes
-Obstructions in small intestine due to thick content
-Infertility in males due to absence of vas deferens
-Excess secretion of NaCl from sweat glands

62
Q

Describe the structure of CFTR

A

-cAMP activated Cl- channel
-cAMP activated protein kinase A which phosphorylates CFTR
-Channel has 12 transmembrane spanning domains
-R domain is regulatory domain where protein kinase A phosphorylates protein to open it

63
Q

What are class 1 CFTR mutations?

A

Impaired production of CFTR

64
Q

What are class 2 CFTR mutations?

A

Impaired trafficking, cell doesn’t reach the membrane

65
Q

What are class 3 CFTR mutations?

A

Impaired gaiting, protein goes to the membrane but has a reduced open probability

66
Q

What are class 4 CFTR mutations?

A

Decreased conductance, less Cl- ions

67
Q

What are class 5 CFTR mutations?

A

Decreased protein production, less than normal of the protein is made

68
Q

What are class 6 CFTR mutations?

A

Decreased membrane stability, protein is removed from the membrane too early

69
Q

What are class 7 CFTR mutations?

A

Impaired production, absence of full length mRNA

70
Q

Describe the lung pathology of patients with cystic fibrosis

A

-Viscous airway mucus. Mucus is the first line of defence but its thick and not easy to remove
-Recurrent bacterial infections
-Antibiotic resistance
-Inflammation
-Tissue degeneration
-Common cause of death because once lung tissue has degenerated, it cannot regenerate

71
Q

Describe upper airway Na+ and Cl- handling and how it’s different in cystic fibrosis patients

A

-Sodium potassium ATPase pumps 3 sodium ions out in exchange for 2 potassium ions, hydrolysing ATP
-Basolateral potassium channel create negative membrane potential
-Negative membrane potential and low intracellular sodium sets driving force for NKCC1
-Sodium brought in with 2 chloride and potassium
-Chloride accumulates in cell, when CFTR is opened, chloride is secreted
-ENaC absorbs sodium which is then lost across basolateral membrane
-With a high liquid layer, cilia can beat properly and clear the mucus, in CF the liquid layer is lower and so cilia cannot beat and mucus can’t be cleared

72
Q

Describe the advantage of having a CF mutation in cholera

A

-Cells secrete chloride and water which moves into lumen and mix with faeces.
-Enterotoxins from bacteria activate CFTR leading to diarrhoea
-Carriers only secreted 50% and so had less dehydration and were less likely to die

73
Q

What are the treatments of CF?

A

-Physiotherapy
-Bronchodilator drugs
-Abtibitoic sterioids
-Mucolytics
-All current treatments treat the symptoms and not the cause
-Gene therapy is challenging and has had poor success so far

74
Q

Why is it important to regulate pH?

A

-Small changes in pH cause large changes in the function of the body
-Proteins in the body are pH sensitive
-Most fluids within the body sit within pH 6.8-8
-Fluctuations have physiological effects:
-Excitability of muscles and nerves
-Enzyme activities
-K+ levels

75
Q

What are the pH’s of:
Gastric secretions, cerebrospinal fluid, pancreatic secretions and urine?

A

Gastric secretions; 0.7
Cerebrospinal fluid; 7.3
Pancreatic secretions; 8.1
Urine; 5.4

76
Q

What systems are involved in regulating pH of the body?

A

-Blood and tissue buffers
-Respiration
-Renal system

77
Q

Describe how carbonic acid/ bicarbonate buffer the extracellular fluid when CO2 is added or taken away

A

-Adding CO2 shifts the equilibrium to the right, so halogen ions will be made and pH will fall. HCO3- will increase
-Taking way CO2 will shift the equilibrium to the left, using halogen ions to make carbon dioxide and water leading to an increase in pH and low HCO3- concentration

78
Q

Where are peripheral chemoreceptors found and what is their main stimulus?

A

-Found in carotid and aortic bodies
-Their main stimulus id hypoxia (fall in pCO2)

79
Q

Describe the mechanisms of peripheral chemoreceptors

A

-BK potassium channels, under normal conditions they are open and drive the membrane potential towards the Nernst potential for potassium.
-When pO2 falls, pCO2 rises and pH falls, they’re open leading to depolarisation. This activates voltage gated sodium channels which open leading to action potential which opens calcium channels in the membrane. This leads to neurotransmitter release (ACh, dopamine, NA, 5-HT, substance P and ANP) and afferent nerve stimulation

80
Q

What is the role of the central chemoreceptors?

A

-High PCO2 levels lead to increase in ventilation

81
Q

What are the 3 mechanisms of the renal system?

A

-HCO3- handling
-Urine acidification
-Ammonia synthesis

82
Q

Describe the proximal cell model

A

-Sodium potassium ATPase and potassium channel on basolateral membrane set negative membrane potential, and low intracellular sodium conc.
-On the apical membrane, sodium influx in exchange for halogen ion by sodium halogen exchange protein.
-Halogen that is secreted combines with bicarbonate to form carbonic acid.
-Carbonic anhydrase splits into carbon dioxide and water which enters cell through aquaporin 1 water channels.
-Within cell form carbonic anhydrase which dissociates into halogen ion and bicarbonate.
-Bicarbonate reabsorbed across basolateral membrane via sodium bicarbonate transport protein.

83
Q

What is urine acidification?

A

-Alkaline salt to an acid salt
-Occurs at any point down the nephron
-Loss of halogen ions
-Halogen ion is then excreted in urine

84
Q

Describe the process of ammonia production in the renal system

A

-Ammonia produced by metabolism of glutamine to alpha kept-gluterate which releases ammonia, joint with halogen ion to make ammonium
-Ammonia is membrane permeable, ammonium is impermeable
-Glutamine leads to ammonia production
-Metabolic processes producing carbon dioxide, joins with water to dorm H2CO3 to HCO3-
-Ammonia then leaves cell, forms ammonium with halogen ion and then the pH of urine is still low.
-This is diffusion trapping because impermeable ammonium is formed so it cannot return.

85
Q

What is respiratory acidosis and what is the body’s response to it?

A

-Struggle to eliminate CO2 from body
-Seen in lung disease and emphysema
-Increase in CO2 impacts the buffer system, leading to more halogen ions and increase in bicarbonate
-Respiratory problem so therefore renal compensation
-Increased H+ secretion, increased reabsorption of bicarbonate and a rise in pH but a further HCO3- rise

86
Q

What is respiratory alkalosis and what is the body’s response?

A

-CO2 elimination increase
-Hyperventilation
-Renal compensation; decreased H+ secretion, decreased reabsorption of HCO3-
-Fall in pH but further HCO3- fall

87
Q

Describe metabolic acidosis and the body’s response

A

-Ingestion of acid or loss of alkaline fluid seen in diarrhoea, cholera or diabetic ketoacidosis
-Respiratory compensation;
-Increased respiratory rate
-Decreased arterial PCO2
-Increase in pH and drop in PCO2
-Renal correction
-Increased secretion of H+
-Increased reabsorption of HCO3-

88
Q

Describe metabolic alkalosis and the body’s response

A

-ingestion of alkaline fluid or loss of acid e.g. through persistent vomiting
-Respiratory compensation
-Fall in respiratory rate
-Increase in arterial PCO2
-pH fall and rise in PCO2

89
Q

What is the effects of the drug Ivacaftor on cystic fibrosis?

A

-The molecule is in the liquid layer on the apical surface of the cell.
-Exposing the cystic fibrosis cells to ivacaftor increases the height of the liquid layer.
-The potentiator changes the channel so it can open. It increases the open probability of the channel.

90
Q

What percentage increase in CFTR function can be sufficient to alleviate symptoms?

A

15%

91
Q

What is the effect of VX-770 on sweat chloride?

A

-Within 2 weeks sweat chloride is reduced to below 60mM which it the clinical threshold for CF

92
Q

What are intercalated disks made from?

A

-Mechanical links; desmosomes
-Electrical links; gap junctions

93
Q

Describe the process of cardiac contraction

A

-Influx of Ca2+ from ECF via L-type Ca2+ channels (Cav1.2)
-Activation of ryanodine receptor type 2 on SR (CICR)
-L type calcium channels linked to ryanodine receptors on sarcoplasmic reticulum
-Depolarisation as a result of action potential activated L type calcium channels which activate ryanodine receptors and lead to rise in intracellular calcium.
-Myofilament interactions increase the tension in muscles leading to contraction

94
Q

Describe the removal of calcium after cardiac contraction mediated by proteins

A
  1. Sarcoplasmic reticulum; SERCA2, primary active transport protein
  2. Plasma membrane PMCA and NCX1
  3. Mitochondrial membrane MiCa channels
95
Q

What influences the strength and velocity of cardiac contraction?

A

-Myocyte level depends on how much Ca2+ increases and the sensitivity of contractile proteins to calcium
-Muscle level depends on the preload EDV (how much blood in ventricles) and after load (arterial pressure)

96
Q

What is passive tension?

A

Tension generated in a muscle at a set sarcomere length. Proteins titin and design create passive tension

97
Q

How is the velocity of shortening calculated?

A

-Adjustable stop is used to change the length of the muscle
-The weight is equal to the after load
-Adjustable stop id removed and muscle contracts, the tension remains the same but the muscle shortens and the after load is lifted
-Speed of muscle shortening is the velocity of shortening, this is the isotonic phase of contraction

98
Q

What are the 3 cardiac cell types?

A

Nodal cells, conducting cells and myocytes

99
Q

Describe the spread of electrical activity through the heart

A

-Heart beat initiated at SAN
-Conduction to atria and AVN. Conduction from right to left through interatrial tract
-Moves to atrioventricular ring and into ventricles
-Passage through bundle of His
-Purkinje system distribution to ventricular muscle cells

100
Q

Where is the SAN and what are its conduction speeds?

A

-Posterior aspect of right atrium, at the junction of the superior vena and right atrium
-Conduction; 0.05m/s

101
Q

Where is the AV node and what is its conduction speed?

A

-Posterior aspect on right side of interatrial septum
-Slow conduction velocity (0.05m/s)
-Slowing down the spread of activity causes a short delay allowing atrial contraction to finish.
-AV refractoriness prevents excess ventricular contraction

102
Q

Describe control of the pacemaker cells

A

-Sympathetic system releases noradrenaline to increase the slope of the pre potential and therefore reach threshold faster and firing rate increases.
-Vagal fibres (ACh) hyperpolarises membrane potential and decreases the pre potential slope, increasing the time taken to reach threshold and reducing heart rate.
-Calcium clock oscillations; rhythmic alterations of SR Ca2+ release. This activates NCX (sodium calcium exchanger) 3 sodium in for one calcium out and therefore mediates depolarisation

103
Q

Describe the process of a cardiac muscle action potential

A

-Voltage gated sodium channels open
-Na+ inflow depolarises the membrane and triggers the opening of still more Na+ channels creating a positive feedback cycle and a rapidly rising membrane voltage
-Na+ channels close when the cell depolarises and the voltage peaks at nearly +30mV
-Ca2+ entering through slow calcium channels prolongs depolarisation of membrane creating plateau. Plateau falls slightly because of some K+ leakage but most K+ channels remain closed until the end of the plateau.
-Ca2+ channels close and Ca2+ is transported out of cell. K+ channels open and rapid K+ outflow returns membrane to its resting potential.

104
Q

How many people die in UK from sudden cardiac death per year?

A

70,000

105
Q

What is QT syndrome?

A

-Where the QT interval is either longer or shorter than normal
-Includes ventricular depolarisation and ventricular repolarization
-Short QT; repolarization is accelerated, T wave happens earlier and the duration is therefore shorter
-Long QT; repolarization is delayed or slowed. QT interval is therefore shorter

106
Q

Describe the ventricular action potential

A

-Voltage gated sodium channels mediate depolarisation
-Voltage gated calcium channels mediate plateau
-Voltage gated potassium channels mediate the repolarization phase

Physiology of cells and systems (2 decks)

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