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In: Anatomy and Physiology

2. What Physiological mechanisms by which plasma levels of the following are controlled: a. plasma pH...

2. What Physiological mechanisms by which plasma levels of the following are controlled: a. plasma pH levels b. plasma tonicity c. plasma glucose levels.

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Expert Solution

Plasma plasma pH levels.

Homeostatic homeostatic control of Plasma pH level ranges from 7.38 to 7.42 is an essential requirement for life. This is achieved through three line of Defence,

Physicochemical buffering

Rapid respiratory changes in pco2

Slow renal changes in in H+ excretion and hco3 - reabsorption and production.

Disturbances in acid is balance are described according to the cause of a primary change in either pco2 (respiratory acidosis and respiratory alkalosis) for Plasma hco3 - concentration(metabolic acidosis and metabolic alkalosis). Buffering and respiratory changes minimises change in pH. Full compensation is affected to renal changes in reabsorption of filtered hco3 - and secretion of h +, leading to generation of hco3 - to replete buffer Store. Factors influencing hco3 - reabsorption(primarily proximal tubule) Include amount filtered, extracellular fluid volume and arterial pco2. Generation of hco3 - along the nephron is influenced by availability and PK of urinary buffer ( fora example acid phosphate and creatinine), renal tubular fluid PH and formation of ammonium salt( for example Ammonium Sulphate). Clinical conditions in which metabolic and respiratory changes in acid base status occur are considered as are the compensatory mechanism which limit changes in pH. Full correction of these disturbances requires removal of the primary disturbance.

Plasma plasma tonicity.

Toni city which is potentially confused with osmolality, denotes the concentration of osmoles.--also known as effective osmoles--that do not freely cross cell membrane. With the exception of specialised epithelia in the distal nephron the concentration inside and outside body cells must be the same since their cell membranes are freely permeable to water due to constitutive presence of aquaporin. Therefore the accumulation of effective osmoles in either intra or extracellular compartment provides a driving force for water movement into the compartment of Greater tonicity to equalise concentration. Hypotonic plasma causes movement of water intracellularly leading to cellular swelling. Conversely hypertonic plasma bigets cellular shrinkage. Sodium and glucose as obligate extracellular solute are thus effective osmoles and and contribute to both osmolality and tonicity, whereas membrane permeable urea contributes to osmolality without affecting tonicity. Plasma tonicity cannot be measured directly but is calculated by subtracting the contribution of Urea to the measured plasma osmolality.

Pituitary regulation of tonicity.

Plasma toniciy is tightly regulated by antidiuretic hormone also known as argenine vesopressin. Hypotonic extracellular environment induce shrinkage of hypothalamic osmoreceptors. The subsequent opening of stretch in activated channels triggers membrane depolarization, intracellular signalling and release of vasopressin from the posterior pituitary gland into the systemic circulation. Vasopressin then acts on the collecting duct of the nephron to increase water reabsorption and decrease serum tonicity. All the plasma hypertonicity serves as a primary stimulus for vasopressin release, hypovolemia also can promote vasopressin secretion. Though mild changes in blood pressure do not affect vasopressin release, modest decreases in perfusion sensed by baroreceptors stimulate pituitary vasopressin release at the expense of potentially lowering serum tonicity. Teleological E1 good argue that retaining water to Foster volume expansion and thus reserve perfusion in the hypovolemic state was evolutionary advantages.

Renal regulation of tonicity

Vasopressin binds to vasopressin V2 receptors on the lateral surface of principal cells of the collecting duct of the distal nephron. In the absence of vasopressin in permeability of the collecting duct to water gives rise to dilute urine, water remains behind in the Tubular lumen is solute is reabsorbed. V2 receptor activation stimulate translocation to the fusion of aquaporin 2 containing vesicles with the apicall membrane of the principal cell, alarming water to flow into the cell, from which it exits into the hypertonic medullary interstitium through constitutively active lateral aquaporin channel. Reabsorption of water in this manner leads to concentrated urine and lowers serum osmolality. Urine osmolality is Hence a surrogate measure of vasopressin activity, high and low urine osmolality equals to high and low vasopressin levels respectively. In the healthy state vasopressin levels are undetectable when plasma tonicity is low and rise in a linear fashion is tonicity increases above normal. The normal human kidney can produce urine with osmolality ranging from 50 to 1200 m O s m per kg H2O. However in advanced Kidney Disease this range narrow significantly. Concentrating ability is markedly impaired and a more modest diluting defect occur as well.

Plasma plasma Glucose level

Glucose glucose is the main source of fuel for the cells in the body but it's too big to simply diffuse into the cells by itself. It needs to be transported into the cells. Insulin is a hormone produced by a pancreas that facilitate glucose transport into the cell. Bus but facilitating glucose transport into cells from the bloodstream, insulin lowers blood glucose level. It also in habit glucose production from amino acids and fatty acids and glycogen which is carbohydrate composed of many glucose subunit. Insulin is actually stimulate glycogen formation from glucose. These functions of insulin helps to lower glucose levels in the blood. Glucagon is a hormone produced by the pancreas that raises blood glucose levels by stimulating The breakdown of glycogen into glucose, stimulating glucose production from amino acids and fatty acids and stimulating release of glucose from the liver. Glucagon and insulin antagonistic effects, with glucagon promoting glucose production and release into the bloodstream and insulin promoting the transport of glucose into cells from the blood stream and inhibiting glucose production. Glucose levels in the blood are usually measured in terms of milligrams per deciliter, with a normal range of 70 to 110 mg per dl. Generally speaking if glucose levels stray out of these range, the amount of insulin and glucagon produced by the pancreas will be adjusted to bring glucose levels back into this range. It should be noted hear that insulin and glucagon signalling are not all or nothing response in normal individual. When the system is functioning properly there is always some insulin and glucagon being produced by the pancreas that is trying to find a balance between glucose release into the blood and glucose uptake in two cells.


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