Saturday, 7 January 2017

PHYSIOLOGY OF MUSCLES


Physiology of muscles
The nervous system 'communicates' with muscle via neuromuscular (also called myoneural) junctions. These junctions (Figure 1) work very much like a synapse between neurons (neuromuscular junction video). In other words:
  • the impulse arrives at the end bulb,
  • chemical transmitter is released from vesicles (each of which contains 5,000 - 10,000 molecules of acetylcholine) and diffuses across the neuromuscular cleft,
  • the transmitter molecules fill receptor sites in the membrane of the muscle & increase membrane permeability to sodium,
  • sodium then diffuses in & the membrane potential becomes less negative,
  • and, if the threshold potential is reached, an action potential occurs, an impulse travels along the muscle cell membrane, and the muscle contracts.

Some muscles (skeletal muscles) will not contract unless stimulated by neurons; other muscles (smooth & cardiac) will contract without nervous stimulation but their contraction can be influenced by the nervous system. Thus, the nervous and muscle systems are closely interconnected. Let's now focus on muscle - what is its structure & how does it work.

Highly magnified view of a neuromuscular junction (Hirsch 2007).  
Characteristics of muscle:
  • excitability - responds to stimuli (e.g., nervous impulses)
  • contractility - able to shorten in length
  • extensibility - stretches when pulled
  • elasticity - tends to return to original shape & length after contraction or extension

Functions of muscle:
  • motion
  • maintenance of posture
  • heat production

Types of muscle:
  • skeletal:
    • attached to bones & moves skeleton
    • also called striated muscle (because of its appearance under the microscope, as shown in the photo to the left)
    • voluntary muscle
  • smooth (photo on the right)
    • involuntary muscle
    • muscle of the viscera (e.g., in walls of blood vessels, intestine, & other 'hollow' structures and organs in the body)
  • cardiac:
    • muscle of the heart
    • involuntary
 


Skeletal muscle structure
Skeletal muscles are usually attached to bone by tendons composed of connective tissue. This connective tissue also ensheaths the entire muscle & is called epimysium. Skeletal muscles consist of numerous subunits or bundles called fasicles (or fascicles). Fascicles are also surrounded by connective tissue (called the perimysium) and each fascicle is composed of numerous muscle fibers (or muscle cells). Muscle cells, ensheathed by endomysium, consist of many fibrils (or myofibrils), and these myofibrils are made up of long protein molecules called myofilaments. There are two types of myofilaments in myofibrils: thick myofilaments and thin myofilaments.

Source: Wikipedia


Skeletal muscles vary considerably in size, shape, and arrangement of fibers. They range from extremely tiny strands such as the stapedium muscle of the middle ear to large masses such as the muscles of the thigh. Skeletal muscles may be made up of hundreds, or even thousands, of muscle fibers bundled together and wrapped in a connective tissue covering. Each muscle is surrounded by a connective tissue sheath called the epimysium. Fascia, connective tissue outside the epimysium, surrounds and separates the muscles. Portions of the epimysium project inward to divide the muscle into compartments. Each compartment contains a bundle of muscle fibers. Each bundle of muscle fiber is called a fasciculus and is surrounded by a layer of connective tissue called the perimysium. Within the fasciculus, each individual muscle cell, called a muscle fiber, is surrounded by connective tissue called the endomysium. Skeletal muscles have an abundant supply of blood vessels and nerves. Before a skeletal muscle fiber can contract, it has to receive an impulse from a neuron. Generally, an artery and at least one vein accompany each nerve that penetrates the epimysium of a skeletal muscle. Branches of the nerve and blood vessels follow the connective tissue components of the muscle of a nerve cell and with one or more minute blood vessels called capillaries (Source: training.seer.cancer.gov).

The cell membrane of a muscle cell is called the sarcolemma, and this membrane, like that of neurons, maintains a membrane potential. So, impulses travel along muscle cell membranes just as they do along nerve cell membranes. However, the 'function' of impulses in muscle cells is to bring about contraction. To understand how a muscle contracts, you need to know a bit about the structure of muscle cells.
Skeletal muscle is the muscle attached to the skeleton. Hundreds or thousands of muscle fibers (cells) bundle together to make up an individual skeletal muscle. Muscle cells are long, cylindrical structures that are bound by a plasma membrane (the sarcolemma) and an overlying basal lamina and when grouped into bundles (fascicles) they make up muscle. The sarcolemma forms a physical barrier against the external environment and also mediates signals between the exterior and the muscle cell.
The sarcoplasm is the specialized cytoplasm of a muscle cell that contains the usual subcellular elements along with the Golgi apparatus, abundant myofibrils, a modified endoplasmic reticulum known as the sarcoplasmic reticulum (SR), myoglobin and mitochondria. Transverse (T)-tubules invaginate the sarcolemma, allowing impulses to penetrate the cell and activate the SR. As shown in the figure, the SR forms a network around the myofibrils, storing and providing the Ca2+ that is required for muscle contraction.
Myofibrils are contractile units that consist of an ordered arrangement of longitudinal myofilaments. Myofilaments can be either thick filaments (comprised of myosin) or thin filaments (comprised primarily of actin). The characteristic 'striations' of skeletal and cardiac muscle are readily observable by light microscopy as alternating light and dark bands on longitudinal sections. The light band, (known as the I-band) is made up of thin filaments, whereas the dark band (known as the A-band) is made up of thick filaments. The Z-line (also known as the Z-disk or Z-band) defines the lateral boundary of each sarcomeric unit. Contraction of the sarcomere occurs when the Z-lines move closer together, making the myofibrils contract, and therefore the whole muscle cell and then the entire muscle contracts (Source: Davies and Nowak 2006).
The SARCOLEMMA has a unique feature: it has holes in it. These "holes" lead into tubes called TRANSVERSE TUBULES (or T-TUBULES for short). These tubules pass down into the muscle cell and go around the MYOFIBRILS. However, these tubules DO NOT open into the interior of the muscle cell; they pass completely through and open somewhere else on the sarcolemma (i.e., these tubules are not used to get things into and out of the muscle cell). The function of T-TUBULES is to conduct impulses from the surface of the cell (SARCOLEMMA) down into the cell and, specifically, to another structure in the cell called the SARCOPLASMIC RETICULUM.

A muscle fiber is excited via a motor nerve that generates an action potential that spreads along the surface membrane (sarcolemma) and the transverse tubular system into the deeper parts of the muscle fiber. A receptor protein (DHP) senses the membrane depolarization, alters its conformation, and activates the ryanodine receptor (RyR) that releases Ca2+ from the SR. Ca2+ then bind to troponin and activates the contraction process (Jurkat-Rott and Lehmann-Horn 2005).

Sarcoplasmic reticulum (SR) membranes in close proximity to a T-tubule. 'RyR' are proteins the aid in the release of calcium from the SR, 'SERCA2' are proteins that aid in the transport of calcium into the SR (Brette and Orchard 2007). The SARCOPLASMIC RETICULUM (SR) is a bit like the endoplasmic reticulum of other cells, e.g., it's hollow. But the primary function of the SARCOPLASMIC RETICULUM is to STORE CALCIUM IONS. Sarcoplasmic reticulum is very abundant in skeletal muscle cells and is closely associated with the MYOFIBRILS (and, therefore, the MYOFILAMENTS). The membrane of the SR is well-equipped to handle calcium: there are "pumps" (active transport) for calcium so that calcium is constantly being "pumped" into the SR from the cytoplasm of the muscle cell (called the SARCOPLASM). As a result, in a relaxed muscle, there is a very high concentration of calcium in the SR and a very low concentration in the sarcoplasm (and, therefore, among the myofibrils & myofilaments). In addition, the membrane has special openings, or "gates", for calcium. In a relaxed muscle, these gates are closed and calcium cannot pass through the membrane. So, the calcium remains in the SR. However, if an impulse travels along the membrane of the SR, the calcium "gates" open &, therefore, calcium diffuses rapidly out of the SR & into the sarcoplasm where the myofibrils & myofilaments are located. This, as you will see, is a key step in muscle contraction. Myofibrils are composed of 2 types of myofilaments: thick and thin. In skeletal muscle, these myofilaments are arranged in a very regular, precise pattern: thick myofilaments are typically surrounded by 6 thin myofilaments (end view). In a side view, thin myofilaments can be seen above and below each thick myofilament.

Myofibril cross-section showing arrangement of thick and thin myofilaments.
Bar = 100 nm. Image from Widrick et al. (2001)

Source: Tskhovrebova and Trinick (2003).

Muscle structure
Each myofibril is composed of many subunits lined up end-to-end. These subunits are, of course, composed of myofilaments and are called SARCOMERES. The drawings above & below show just a very small section of the entire length of a myofibril and so you can only see one complete SARCOMERE.
In each sarcomere, thin myofilaments extend in from each end. Thick myofilaments are found in the middle of the sarcomere and do not extend to the ends. Because of this arrangement, when skeletal muscle is viewed with a microscope, the ends of a sarcomere (where only thin myofilaments are found) appear lighter than the central section (which is dark because of the presence of the thick myofilaments). Thus, a myofibril has alternating light and dark areas because each consists of many sarcomeres lined up end-to-end. This is why skeletal muscle is called STRIATED MUSCLE (i.e., the alternating light and dark areas look like stripes or striations). The light areas are called the I-BANDS and the darker areas the A-BANDS. Near the center of each I-BAND is a thin dark line called the Z-LINE (or Z-membrane in the drawing below). The Z-LINE is where adjacent sarcomeres come together and the thin myofilaments of adjacent sarcomeres overlap slightly. Thus, a sarcomere can be defined as the area between Z-lines.

Used by permission of John W. Kimball
Thick myofilaments are composed of a protein called MYOSIN. Each MYOSIN molecule has a tail which forms the core of the thick myofilament plus a head that projects out from the core of the filament. These MYOSIN heads are also commonly referred to as CROSS-BRIDGES.
The MYOSIN HEAD has several important characteristics:
  • it has ATP-binding sites into which fit molecules of ATP. ATP represents potential energy.
  • it has ACTIN-binding sites into which fit molecules of ACTIN. Actin is part of the thin myofilament and will be discussed in more detail shortly.
  • it has a "hinge"at the point where it leaves the core of the thick myofilament. This allows the head to swivel back and forth, and the "swivelling" is, as will be described shortly, what actually causes muscle contraction.
Thin myofilaments are composed of 3 types of protein: ACTIN, TROPONIN, and TROPOMYOSIN.
The actin molecules (or G-actin as above) are spherical and form long chains. Each thin myofilament contains two such chains that coil around each other. TROPOMYOSIN molecules are lone, thin molecules that wrap around the chain of ACTIN. At the end of each tropomyosin is an TROPONIN molecule. The TROPOMYOSIN and TROPONIN molecules are connected to each other. Each of these 3 proteins plays a key role in muscle contraction:
 
  • ACTIN - when actin combines with MYOSIN HEAD the ATP associated with the head breaks down into ADP. This reaction released energy that causes the MYOSIN HEAD to SWIVEL.
  • TROPOMYOSIN - In a relaxed muscle, the MYOSIN HEADS of the thick myofilament lie against TROPOMYOSIN molecules of the thin myofilament. As long as the MYOSIN HEADS remain in contact with TROPOMYOSIN nothing happens (i.e., a muscle remains relaxed).
  • TROPONIN - Troponin molecules have binding sites for calcium ions. When a calcium ion fills this site it causes a change in the shape and position of TROPONIN. And, when TROPONIN shifts, it pulls the TROPOMYOSIN to which it is attached. When TROPOMYOSIN is moved, the MYOSIN HEAD that was touching the tropomyosin now comes in contact with an underlying ACTIN molecule.
 
Sliding filaments



Muscle contraction
1 - Because skeletal muscle is voluntary muscle, contraction requires a nervous impulse. So, step 1 in contraction is when the impulse is transferred from a neuron to the SARCOLEMMA of a muscle cell.
2 - The impulse travels along the SARCOLEMMA and down the T-TUBULES. From the T-TUBULES, the impulse passes to the SARCOPLASMIC RETICULUM.
3 - As the impulse travels along the Sarcoplasmic Reticulum (SR), the calcium gates in the membrane of the SR open. As a result, CALCIUM diffuses out of the SR and among the myofilaments.
4 - Calcium fills the binding sites in the TROPONIN molecules. As noted previously, this alters the shape and position of the TROPONIN which in turn causes movement of the attached TROPOMYOSIN molecule.
5 - Movement of TROPOMYOSIN permits the MYOSIN HEAD to contact ACTIN (Animations: Myofilament Contraction & Breakdown of ATP and cross-bridge movement).
6 - Contact with ACTIN causes the MYOSIN HEAD to swivel.
7 - During the swivel, the MYOSIN HEAD is firmly attached to ACTIN. So, when the HEAD swivels it pulls the ACTIN (and, therefore, the entire thin myofilament) forward. (Obviously, one MYOSIN HEAD cannot pull the entire thin myofilament. Many MYOSIN HEADS are swivelling simultaneously, or nearly so, and their collective efforts are enough to pull the entire thin myofilament).
 
 

8 - At the end of the swivel, ATP fits into the binding site on the cross-bridge & this breaks the bond between the cross-bridge (myosin) and actin. The MYOSIN HEAD then swivels back. As it swivels back, the ATP breaks down to ADP & P and the cross-bridge again binds to an actin molecule.
9 -  As a result, the HEAD is once again bound firmly to ACTIN. However, because the HEAD was not attached to actin when it swivelled back, the HEAD will bind to a different ACTIN molecule (i.e., one further back on the thin myofilament). Once the HEAD is attached to ACTIN, the cross-bridge again swivels, SO STEP 7 IS REPEATED.
As long as calcium is present (attached to TROPONIN), steps 7 through 9 will continue. And, as they do, the thin myofilament is being "pulled" by the MYOSIN HEADS of the thick myofilament. Thus, the THICK & THIN myofilaments are actually sliding past each other. As this occurs, the distance between the Z-lines of the sarcomere decreases. As sarcomeres get shorter, the myofibril, of course, gets shorter. And, obviously, the muscle fibers (and entire muscle) get shorter.
Skeletal muscle relaxes when the nervous impulse stops. No impulse means that the membrane of the SARCOPLASMIC RETICULUM is no longer permeable to calcium (i.e., no impulse means that the CALCIUM GATES close). So, calcium no longer diffuses out. The CALCIUM PUMP in the membrane will now transport the calcium back into the SR. As this occurs, calcium ions leave the binding sites on the TOPONIN MOLECULES. Without calcium, TROPONIN returns to its original shape and position as does the attached TROPOMYOSIN. This means that TROPOMYOSIN is now back in position, in contact with the MYOSIN HEAD. So, the MYOSIN head is no longer in contact with ACTIN and, therefore, the muscle stops contracting (i.e., relaxes).

Contraction
So, under most circumstances, calcium is the "switch" that turns muscle "on and off" (contracting and relaxing). When a muscle is used for an extended period, ATP supplies can diminish. As ATP concentration in a muscle declines, the MYOSIN HEADS remain bound to actin and can no longer swivel. This decline in ATP levels in a muscle causes MUSCLE FATIGUE. Even though calcium is still present (and a nervous impulse is being transmitted to the muscle), contraction (or at least a strong contraction) is not possible.
Animations illustrating muscle contraction: Muscle cell contraction Skeletal muscle contraction Mechanism of filament sliding during contraction of a myofibril (Wiley) Action potentials and muscle contraction
1 - Calcium released from sarcoplasmic reticulum
2  - Myosin head energized via myosin-ATPase activity which converts the bound ATP to ADP + Pi
3 - Calcium binds to troponin
4 - Tropomyosin translocates to uncover the cross-bridge binding sites
5 - The energized myosin binding sites approach the binding sites
6 - The first myosin head binds to actin
7 - The bound myosin head releases ADP + Pi, flips and the muscle shortens
8 - The second myosin head binds to actin
9 - The first myosin head binds ATP to allow the actin and myosin to unbind
10 - The second myosin head releases its ADP + Pi, flips& the muscle shortens further
11 - The second myosin head binds to ATP to allow the actin and myosin to unbind
12 - The second myosin head unbinds from the actin, flips back and is ready for the next cycle
13 - The cross-bridge cycle is terminated by the loss of calcium from the troponin
14 - Tropomyosin translocates to cover the cross-bridge binding sites
15 - The calcium returns to the sarcoplasmic reticulum, the muscle relaxes & returns to the resting state
Types of contractions:
    1 - isotonic - tension or force generated by the muscle is greater than the load & the muscle shortens
    2 - isometric - load is greater than the tension or force generated by the muscle & the muscle does not shorten
Twitch - the response of a skeletal muscle to a single stimulation (or action potential):
  • latent period - no change in length; time during which impulse is traveling along sarcolemma & down t-tubules to sarcoplasmic reticulum, calcium is being released, and so on (in other words, muscle cannot contract instantaneously!)
  • contraction period -  tension increases (cross-bridges are swivelling)
  • relaxation period - muscle relaxes (tension decreases) & tends to return to its original length
    An important characteristic of skeletal muscle is its ability to contract to varying degrees. A muscle, like the biceps, contracts with varying degrees of force depending on the circumstance (this is also referred to as a graded response). Muscles do this by a process called summation, specifically by motor unit summation and wave summation.
    Motor Unit Summation - the degree of contraction of a skeletal muscle is influenced by the number of motor units being stimulated (with a motor unit being a motor neuron plus all of the muscle fibers it innervates; see diagram below). Skeletal muscles consist of numerous motor units and, therefore, stimulating more motor units creates a stronger contraction.
    Wave Summation - an increase in the frequency with which a muscle is stimulated increases the strength of contraction. This is illustrated in (b). With rapid stimulation (so rapid that a muscle does not completely relax between successive stimulations), a muscle fiber is re-stimulated while there is still some contractile activity. As a result, there is a 'summation' of the contractile force. In addition, with rapid stimulation there isn't enough time between successive stimulations to remove all the calcium from the sarcoplasm. So, with several stimulations in rapid succession, calcium levels in the sarcoplasm increase. More calcium means more active cross-bridges and, therefore, a stronger contraction. (Wiley animation)
    If a muscle fiber is stimulated so rapidly that it does not relax at all between stimuli, a smooth, sustained contraction called tetanus occurs (illustrated by the straight line in c above & in the diagram below).
     
     


    Used by permission of John W. Kimball
    SMOOTH MUSCLE:
    • involuntary muscle; innervated by the Autonomic Nervous System (visceral efferent fibers)
    • found primarily in the walls of hollow organs & tubes
    • spindle-shaped cells typically arranged in sheets
    • cells do not have t-tubules & have very little sarcoplasmic reticulum
    • cells do not contain sarcomeres (so are not striated) but are made up of thick & thin myofilaments. Thin filaments in smooth muscle do not contain troponin.
    • calcium does not bind to troponin but, rather, to a protein called calmodulin. The calcium-calmodulin complex 'activates' myosin which then binds to actin & contraction (swivelling of cross-bridges) begins.

    Two types of smooth muscle:
               1 - visceral, or unitary, smooth muscle
      • found in the walls of hollow organs (e.g., small blood vessels, digestive tract, urinary system, & reproductive system)
      • multiple fibers contract as a unit (because impulses travel easily across gap junctions from cell to cell) &, in some cases, are self-excitable (generate spontaneous action potentials & contractions)
      2 - multiunit smooth muscle
       
      • consists of motor units that are activated by nervous stimulation
      • found in the walls of large blood vessels, in the eye (adusting the shape of the lens to permit accommodation & the size of the pupil to adjust the amount of light entering the eye), & at the base of hair follicle (the 'goose bump' muscles)
      Useful links: Actin Myosin animation Introduction to Muscle Physiology and Design McGraw-Hill: Musculoskeletal system
      Literature cited:
      Brette, F., and C. Orchard. 2007. Resurgence of cardiac T-tubule research. Physiology 22: 167-173.
      Davies, K. E., and K. J. Nowak. 2006. Molecular mechanisms of muscular dystrophies: old and new players. Nature Reviews Molecular Cell Biology 7: 762-773.
      Hirsch, N. P. 2007. Neuromuscular junction in health and disease. British Journal of Anaesthesia 99: 132-138.
      Hopkins, P. M. 2005. Foundations of anethesia, second ed. Mosby, London.
      Jurkat-Rott, K., and F. Lehmann-Horn. 2005. Muscle channelopathies and critical points in functional and genomic studies. Journal of Clinical Investigation 115: 2000-2009.
      Tskhovrebova, L., and J. Trinick. 2003. Titin: properties and family relationships. Nature Reviews Molecular Cell Biology 4: 679-689.
      Widrick, J. J., J. G. Romatowski, K. M. Norenberg, S. T. Knuth, J. L. W. Bain, D. A. Riley, S. W. Trappe, T. A. Trappe, D. L. Costill, and R. H. Fitts. 2001. Functional properties of slow and fast gastrocnemius muscle fibers after a 17-day spaceflight. Journal of Applied Physiology 90: 2203-2211.
      Back to BIO 301 syllabus
        Lecture Notes 4 - Blood & Body Defenses

      Posted by at No comments:
      REGULATION OF WATER IN HUMAN BODY
      The maintenance of a correct water balance (the net difference between water gain and water losses) is essential to good health.
      It is all the more essential as there is no real water storage in the body: the water we lose needs be replaced, and humans cannot survive more than a few days without water.1,2
      We lose water on a daily basis.
      • Through the respiratory tract (by breathing)
      • Through the gastro-intestinal tract (faeces)
      • Through the skin (perspiration and sweating)
      • Through the kidneys (urine excretion)Lifestyle and environmental conditions have a significant impact on an individual’s own level of water loss, but on average, a typical adult loses about 2.6 litres (L) per day.3
        Table: Average daily water loss from different organs in adults3
        A table showing average daily water loss
        Additional water losses via sweat will be induced by physical exercise and/or a hot environment and could contribute to water losses of up to several litres.
        We gain water through fluid and food intake and metabolic water production mainly through food nutrient utilization by the body. Metabolic water production represents 0.3 L per day, on average, and water from foods can vary greatly according to dietary habits. Our remaining requirement needs to be provided by fluids. Water balance in the human body Stock Vector - 48256155The endocrine system mediates many of the physiological responses to the homeostatic and acclimation demands of salt and water transport. Many of the hormones involved in the control of salt and water transport are common to all vertebrates, although their precise function and target tissues have changed during evolution. Arginine vasopressin (vasotocin), angiotensin II, natriuretic peptides, vasoactive intestinal peptide, urotensin II, insulin and non-genomic actions of corticosteroids are involved in acute (minutes and hours) alterations in ion and water transport. This rapid alteration in transport is primarily the result changes in behavior, blood flow to osmoregulatory organs, and membrane insertion or activation (e.g., phosphorylation) of existing transport proteins, ion and water channels, contransporters and pumps. Corticosteroids (through genomic actions), prolactin, growth hormone, and insulin-like growth factor I primarily control long-term (several hours to days) changes in transport capacity that are the result of synthesis of new transport proteins, cell proliferation, and differentiation. In addition to the important task of establishing broad evolutionary patterns in hormones involved in ion regulation, comparative endocrinology can determine species and population level differences in signaling pathways that may be critical for adaptation to extreme or rapidly changing environment


      • links;www.bio.umass.edu/biology/mccormick/pdf/GCE
      • https://quizlet.com/11975873/hormonal-control-of-water-and-sodium
      Posted by at No comments:

      Friday, 6 January 2017

      BODY FLUIDS




      CONTENTS OF BODY FLUIDS
      Body fluids can either be intracellular or extracellular.Intracellular fluids are those found within the cell while the extracellular fluids are found outside the cell.The extracellular fluids consists of plasma and interstitial fluids.


      Image result for body fluids pics


      CONTENTS OF INTRACELLULAR FLUIDS
      -Water
      -Proteins
      -Potassium
      -Electrolytes

      CONTENTS OF EXTRACELLULAR FLUID
      -Proteins
      -Chlorine
      -Sodium
      -Calcium

      Image result for intracellular fluid contents pics

        Two thirds of the body fluids is intracellular fluid,and the rest is extracellular fluid.Also in the extracellular fluid 80% is the interstitial fluid and the remaining 20% is the plasma.
         The amount of the fluids in the compartments may vary due to the movement of fluids from one compartment to another due to the difference in concentrations.http://www.wisegeek.org/what-are-the-different-types-of-body-fluids.htm.

      ESTIMATION OF BODY FLUIDS VOLUME

        
      Estimation of body fluid volume in hyponatremia is useful for diagnosis and therapeutic decision-making. Physical examination has been generally used to estimate body fluid volume, but it depends on the physician's abilities. Bioimpedance spectroscopy has been suggested to be a reliable method for the estimation of body fluid volume. Therefore, this study investigated whether bioimpedance spectroscopy could replace physical examination in hyponatremia.

      Materials and Methods

      The study included 30 patients with hyponatremia. At the time of the initial visit, body fluid volume was estimated simultaneously by both physical examination and bioimpedance spectroscopy. Estimation of body fluid status by clinical diagnosis was performed as well, which determined body fluid status corresponds with the most likely cause of hyponatremia (clinical body fluid estimation).

      Results

      The results of body fluid volume estimated by physical examination, bioimpedance spectroscopy, and clinical body fluid estimation showed that 9, 10, and 9 patients, respectively, were hypervolemic; 13, 15 and 16 patients, respectively, were euvolemic; and 8, 5, and 5 patients, respectively, were hypovolemic. Cohen's kappa analysis showed a significant agreement between physical examination and bioimpedance spectroscopy (kappa coefficient, 0.632, p<0.001). In addition, bioimpedance spectroscopy showed a higher level of agreement with clinical body fluid estimation than physical examination (kappa coefficient, 0.602 vs. 0.524).
      Image result for body fluids measurement pics
      BODY FLUID AND ELECTROLYTES BALANCE

      Electrolytes are minerals in your body that have an electric charge. They are in your blood, urine and body fluids. Maintaining the right balance of electrolytes helps your body's blood chemistry, muscle action and other processes. Sodium, calcium, potassium, chlorine, phosphate and magnesium are all electrolytes. You get them from the foods you eat and the fluids you drink.
      Levels of electrolytes in your body can become too low or too high. That can happen when the amount of water in your body changes, causing dehydration or overhydration. Causes include some medicines, vomiting, diarrhea, sweating or kidney problems. Problems most often occur with levels of sodium, potassium or calcium




      BODY FLUIDS BALANCE DISORDERS
      Every part of your body needs water to function. When you are healthy, your body is able to balance the amount of water that enters or leaves your body.
      A fluid imbalance may occur when you lose more water or fluid than your body can take in. It can also occur when you take in more water or fluid than your body is able to get rid of.

      Causes

      Your body is constantly losing water through breathing, sweating, and urinating. If you do not take in enough fluids or water, you become dehydrated.
      Your body may also have a hard time getting rid of fluids. As a result, excess fluid builds up in the body. This is called fluid overload (volume overload). This can lead to edema (excess fluid in the skin and tissues).
      Many medical problems can cause fluid imbalance:
      • After surgery, the body usually retains large amounts of fluid for several days, causing swelling of the body.
      • In heart failure, fluid collects in the lungs, liver, blood vessels, and body tissues because the heart does a poor job of pumping it to the kidneys.
      • When the kidneys do not work well because of chronic kidney disease, the body cannot get rid of unneeded fluids.
      • The body may lose too much fluid due to diarrhea, vomiting, severe blood loss, or high fever.
      • Lack of a hormone called antidiuretic hormone (ADH) can cause the kidneys to get rid of too much fluid. This results in extreme thirst and dehydration.
      Often, a high or low level of sodium or potassium is present as well.
      Medicines can also affect fluid balance. The most common are water pills (diuretics) to treat blood pressure.

      Treatment

      Treatment depends on the specific condition that is causing the fluid imbalance.


      EDEMA
      Edema is a swelling, usually of the legs, feet, and/or hands due to the accumulation of excessive fluid in the tissues.
    • The edema that occurs in diseases of the heart, liver, and kidneys is mainly caused by salt retention, which holds the excess fluid in the body.
    • In certain liver and kidney diseases, low levels of albumin in the blood can contribute to fluid retention.
    • Heart failure, cirrhosis of the liver, venous insufficiency, and a kidney disease called nephrotic syndrome are the most common systemic diseases that cause edema.
    • Excess fluid that accumulates in the lungs is called pulmonary edema.
    • Excess fluid that accumulates in the abdominal cavity is called ascites.
    • Edema of unknown cause (idiopathic edema) occurs primarily in women.
    • Varicose veins or thrombophlebitis (a blood clot in an inflamed vein) of the deep veins in the legs causes edema that is localized to the legs.
    • Therapy for edema consists of treating the underlying conditions, restricting salt intake, compression stockings, elevation of the extremity, and often using diuretics (medicines that induce urination).

      • Image result for edema pics
      Pitting Edema - EMTprep.com
      Add caption
      Image result for edema pics


      LINKS

      For more information about body fluids the following links may be followed
      www.webmd.com/heart-disease/heart-failure/edema-overview www.medicinenet.com/edema/article.htm
      www.medicalnewstoday.com/articles/159111


      Posted by at No comments:
      Subscribe to: Posts (Atom)