Types of ion channels and their functions
Leak channels: Leak channels are passive ion channels. They are always open and ions pass through them continuously. The leak channels allow Na+ (sodium ions) and K+ (potassium ions) ions move across the cell membrane down their concentration gradient (from higher potential to lower potential). It does not require any ligand or ATP for functioning. This is known as passive transport.
ATP Pumps: Na+ and K+ ions also get transmitted across the cell membrane in the response of the action potential. This transport occurs via ATP mediated pump. The hydrolysis of ATP provides the desired energy required for the influx or the efflux of the ions across the cell membrane. Here single hydrolysis of ATP into ADP transports three Na+ ions out of the cell membrane and 2K+ ions inside the cell membrane, restoring the resting membrane potential. This is known as active transport.
Voltage gated ion channels are a class of transmembrane proteins that form pores through the cell membrane and providing a passage for ion transfer. They are activated in the response of change in the membrane potential. The change in potential alters the structure of the channels and help in the passage of ion and thus restoring the membrane potential.
Example: voltage gated Na+ ion channel
Ligand gated ion channels are integral membrane protein but they open in response to a chemical messenger or ligand (neurotransmitter). The ligand binds to the extracellular domain of the channel, causing structural changes and subsequent opening of the channel. They are also known as ionotropic receptor.
Examples: Acetycholine receptors and Serotonin receptors
Depolarization: Depolarization is caused by the inward flow of the passive Na+ ion channels. The inwatd flow of the Na+ ions inside the cell membrane changes the resting membrane potential (-70mV), making it positive.
Repolarization: As the Na+ions moves inward, the exterior of the cell membrane becomes negative. When it reaches a certain threshold, the ligand gated Na+/K+ ion channels opens. Restoring the membrane potential.
Hyperpolarization: As the efflux of the K+ ion channel outside the cell causes the interior of the cell to become more negative causing hyperpolarization.
At resting membrane potential, the ligand gated Na+ and K+ ion channel remain closed
The opening of the voltage gated K+ ion channel is promoted by the depolarization of the membrane. Voltage gated K+ion channels open causing increase permeability of the of K+ ions inside the cytosol. The causes repolarization of the membrane into the resting membrane potential. Unlike Na+ channels, the majority of the K+ channels remain open as long as the membrane id being depolarized and close only when the the membrane potential has been restored (inside negative). As they the voltage gated K+ ion channels open for after a fraction mili-second of depolarization they are also termed as delayed K+ channels. The only open channel during the resting membrane potential is the non-voltage gated K+ ion channels that generates the inside negative potential.
Regulation of hormones such as thyroid hormones and TRH
Ligand gated ion channels, Cell membrane
ATPase takes up the place
The primary function is to keep the channel deactivated while in resting potential
In case of losing the structure, the channel remains active irrespective of polarization, resting or hyperpolarization.
1: Resting membrane potential
2: Thershold of excitation
- Peak of action potential
- Hyperpolarization
- Membrane is slowly attaining towards the resting potential
2: Threshold of polarization or threshold or excitation. At this point, the Na+ ion channels open and Na+ ions moves inside the cell
3: Peak action potential
4: Hyperpolarization
In between the 3 and 4, the neuronal impulses is being transmitted. The Na+ ions becomes refractory and no more Na+ ions enters the cell. The K+ channels gradually close and Na+ channels reset (attaining the resting membrane potential). The opening of the K+ and Cl- channels causes hyperpolarization of the membrane potential. The K+ ions flows outward the membrane and Cl- flows inwards, causing the membrane potential to become more negative.
K+ channels opens, leading to the efflux of K+ ions outside the cell and Na+ ion channels become refractory and no more Na+ ions enter the cells.
Elevated levels of T3 and T4 are responsible for hyperthyroidism. T3 and T4 are thyroid hormones are increased levels of T3 and T4 cause thyrotoxicosis. Since the thyroid control the metabolism, the increased level of T3 and T4 is making Helen loose excessive weight. The thyroid hormone also controls the body’s temperature balance and hence increased level of T3 and T4 is making Helen feel over heated.
True
Blank 1: Inactive or in a protein-bound manner
Blank 2: target site
Blank3: Yes
|
Normal mechanism (Negative feedback mechanism0 Neurons in the hypothalamus secrete thyroid releasing hormone or thyrotropin releasing hormone (TRH). This hormone stimulates the anterior portion of the pituitary gland to secrete thyroid-stimulating hormone (TSH). TSH once activated, binds to receptors on epithelial cells present in the thyroid gland, promoting the secretion of the thyroid hormones. When concentrations of thyroid hormones in the blood increase beyond the threshold, it generates a negative feedback and the TRH-secreting neurons in the hypothalamus are down regulated. Inhibition of TRH secretion inhibits the secretion of the TSH. |
In case of Helen, the TSH binding to its receptors is not getting affected via the decrease in the TRH and hence leading to the elevated levels of T3 and T4. Moreover, TSH might have bonded with faulty receptors, leading to zero effect with negative feedback mechanism.
Suggested treatment chart (no questions)
Blank1: increased
Blank2: hypothyroidism
Blank1: decrease in comparison to before surgery but will gradually increase
Blank2: lack of negative feedback mechanism
Blank3: autoimmune disease
Helen might be suffering from autoimmune disease, as the removal of the thyroid gland does not lower the level of T4 and T3 secretion.
Cardiac Output (CO): Heart Rate (HR) x Stroke Volume (SV)
Blank1: decrease; Blank 2: Decrease
Blank1: Increase; Blank2: Increase
The two most critical physiological parameter affecting Moes blood pressure are
- Peripheral resistance
- Cardiac output
Drinking coffee causes vasoconstriction. Vasoconstriction or the contraction of the smooth muscles prevents the normal flow of the heart. Prevention of the normal blood flow caused increase in the cardiac output. The heart needs to pump more blood and leading to the increase in blood pressure, the principal cause behind hypertension.
Physiological conditions affecting blood pressure, lung function, and nerve signals
Physiological condition for increase peripheral resistance:
- Low blood vessel diameter
- High blood viscosity
Reason: defects in vasopressin or angiotensin
Physiological condition for low peripheral resistance:
- Vasodilation or relaxation of the smooth muscle)
- Less blood viscosity
Reason: defects in vasopressin or angiotensin
MAP before medication: 124.66
MAP after 1 month: 103
MAP after 3 months: 93
(Source: Created by Author)
Smokers cough is a persistent cough that occurs in long term smokers. Block in the cilia means less flow of oxygen and hence less aeration.
Emphysema is a long-term, progressive disease of the lungs. It causes destruction of lung tissue around smaller airways or bronchioles.
Destruction in the lung tissue caused obstruction in the proper passage of the oxygen and cardon dioxide, causing labored breathing.
The partial pressure of oxygen inside the lungs affects the rate of diffusion of gases inside the lungs.
Blank1: reduce; Blank2: increase
Taking dead space (DS) as 150 (normal value) [since not provided in the question]
The Alveloar ventilation (AV)is [AV= (TV-DS)RR]
March: 4550
April: 4020
May: 3900
June: 3480
July: 3025
(Source: Created by Author)
Axon hillock is the site of generation of the action potential in neurons. Once generated, it is propagated as a wave along the axon body and is passed on to the next axon at the axon terminal. In order to ensure swift and efficient signals transduction, the axon body is covered with neuronal sheet. The Myelin sheet prevents ions carrying the electrical signals from entering or leaving the axon along. The gap in the myelin sheet is known as node of Ranvire. It is where the ion channels are present (Barbero, Merletti & Rainoldi, 2012) (De Mello, 2013)
In case of multiple sclerosis, there occurs demylination and hence loss of the ions travelling through the axon (Lassmann, Van Horssen & Mahad, 2012) (Srivastava et al. 2012). It is due to the inappropriate propagation of the nerve impulses that Edna is experiencing numbness in her torso and tingling sensation at the finger tips.
Neurons in the hypothalamus secrete thyroid releasing hormone or thyrotropin releasing hormone (TRH). This hormone stimulates the anterior portion of the pituitary gland to secrete thyroid-stimulating hormone (TSH). TSH once activated, binds to receptors on epithelial cells present in the thyroid gland, promoting the secretion of the thyroid hormones. When concentrations of thyroid hormones in the blood increase beyond the threshold, it generates a negative feedback and the TRH-secreting neurons in the hypothalamus are down regulated. Inhibition of TRH secretion inhibits the secretion of the TSH. (Flier, Kalsbeek & Boelen, 2014) (Brent, 2012).
Common cause of hypothyroidism is Hasimoto’s disease. It is an autoimmune disease. Auto antibodies are formed to thymoglobulin and thyroid peroxides. Both of them are responsible for the uptake of the iodine. Binding of autoantibodies to these proteins interferes with the iodine uptake and leads to the decreased production of the thyroid hormones (Sugiyama et al., 2015) (Owen, Punt & Stranford, 2013).
Common cause of hyperthyroidism is Grave’s disease. It is an autoimmune disease. Binding of the autoantibody to the receptor of the thyroid stimulating hormone induces unregulated activation of the thyroid, leading to over production of the thyroid hormone (Annerbo, Stålberg & Hellman, 2012) (Owen, Punt & Stranford, 2013).
References:
Annerbo, M., Stålberg, P., & Hellman, P. (2012). Management of Grave’s disease is improved by total thyroidectomy. World journal of surgery, 36(8), 1943-1946.
Barbero, M., Merletti, R., & Rainoldi, A. (2012). Generation, propagation, and extinction of single-fiber and motor unit action potentials. In Atlas of Muscle Innervation Zones (pp. 21-38). Springer Milan.
Brent, G. A. (2012). Mechanisms of thyroid hormone action. The Journal of clinical investigation, 122(9), 3035.
De Mello, W. C. (Ed.). (2013). Electrical phenomena in the heart. Academic Press.
Fliers, E., Kalsbeek, A., & Boelen, A. (2014). MECHANISMS IN ENDOCRINOLOGY: Beyond the fixed setpoint of the hypothalamus–pituitary–thyroid axis. European journal of endocrinology, 171(5), R197-R208.
Lassmann, H., Van Horssen, J., & Mahad, D. (2012). Progressive multiple sclerosis: pathology and pathogenesis. Nature Reviews Neurology, 8(11), 647-656.
Owen, J. A., Punt, J., & Stranford, S. A. (2013). Kuby immunology (pp. 427-444). New York: WH Freeman.
Srivastava, R., Aslam, M., Kalluri, S. R., Schirmer, L., Buck, D., Tackenberg, B., … & Bennett, J. L. (2012). Potassium channel KIR4. 1 as an immune target in multiple sclerosis. New England Journal of Medicine, 367(2), 115-123.
Sugiyama, A., Nishie, H., Takeuchi, S., Yoshinari, M., & Furue, M. (2015). Hashimoto’s disease is a frequent comorbidity and an exacerbating factor of chronic spontaneous urticaria. Allergologia et immunopathologia, 43(3), 249-253.
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