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I discussed a leather store about the white border aka salt border on leather shoes. They said that it is due to inner features of leather and you could try to add some fat/cream to push it back inside the shoes. I haven't yet understood physiology of skin here,
"why does it act like that?"is the first doubt and then the second
"does human skin act the same way?"-- I can see this kind of salt borders in gym clothes when they cry uncleaned but haven't seen them yet on my skin at least. The extra salty water from legs causes real damage, such as getting the inner fluids out, to the leather. When you do heavy training, the salty sweat in the human skin acts apparently the same way. So:
how to manage the skin in living human skin and how does it differ from leather maintenance? What is the common physiological background with the different kinds of skins?
I try to answer it myself:
- leather: you can add the fat/cream/etc only externally
- living human ski: you can add the fat/cream-etc both internally (fatty food) and externally (lotions)
The two processes are quite different: On leather shoes no active transport takes place. The salt either comes with the snow (most likely most of it) when the streets get salted to avoid ice. Your shoe soaks up the salt-water mixture and when the water dries up, the salt stays behind. The other possibility (more for new leather shoes) is that water goes into the leather and dissolves salts, which remain from the tanning process of the leather. With older shoes I have never observed this "snow marks" in the summer when the shoes got wet in rain. Using a wet cloth removes the salt, subsequent treatment of the shoe prevents that water can enter the leather.
The skin is quite different: Here we have living cells and an active transport of water through pores when you body get warm. This is to cool you and prevent overheating and since the body fluids contain salt, so does sweat.
8: Bacterial Colony Morphology
Bacteria grow on solid media as colonies. A colony is defined as a visible mass of microorganisms all originating from a single mother cell, therefore a colony constitutes a clone of bacteria all genetically alike.
In the identification of bacteria and fungi much weight is placed on how the organism grows in or on media. This exercise will help you identify the cultural characteristics of a bacterium on an agar plate - called colony morphology. Although one might not necessarily see the importance of colonial morphology at first, it really can be important when identifying the bacterium. Features of the colonies may help to pinpoint the identity of the bacterium. Different species of bacteria can produce very different colonies.
In the above picture of a mixed culture, an agar plate that has been exposed to the air and many different colony morphologies can be identified. Nine obviously different colonies are numbered: some colony types recur in various areas of the plate (note # 3 and # 4). Not only are pigment differences seen, but also size, edge, pattern, opacity, and shine. Two circles have been drawn around merging colonies, where the species of the 2 colonies are different. Trying to pick a bit of one of those adjacent colonies increases the chances of picking up another mixed culture, consisting of the 2 species that were merged together. ALWAYS pick a well-isolated colony when subculturing.
WHOLE SHAPE OF COLONY
Varies from round to irregular to filamentous and rhizoid (root-like)
SIZE OF COLONY
Can vary from large colonies to tiny colonies less than 1mm = punctiform (pin-point). Measure with a millimeter rule.
EDGE/MARGIN OF COLONY
Magnified edge shape (use a dissecting microscope to see the margin edge well)
Color of colonies, pigmentation: white, buff, red, purple, etc.
Some pigments are water-soluble, others are not.
If you take a large inoculum and place it in a tube of water or saline, do you see color?
Do you see any pigment if the organism is growing in a broth medium?
Does incubation temperature affect the color?
Does the entire colony have the color, or is it more like a bull&rsquos eye?
OPACITY OF COLONY
Is the colony transparent (clear), opaque (not transparent or clear), translucent (almost clear, but distorted vision&ndashlike looking through frosted glass), iridescent (changing colors in reflected light)?
ELEVATION OF COLONY
How much does the colony rise above the agar (turn the plate on end to determine height)?
SURFACE OF COLONY
Smooth, glistening, rough, dull (opposite of glistening), rugose (wrinkled)
CONSISTENCY or TEXTURE
Butyrous (buttery), viscid (sticks to loop, hard to get off), brittle/friable (dry, breaks apart), mucoid (sticky, mucus-like)
Thick Ascending Limb
The primary site of sodium reabsorption in the Loop of Henle is the thick ascending limb (TAL). The TAL is impermeable to water. Sodium (Na + ) reabsorption is active- the driver is the Na + /K + ATPase on the basolateral membrane which actively pumps three Na + ions out the cell into the interstitium and two potassium(K + ) ions into the cell. By creating a low intracellular concentration of sodium, the inside of the cell becomes negatively charged, creating an electrochemical gradient.
Sodium then moves into the cell (from the tubular lumen) down the electrical and chemical gradient, through the NKCC2 transporter on the apical membrane This transporter moves one Na + ion, one K + ion and two Cl – ions across the apical membrane. .
Potassium ions are transported back into the tubule by ROMK channels on the apical membrane to prevent toxic build up within the cell. Chloride ions are transported into the tissue fluid via CIC-KB channels.
The overall effects of this process are:
- Removal of Na + whilst retaining water in the tubules – this leads to a hypotonic solution arriving at the DCT.
- Pumping Na + into the interstitial space contributes to a hyperosmotic environment in the kidney medulla (see below)
There is also significant paracellular reabsorption of magnesium, calcium, sodium and potassium.
Thin Ascending Limb
Sodium reabsorption in the thin ascending limb is passive. It occurs paracellularly due to the difference in osmolarity between the tubule and the interstitium.
As the thick ascending limb is impermeable to water, the interstitium becomes concentrated with ions, increasing the osmolarity. This drives water reabsorption from the descending limb as water moves from areas of low osmolarity to areas of high osmolarity. This system is known as counter-current multiplication.
For further explanation of counter-current multiplication, please see this helpful video: https://www.youtube.com/watch?v=Vqce2dtg45U
Thin Descending Limb
The descending limb is highly permeable to water, with reabsorption occurring passively via AQP1 channels. Very low amounts of urea, Na + and other ions are also reabsorbed. . As mentioned above, water reabsorption is driven by the counter-current multiplier system set up by the active reabsorption of sodium in the TAL.
Fig 1 – Diagram showing ion and water reabsorption within the Loop of Henle.
A large amount of reabsorption occurs in the proximal convoluted tubule. Reabsorption is when water and solutes within the PCT are transported into the bloodstream. In the PCT this process occurs via bulk transport. The solutes and water move from the PCT to the interstitium and then into peritubular capillaries. The reabsorption in the proximal tubule is isosmotic.
The proximal tubules reabsorb about 65% of water, sodium, potassium and chloride, 100% of glucose, 100% amino acids, and 85-90% of bicarbonate. This reabsorption occurs due to the presence of channels on the basolateral (facing the interstitium) and apical membranes (facing the tubular lumen).
There are two routes through which reabsorption can take place: paracellular and transcellular. The transcellular route transports solutes through a cell. The paracellular route transports solutes between cells, through the intercellular space.
The driving force for the reabsorption in the PCT is sodium, due to the presence of many sodium-linked symporters e.g. sodium glucose linked transporters (SGLTs) on the apical membrane. Sodium is usually co-transported with other solutes e.g. amino acids and glucose, or in later segments of the tubule with chloride ions. Thus sodium moving down its concentration allows other solutes to move against their own concentration gradient.
To create an electrochemical gradient for sodium, Na + -K + -ATPases on the basolateral surface pump out 3 Na + ions, in exchange for bringing 2 K + ions into the cell. This transporter uses primary active transport . This movement of Na + creates an electrochemical gradient favouring the movement of Na + into the cell from the tubule lumen.
The S1 segment of the PCT is not permeable to urea and chloride ions, hence their concentration increases in S1 which creates a concentration gradient which can be utilised in the S2 and S3 segments. Additional sodium is transported via an antiporter mechanism that reabsorbs sodium whilst secreting other ions, especially H + .
Co-transport refers to the movement of multiple solutes through the same channel.
The sodium concentration gradient allows other molecules, such as glucose, to be transported across the apical membrane against their concentration gradient. For example, SGLT transporters move glucose together with two sodium ions across the apical membrane. Glucose then crosses the basolateral membrane via facilitated diffusion.
Na + /Amino acid symporters are present on the apical side of cells in the S1 segment of the PCT which reabsorbs all the amino acids in the PCT.
Na + /H + antiporter is found on the apical surface of PCT cells. It is an antiporter and therefore transports ions across the cell membrane in opposite directions. In this case, the Na + ions move into the tubular cells, while the H + is expelled into the lumen. The primary function of this transporter is to maintain the pH.
Movement of Water
In the PCT, large volumes of solute are transported into the bloodstream. This means that as we move along the tubule, solute concentration in the tubule decreases while the solute concentration in the interstitium increases.
The difference in concentration gradient results in the water moving into the interstitium via osmosis. Water mainly takes the paracellular route to move out of the renal tubule but it can also take the transcellular route.
Fig 2 – Diagram showing ion absorption and secretion within the proximal convoluted tubule.
Secretion is when substances are removed from the blood and transported into the PCT. This is very useful as only 20% of the blood is filtered in the glomerulus every minute, so this provides an alternative route for substances to enter the tubular lumen. The PCT secretes:
- Organic acids and bases – e.g. bile salts, oxalate and catecholamines (waste products of metabolism)
- Hydrogen ions (H + ) – important in maintaining acid/base balance in the body. H + secretion allows reabsorption of bicarbonate via the use of the enzyme carbonic anhydrase (Fig 2). The net result is for every one molecule of H + secreted, one molecule of bicarbonate and Na + is reabsorbed into the blood stream. As the H + is consumed in the reaction in the tubular lumen, there is no net excretion of H + . In this way, about 85% of filtered bicarbonate is reabsorbed in the PCT (the rest is reabsorbed by the intercalated cells at the DCT/CD later on)..
- Drugs/toxins – Secretion of organic cations such as dopamine or morphine occurs via the H + /OC + exchanger on the apical side of the tubule cell, which is driven by the Na + /H + antiporter.
Physiology of skin and leather: why do salt borders occur? - Biology
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3.1 The Cell Membrane
Despite differences in structure and function, all living cells in multicellular organisms have a surrounding cell membrane. Just as the outer layer of your skin separates your body from its environment, the cell membrane (also known as the plasma membrane) separates the inner contents of a cell from its exterior environment. This cell membrane provides a protective barrier around the cell and regulates which materials can pass in or out.
Structure and Composition of the Cell Membrane
The cell membrane is an extremely pliable structure composed primarily of two layers of phospholipids (a “bilayer”). Cholesterol and various proteins are also embedded within the membrane giving the membrane a variety of functions described below.
A single phospholipid molecule has a phosphate group on one end, called the “head,” and two side-by-side chains of fatty acids that make up the lipid “tails” (Figure 3.1.1). The lipid tails of one layer face the lipid tails of the other layer, meeting at the interface of the two layers. The phospholipid heads face outward, one layer exposed to the interior of the cell and one layer exposed to the exterior (Figure 3.1.1).
Figure 3.1.1 – Phospholipid Structure and Bilayer: A phospholipid molecule consists of a polar phosphate “head,” which is hydrophilic and a non-polar lipid “tail,” which is hydrophobic. Unsaturated fatty acids result in kinks in the hydrophobic tails. The phospholipid bilayer consists of two adjacent sheets of phospholipids, arranged tail to tail. The hydrophobic tails associate with one another, forming the interior of the membrane. The polar heads contact the fluid inside and outside of the cell.
The phosphate group is negatively charged, making the head polar and hydrophilic—or “water loving.” A hydrophilic molecule (or region of a molecule) is one that is attracted to water. The phosphate heads are thus attracted to the water molecules of both the extracellular and intracellular environments. The lipid tails, on the other hand, are uncharged, or nonpolar, and are hydrophobic—or “water fearing.” A hydrophobic molecule (or region of a molecule) repels and is repelled by water. Phospholipids are thus amphipathic molecules. An amphipathic molecule is one that contains both a hydrophilic and a hydrophobic region. In fact, soap works to remove oil and grease stains because it has amphipathic properties. The hydrophilic portion can dissolve in the wash water while the hydrophobic portion can trap grease in stains that then can be washed away. A similar process occurs in your digestive system when bile salts (made from cholesterol, phospholipids and salt) help to break up ingested lipids.
Since the phosphate groups are polar and hydrophilic, they are attracted to water in the intracellular fluid. Intracellular fluid (ICF) is the fluid interior of the cell. The phosphate groups are also attracted to the extracellular fluid. Extracellular fluid (ECF) is the fluid environment outside the enclosure of the cell membrane (see above Figure). Since the lipid tails are hydrophobic, they meet in the inner region of the membrane, excluding watery intracellular and extracellular fluid from this space. In addition to phospholipids and cholesterol, the cell membrane has many proteins detailed in the next section.
The lipid bilayer forms the basis of the cell membrane, but it is peppered throughout with various proteins. Two different types of proteins that are commonly associated with the cell membrane are the integral protein and peripheral protein (Figure 3.1.2). As its name suggests, an integral protein is a protein that is embedded in the membrane. Many different types of integral proteins exist, each with different functions. For example, an integral protein that extends an opening through the membrane for ions to enter or exit the cell is known as a channel protein. Peripheral proteins are typically found on the inner or outer surface of the lipid bilayer but can also be attached to the internal or external surface of an integral protein.
Figure 3.1.2- Cell Membrane: The cell membrane of the cell is a phospholipid bilayer containing many different molecular components, including proteins and cholesterol, some with carbohydrate groups attached.
Some integral proteins serve as cell recognition or surface identity proteins, which mark a cell’s identity so that it can be recognized by other cells. Some integral proteins act as enzymes, or in cell adhesion, between neighboring cells. A receptor is a type of recognition protein that can selectively bind a specific molecule outside the cell, and this binding induces a chemical reaction within the cell. Some integral proteins serve dual roles as both a receptor and an ion channel. One example of a receptor-channel interaction is the receptors on nerve cells that bind neurotransmitters, such as dopamine. When a dopamine molecule binds to a dopamine receptor protein, a channel within the transmembrane protein opens to allow certain ions to flow into the cell. Peripheral proteins are often associated with integral proteins along the inner cell membrane where they play a role in cell signaling or anchoring to internal cellular components (ie: cytoskeleton discussed later).
Some integral membrane proteins are glycoproteins. A glycoprotein is a protein that has carbohydrate molecules attached, which extend into the extracellular environment. The attached carbohydrate tags on glycoproteins aid in cell recognition. The carbohydrates that extend from membrane proteins and even from some membrane lipids collectively form the glycocalyx. The glycocalyx is a fuzzy-appearing coating around the cell formed from glycoproteins and other carbohydrates attached to the cell membrane. The glycocalyx can have various roles. For example, it may have molecules that allow the cell to bind to another cell, it may contain receptors for hormones, or it might have enzymes to break down nutrients. The glycocalyces found in a person’s body are products of that person’s genetic makeup. They give each of the individual’s trillions of cells the “identity” of belonging in the person’s body. This identity is the primary way that a person’s immune defense cells “know” not to attack the person’s own body cells, but it also is the reason organs donated by another person might be rejected.
Transport Across the Cell Membrane
One of the great wonders of the cell membrane is its ability to regulate the concentration of substances inside the cell. These substances include ions such as Ca ++ , Na + , K + , and Cl – , nutrients including sugars, fatty acids, and amino acids, and waste products, particularly carbon dioxide (CO2), which must leave the cell.
The membrane’s lipid bilayer structure provides the first level of control. The phospholipids are tightly packed together, and the membrane has a hydrophobic interior. This structure causes the membrane to be selectively permeable. A membrane that has selective permeability allows only substances meeting certain criteria to pass through it unaided. In the case of the cell membrane, only relatively small, nonpolar materials can move through the lipid bilayer (remember, the lipid tails of the membrane are nonpolar). Some examples of these are other lipids, oxygen and carbon dioxide gases, and alcohol. However, water-soluble materials—like glucose, amino acids, and electrolytes—need some assistance to cross the membrane because they are repelled by the hydrophobic tails of the phospholipid bilayer. All substances that move through the membrane do so by one of two general methods, which are categorized based on whether or not energy is required. Passive transport is the movement of substances across the membrane without the expenditure of cellular energy. In contrast, active transport is the movement of substances across the membrane using energy from adenosine triphosphate (ATP).
In order to understand how substances move passively across a cell membrane, it is necessary to understand concentration gradients and diffusion. A concentration gradient is the difference in concentration of a substance across a space. Molecules (or ions) will spread/diffuse from where they are more concentrated to where they are less concentrated until they are equally distributed in that space. (When molecules move in this way, they are said to move down their concentration gradient, from high concentration to low concentration.) Diffusion is the movement of particles from an area of higher concentration to an area of lower concentration. A couple of common examples will help to illustrate this concept. Imagine being inside a closed room. If a bottle of perfume were sprayed, the scent molecules would naturally diffuse from the spot where they left the bottle to all corners of the room, and this diffusion would go on until the molecules were equally distributed in the room. Another example is a spoonful of sugar placed in a cup of tea. Eventually the sugar will diffuse throughout the tea until no concentration gradient remains. In both cases, if the room is warmer or the tea hotter, diffusion occurs even faster as the molecules are bumping into each other and spreading out faster than at cooler temperatures.
Visit this link to see diffusion and how it is propelled by the kinetic energy of molecules in solution. How does temperature affect diffusion rate, and why?
Whenever a substance exists in greater concentration on one side of a semipermeable membrane, such as cell membranes, any substance that can move down its concentration gradient across the membrane will do so. If the substances can move across the cell membrane without the cell expending energy, the movement of molecules is called passive transport. Consider substances that can easily diffuse through the lipid bilayer of the cell membrane, such as the gases oxygen (O2) and carbon dioxide (CO2). These small, fat soluble gasses and other small lipid soluble molecules can dissolve in the membrane and enter or exit the cell following their concentration gradient. This mechanism of molecules moving across a cell membrane from the side where they are more concentrated to the side where they are less concentrated is a form of passive transport called simple diffusion. O2 generally diffuses into cells because it is more concentrated outside of them, and CO2 typically diffuses out of cells because it is more concentrated inside of them.
Before moving on, it is important to realize that the concentration gradients for oxygen and carbon dioxide will always exist across a living cell and never reach equal distribution. This is because cells rapidly use up oxygen during metabolism and so, there is typically a lower concentration of O2 inside the cell than outside. As a result, oxygen will diffuse from outside the cell directly through the lipid bilayer of the membrane and into the cytoplasm within the cell. On the other hand, because cells produce CO2 as a byproduct of metabolism, CO2 concentrations rise within the cytoplasm therefore, CO2 will move from the cell through the lipid bilayer and into the extracellular fluid, where its concentration is lower. (Figure 3.1.3).
Figure 3.1.3 – Simple Diffusion Across the Cell (Plasma) Membrane: The structure of the lipid bilayer allows small, uncharged substances such as oxygen and carbon dioxide, and hydrophobic molecules such as lipids, to pass through the cell membrane, down their concentration gradient, by simple diffusion.
Large polar or ionic molecules, which are hydrophilic, cannot easily cross the phospholipid bilayer. Charged atoms or molecules of any size cannot cross the cell membrane via simple diffusion as the charges are repelled by the hydrophobic tails in the interior of the phospholipid bilayer. Solutes dissolved in water on either side of the cell membrane will tend to diffuse down their concentration gradients, but because most substances cannot pass freely through the lipid bilayer of the cell membrane, their movement is restricted to protein channels and specialized transport mechanisms in the membrane. Facilitated diffusion is the diffusion process used for those substances that cannot cross the lipid bilayer due to their size, charge, and/or polarity but do so down their concentration gradients (Figure 3.1.4). As an example, even though sodium ions (Na + ) are highly concentrated outside of cells, these electrolytes are charged and cannot pass through the nonpolar lipid bilayer of the membrane. Their diffusion is facilitated by membrane proteins that form sodium channels (or “pores”), so that Na+ ions can move down their concentration gradient from outside the cells to inside the cells. A common example of facilitated diffusion using a carrier protein is the movement of glucose into the cell, where it is used to make ATP. Although glucose can be more concentrated outside of a cell, it cannot cross the lipid bilayer via simple diffusion because it is both large and polar, and therefore, repelled by the phospholipid membrane. To resolve this, a specialized carrier protein called the glucose transporter will transfer glucose molecules into the cell to facilitate its inward diffusion. The difference between a channel and a carrier is that the carrier usually changes shape during the diffusion process, while the channel does not. There are many other solutes that must undergo facilitated diffusion to move into a cell, such as amino acids, or to move out of a cell, such as wastes.
Figure 3.1.4 – Facilitated Diffusion: (a) Facilitated diffusion of substances crossing the cell (plasma) membrane takes place with the help of proteins such as channel proteins and carrier proteins. Channel proteins are less selective than carrier proteins, and usually mildly discriminate between their cargo based on size and charge. (b) Carrier proteins are more selective, often only allowing one particular type of molecule to cross.
A specialized example of facilitated transport is water moving across the cell membrane of all cells, through protein channels known as aquaporins. Osmosis is the diffusion of water through a semipermeable membrane from where there is more relative water to where there is less relative water (down its water concentration gradient) (Figure 3.1.5).
Figure 3.1.5 – Osmosis: Osmosis is the diffusion of water through a semipermeable membrane down its concentration gradient. If a membrane is permeable to water, though not to a solute, water will equalize its own concentration by diffusing to the side of lower water concentration (and thus the side of higher solute concentration). In the beaker on the left, the solution on the right side of the membrane is hypertonic.
On their own, cells cannot regulate the movement of water molecules across their membrane, so it is important that cells are exposed to an environment in which the concentration of solutes outside of the cells (in the extracellular fluid) is equal to the concentration of solutes inside the cells (in the cytoplasm). Two solutions that have the same concentration of solutes are said to be isotonic (equal tension). When cells and their extracellular environments are isotonic, the concentration of water molecules is the same outside and inside the cells, and the cells maintain their normal shape (and function).
Osmosis occurs when there is an imbalance of solutes outside of a cell versus inside the cell. A solution that has a higher concentration of solutes than another solution is said to be hypertonic, and water molecules tend to diffuse into a hypertonic solution (Figure 3.1.6). Cells in a hypertonic solution will shrivel as water leaves the cell via osmosis. In contrast, a solution that has a lower concentration of solutes than another solution is said to be hypotonic, and water molecules tend to diffuse out of a hypotonic solution. Cells in a hypotonic solution will take on too much water and swell, with the risk of eventually bursting. A critical aspect of homeostasis in living things is to create an internal environment in which all of the body’s cells are in an isotonic solution. Various organ systems, particularly the kidneys, work to maintain this homeostasis.
Figure 3.1.6 – Concentration of Solution: A hypertonic solution has a solute concentration higher than another solution. An isotonic solution has a solute concentration equal to another solution. A hypotonic solution has a solute concentration lower than another solution.
For all of the transport methods described above, the cell expends no energy. Membrane proteins that aid in the passive transport of substances do so without the use of ATP. During primary active transport, ATP is required to move a substance across a membrane, with the help of membrane protein, and against its concentration gradient.
One of the most common types of active transport involves proteins that serve as pumps. The word “pump” probably conjures up thoughts of using energy to pump up the tire of a bicycle or a basketball. Similarly, energy from ATP is required for these membrane proteins to transport substances—molecules or ions—across the membrane, against their concentration gradients (from an area of low concentration to an area of high concentration).
The sodium-potassium pump, which is also called Na + /K + ATPase, transports sodium out of a cell while moving potassium into the cell. The Na + /K + pump is an important ion pump found in the membranes of all cells. The activity of these pumps in nerve cells is so great that it accounts for the majority of their ATP usage.
Figure 3.1.7 The sodium-potassium pump is found in many cell (plasma) membranes. Powered by ATP, the pump moves sodium and potassium ions in opposite directions, each against its concentration gradient. In a single cycle of the pump, three sodium ions are extruded from and two potassium ions are imported into the cell.
Active transport pumps can also work together with other active or passive transport systems to move substances across the membrane. For example, the sodium-potassium pump maintains a high concentration of sodium ions outside of the cell. Therefore, if the cell needs sodium ions, all it has to do is open a passive sodium channel, as the concentration gradient of the sodium ions will drive them to diffuse into the cell. In this way, the action of an active transport pump (the sodium-potassium pump) powers the passive transport of sodium ions by creating a concentration gradient. When active transport powers the transport of another substance in this way, it is called secondary active transport.
Symporters are secondary active transporters that move two substances in the same direction. For example, the sodium-glucose symporter uses sodium ions to “pull” glucose molecules into the cell. Since cells store glucose for energy, glucose is typically at a higher concentration inside of the cell than outside however, due to the action of the sodium-potassium pump, sodium ions will easily diffuse into the cell when the symporter is opened. The flood of sodium ions through the symporter provides the energy that allows glucose to move through the symporter and into the cell, against its concentration gradient.
Conversely, antiporters are secondary active transport systems that transport substances in opposite directions. For example, the sodium-hydrogen ion antiporter uses the energy from the inward flood of sodium ions to move hydrogen ions (H + ) out of the cell. The sodium-hydrogen antiporter is used to maintain the pH of the cell’s interior.
Other Forms of Membrane Transport
Other forms of active transport do not involve membrane carriers. Endocytosis (bringing “into the cell”) is the process of a cell ingesting material by enveloping it in a portion of its cell membrane, and then pinching off that portion of membrane (Figure 3.1.8). Once pinched off, the portion of membrane and its contents becomes an independent, intracellular vesicle. A vesicle is a membranous sac—a spherical and hollow organelle bounded by a lipid bilayer membrane. Endocytosis often brings materials into the cell that must to be broken down or digested. Phagocytosis (“cell eating”) is the endocytosis of large particles. Many immune cells engage in phagocytosis of invading pathogens. Like little Pac-men, their job is to patrol body tissues for unwanted matter, such as invading bacterial cells, phagocytize them, and digest them. In contrast to phagocytosis, pinocytosis (“cell drinking”) brings fluid containing dissolved substances into a cell through membrane vesicles.
Figure 3.1.8 – Three Forms of Endocytosis: Endocytosis is a form of active transport in which a cell envelopes extracellular materials using its cell membrane. (a) In phagocytosis, which is relatively nonselective, the cell takes in large particles into larger vesicles known as vacuoles. (b) In pinocytosis, the cell takes in small particles in fluid. (c) In contrast, receptor-mediated endocytosis is quite selective. When external receptors bind a specific ligand, the cell responds by endocytosing the ligand.
Phagocytosis and pinocytosis take in large portions of extracellular material, and they are typically not highly selective in the substances they bring in. Cells regulate the endocytosis of specific substances via receptor-mediated endocytosis. Receptor-mediated endocytosis is endocytosis by a portion of the cell membrane which contains many receptors that are specific for a certain substance. Once the surface receptors have bound sufficient amounts of the specific substance (the receptor’s ligand), the cell will endocytose the part of the cell membrane containing the receptor-ligand complexes. Iron, a required component of hemoglobin, is endocytosed by red blood cells in this way. Iron is bound to a protein called transferrin in the blood. Specific transferrin receptors on red blood cell surfaces bind the iron-transferrin molecules, and the cell endocytoses the receptor-ligand complexes.
In contrast with endocytosis, exocytosis (taking “out of the cell”) is the process of a cell exporting material using vesicular transport (Figure 3.1.9). Many cells manufacture substances that must be secreted, like a factory manufacturing a product for export. These substances are typically packaged into membrane-bound vesicles within the cell. When the vesicle membrane fuses with the cell membrane, the vesicle releases its contents into the interstitial fluid. The vesicle membrane then becomes part of the cell membrane.
Specific examples of exocytosis include cells of the stomach and pancreas producing and secreting digestive enzymes through exocytosis (Figure 3.1.10) and endocrine cells producing and secreting hormones that are sent throughout the body.
The addition of new membrane to the plasma membrane is usually coupled with endocytosis so that the cell is not constantly enlarging. Through these processes, the cell membrane is constantly renewing and changing as needed by the cell.
Figure 3.1.9 – Exocytosis: Exocytosis is much like endocytosis in reverse. Material destined for export is packaged into a vesicle inside the cell. The membrane of the vesicle fuses with the cell membrane, and the contents are released into the extracellular space. Figure 3.1.10 – Pancreatic Cells’ Enzyme Products: The pancreatic acinar cells produce and secrete many enzymes that digest food. The tiny black granules in this electron micrograph are secretory vesicles filled with enzymes that will be exported from the cells via exocytosis. LM × 2900. (Micrograph provided by the Regents of University of Michigan Medical School © 2012)
Diseases of the Cell: Cystic Fibrosis
Cystic fibrosis (CF) affects approximately 30,000 people in the United States, with about 1,000 new cases reported each year. The genetic disease is most well-known for its damage to the lungs, causing breathing difficulties and chronic lung infections, but it also affects the liver, pancreas, and intestines. Only about 50 years ago, the prognosis for children born with CF was very grim—a life expectancy rarely over 10 years. Today, with advances in medical treatment, many CF patients live into their 30s.
The symptoms of CF result from a malfunctioning membrane ion channel called the Cystic Fibrosis Transmembrane Conductance Regulator, or CFTR. In healthy people, the CFTR protein is an integral membrane protein that transports Cl– ions out of the cell. In a person who has CF, the gene for the CFTR is mutated, thus, the cell manufactures a defective channel protein that typically is not incorporated into the membrane, but is instead degraded by the cell.
The CFTR requires ATP in order to function, making its Cl– transport a form of active transport. This puzzled researchers for a long time because the Cl– ions are actually flowing down their concentration gradient when transported out of cells. Active transport generally pumps ions against their concentration gradient, but the CFTR presents an exception to this rule.
In normal lung tissue, the movement of Cl– out of the cell maintains a Cl–-rich, negatively charged environment immediately outside of the cell. This is particularly important in the epithelial lining of the respiratory system. Respiratory epithelial cells secrete mucus, which serves to trap dust, bacteria, and other debris. A cilium (plural = cilia) is one of the hair-like appendages found on certain cells. Cilia on the epithelial cells move the mucus and its trapped particles up the airways away from the lungs and toward the outside. In order to be effectively moved upward, the mucus cannot be too viscous, rather, it must have a thin, watery consistency. The transport of Cl– and the maintenance of an electronegative environment outside of the cell attracts positive ions such as Na+ to the extracellular space. The accumulation of both Cl– and Na+ ions in the extracellular space creates solute-rich mucus, which has a low concentration of water molecules. As a result, through osmosis, water moves from cells and extracellular matrix into the mucus, “thinning” it out. In a normal respiratory system, this is how the mucus is kept sufficiently watered-down to be propelled out of the respiratory system.
If the CFTR channel is absent, Cl– ions are not transported out of the cell in adequate numbers, thus preventing them from drawing positive ions. The absence of ions in the secreted mucus results in the lack of a normal water concentration gradient. Thus, there is no osmotic pressure pulling water into the mucus. The resulting mucus is thick and sticky, and the ciliated epithelia cannot effectively remove it from the respiratory system. Passageways in the lungs become blocked with mucus, along with the debris it carries. Bacterial infections occur more easily because bacterial cells are not effectively carried away from the lungs.
The cell membrane provides a barrier around the cell, separating its internal components from the extracellular environment. It is composed of a phospholipid bilayer, with hydrophobic internal lipid “tails” and hydrophilic external phosphate “heads.” Various membrane proteins are scattered throughout the bilayer, both inserted within it and attached to it peripherally. The cell membrane is selectively permeable, allowing only a limited number of materials to diffuse through its lipid bilayer. All materials that cross the membrane do so using passive (non-energy-requiring) or active (energy-requiring) transport processes. During passive transport, materials move by simple diffusion or by facilitated diffusion through the membrane, down their concentration gradient. Water passes through the membrane in a diffusion process called osmosis. During active transport, energy is expended to assist material movement across the membrane in a direction against their concentration gradient. Active transport may take place with the help of protein pumps or through the use of vesicles.
Interactive Link Questions
Visit this link to see diffusion and how it is propelled by the kinetic energy of molecules in solution. How does temperature affect diffusion rate, and why?
Higher temperatures speed up diffusion because molecules have more kinetic energy at higher temperatures.
Bone tissue (osseous tissue) differs greatly from other tissues in the body. Bone is hard and many of its functions depend on that characteristic hardness. Later discussions in this chapter will show that bone is also dynamic in that its shape adjusts to accommodate stresses. This section will examine the gross anatomy of bone first and then move on to its histology.
Gross Anatomy of Bone
The structure of a long bone allows for the best visualization of all of the parts of a bone ((Figure)). A long bone has two parts: the diaphysis and the epiphysis . The diaphysis is the tubular shaft that runs between the proximal and distal ends of the bone. The hollow region in the diaphysis is called the medullary cavity , which is filled with yellow marrow. The walls of the diaphysis are composed of dense and hard compact bone .
The wider section at each end of the bone is called the epiphysis (plural = epiphyses), which is filled with spongy bone. Red marrow fills the spaces in the spongy bone. Each epiphysis meets the diaphysis at the metaphysis, the narrow area that contains the epiphyseal plate (growth plate), a layer of hyaline (transparent) cartilage in a growing bone. When the bone stops growing in early adulthood (approximately 18–21 years), the cartilage is replaced by osseous tissue and the epiphyseal plate becomes an epiphyseal line.
The medullary cavity has a delicate membranous lining called the endosteum (end- = “inside” oste- = “bone”), where bone growth, repair, and remodeling occur. The outer surface of the bone is covered with a fibrous membrane called the periosteum (peri– = “around” or “surrounding”). The periosteum contains blood vessels, nerves, and lymphatic vessels that nourish compact bone. Tendons and ligaments also attach to bones at the periosteum. The periosteum covers the entire outer surface except where the epiphyses meet other bones to form joints ((Figure)). In this region, the epiphyses are covered with articular cartilage , a thin layer of cartilage that reduces friction and acts as a shock absorber.
Flat bones, like those of the cranium, consist of a layer of diploë (spongy bone), lined on either side by a layer of compact bone ((Figure)). The two layers of compact bone and the interior spongy bone work together to protect the internal organs. If the outer layer of a cranial bone fractures, the brain is still protected by the intact inner layer.
The surface features of bones vary considerably, depending on the function and location in the body. (Figure) describes the bone markings, which are illustrated in ((Figure)). There are three general classes of bone markings: (1) articulations, (2) projections, and (3) holes. As the name implies, an articulation is where two bone surfaces come together (articulus = “joint”). These surfaces tend to conform to one another, such as one being rounded and the other cupped, to facilitate the function of the articulation. A projection is an area of a bone that projects above the surface of the bone. These are the attachment points for tendons and ligaments. In general, their size and shape is an indication of the forces exerted through the attachment to the bone. A hole is an opening or groove in the bone that allows blood vessels and nerves to enter the bone. As with the other markings, their size and shape reflect the size of the vessels and nerves that penetrate the bone at these points.
|Articulations||Where two bones meet||Knee joint|
|Head||Prominent rounded surface||Head of femur|
|Condyle||Rounded surface||Occipital condyles|
|Projections||Raised markings||Spinous process of the vertebrae|
|Process||Prominence feature||Transverse process of vertebra|
|Spine||Sharp process||Ischial spine|
|Tubercle||Small, rounded process||Tubercle of humerus|
|Tuberosity||Rough surface||Deltoid tuberosity|
|Line||Slight, elongated ridge||Temporal lines of the parietal bones|
|Holes||Holes and depressions||Foramen (holes through which blood vessels can pass through)|
|Fossa||Elongated basin||Mandibular fossa|
|Fovea||Small pit||Fovea capitis on the head of the femur|
|Sulcus||Groove||Sigmoid sulcus of the temporal bones|
|Canal||Passage in bone||Auditory canal|
|Fissure||Slit through bone||Auricular fissure|
|Foramen||Hole through bone||Foramen magnum in the occipital bone|
|Meatus||Opening into canal||External auditory meatus|
|Sinus||Air-filled space in bone||Nasal sinus|
Bone Cells and Tissue
Bone contains a relatively small number of cells entrenched in a matrix of collagen fibers that provide a surface for inorganic salt crystals to adhere. These salt crystals form when calcium phosphate and calcium carbonate combine to create hydroxyapatite, which incorporates other inorganic salts like magnesium hydroxide, fluoride, and sulfate as it crystallizes, or calcifies, on the collagen fibers. The hydroxyapatite crystals give bones their hardness and strength, while the collagen fibers give them flexibility so that they are not brittle.
Although bone cells compose a small amount of the bone volume, they are crucial to the function of bones. Four types of cells are found within bone tissue: osteoblasts, osteocytes, osteogenic cells, and osteoclasts ((Figure)).
The osteoblast is the bone cell responsible for forming new bone and is found in the growing portions of bone, including the periosteum and endosteum. Osteoblasts, which do not divide, synthesize and secrete the collagen matrix and calcium salts. As the secreted matrix surrounding the osteoblast calcifies, the osteoblast become trapped within it as a result, it changes in structure and becomes an osteocyte , the primary cell of mature bone and the most common type of bone cell. Each osteocyte is located in a space called a lacuna and is surrounded by bone tissue. Osteocytes maintain the mineral concentration of the matrix via the secretion of enzymes. Like osteoblasts, osteocytes lack mitotic activity. They can communicate with each other and receive nutrients via long cytoplasmic processes that extend through canaliculi (singular = canaliculus), channels within the bone matrix.
If osteoblasts and osteocytes are incapable of mitosis, then how are they replenished when old ones die? The answer lies in the properties of a third category of bone cells—the osteogenic cell . These osteogenic cells are undifferentiated with high mitotic activity and they are the only bone cells that divide. Immature osteogenic cells are found in the deep layers of the periosteum and the marrow. They differentiate and develop into osteoblasts.
The dynamic nature of bone means that new tissue is constantly formed, and old, injured, or unnecessary bone is dissolved for repair or for calcium release. The cell responsible for bone resorption, or breakdown, is the osteoclast . They are found on bone surfaces, are multinucleated, and originate from monocytes and macrophages, two types of white blood cells, not from osteogenic cells. Osteoclasts are continually breaking down old bone while osteoblasts are continually forming new bone. The ongoing balance between osteoblasts and osteoclasts is responsible for the constant but subtle reshaping of bone. (Figure) reviews the bone cells, their functions, and locations.
|Osteogenic cells||Develop into osteoblasts||Deep layers of the periosteum and the marrow|
|Osteoblasts||Bone formation||Growing portions of bone, including periosteum and endosteum|
|Osteocytes||Maintain mineral concentration of matrix||Entrapped in matrix|
|Osteoclasts||Bone resorption||Bone surfaces and at sites of old, injured, or unneeded bone|
Compact and Spongy Bone
The differences between compact and spongy bone are best explored via their histology. Most bones contain compact and spongy osseous tissue, but their distribution and concentration vary based on the bone’s overall function. Compact bone is dense so that it can withstand compressive forces, while spongy (cancellous) bone has open spaces and supports shifts in weight distribution.
Compact bone is the denser, stronger of the two types of bone tissue ((Figure)). It can be found under the periosteum and in the diaphyses of long bones, where it provides support and protection.
The microscopic structural unit of compact bone is called an osteon , or Haversian system. Each osteon is composed of concentric rings of calcified matrix called lamellae (singular = lamella). Running down the center of each osteon is the central canal , or Haversian canal, which contains blood vessels, nerves, and lymphatic vessels. These vessels and nerves branch off at right angles through a perforating canal , also known as Volkmann’s canals, to extend to the periosteum and endosteum.
The osteocytes are located inside spaces called lacunae (singular = lacuna), found at the borders of adjacent lamellae. As described earlier, canaliculi connect with the canaliculi of other lacunae and eventually with the central canal. This system allows nutrients to be transported to the osteocytes and wastes to be removed from them.
Spongy (Cancellous) Bone
Like compact bone, spongy bone , also known as cancellous bone, contains osteocytes housed in lacunae, but they are not arranged in concentric circles. Instead, the lacunae and osteocytes are found in a lattice-like network of matrix spikes called trabeculae (singular = trabecula) ((Figure)). The trabeculae may appear to be a random network, but each trabecula forms along lines of stress to provide strength to the bone. The spaces of the trabeculated network provide balance to the dense and heavy compact bone by making bones lighter so that muscles can move them more easily. In addition, the spaces in some spongy bones contain red marrow, protected by the trabeculae, where hematopoiesis occurs.
Skeletal System: Paget’s Disease Paget’s disease usually occurs in adults over age 40. It is a disorder of the bone remodeling process that begins with overactive osteoclasts. This means more bone is resorbed than is laid down. The osteoblasts try to compensate but the new bone they lay down is weak and brittle and therefore prone to fracture.
While some people with Paget’s disease have no symptoms, others experience pain, bone fractures, and bone deformities ((Figure)). Bones of the pelvis, skull, spine, and legs are the most commonly affected. When occurring in the skull, Paget’s disease can cause headaches and hearing loss.
What causes the osteoclasts to become overactive? The answer is still unknown, but hereditary factors seem to play a role. Some scientists believe Paget’s disease is due to an as-yet-unidentified virus.
Paget’s disease is diagnosed via imaging studies and lab tests. X-rays may show bone deformities or areas of bone resorption. Bone scans are also useful. In these studies, a dye containing a radioactive ion is injected into the body. Areas of bone resorption have an affinity for the ion, so they will light up on the scan if the ions are absorbed. In addition, blood levels of an enzyme called alkaline phosphatase are typically elevated in people with Paget’s disease.
Bisphosphonates, drugs that decrease the activity of osteoclasts, are often used in the treatment of Paget’s disease. However, in a small percentage of cases, bisphosphonates themselves have been linked to an increased risk of fractures because the old bone that is left after bisphosphonates are administered becomes worn out and brittle. Still, most doctors feel that the benefits of bisphosphonates more than outweigh the risk the medical professional has to weigh the benefits and risks on a case-by-case basis. Bisphosphonate treatment can reduce the overall risk of deformities or fractures, which in turn reduces the risk of surgical repair and its associated risks and complications.
Blood and Nerve Supply
The spongy bone and medullary cavity receive nourishment from arteries that pass through the compact bone. The arteries enter through the nutrient foramen (plural = foramina), small openings in the diaphysis ((Figure)). The osteocytes in spongy bone are nourished by blood vessels of the periosteum that penetrate spongy bone and blood that circulates in the marrow cavities. As the blood passes through the marrow cavities, it is collected by veins, which then pass out of the bone through the foramina.
In addition to the blood vessels, nerves follow the same paths into the bone where they tend to concentrate in the more metabolically active regions of the bone. The nerves sense pain, and it appears the nerves also play roles in regulating blood supplies and in bone growth, hence their concentrations in metabolically active sites of the bone.
Watch this video to see the microscopic features of a bone.
A hollow medullary cavity filled with yellow marrow runs the length of the diaphysis of a long bone. The walls of the diaphysis are compact bone. The epiphyses, which are wider sections at each end of a long bone, are filled with spongy bone and red marrow. The epiphyseal plate, a layer of hyaline cartilage, is replaced by osseous tissue as the organ grows in length. The medullary cavity has a delicate membranous lining called the endosteum. The outer surface of bone, except in regions covered with articular cartilage, is covered with a fibrous membrane called the periosteum. Flat bones consist of two layers of compact bone surrounding a layer of spongy bone. Bone markings depend on the function and location of bones. Articulations are places where two bones meet. Projections stick out from the surface of the bone and provide attachment points for tendons and ligaments. Holes are openings or depressions in the bones.
Bone matrix consists of collagen fibers and organic ground substance, primarily hydroxyapatite formed from calcium salts. Osteogenic cells develop into osteoblasts. Osteoblasts are cells that make new bone. They become osteocytes, the cells of mature bone, when they get trapped in the matrix. Osteoclasts engage in bone resorption. Compact bone is dense and composed of osteons, while spongy bone is less dense and made up of trabeculae. Blood vessels and nerves enter the bone through the nutrient foramina to nourish and innervate bones.
The Bends(Decompression Syndromes)
Nitrogen or any gas from a diver's air tank increases in pressure as a diver descends. For every 33 feet in ocean water, the pressure due to nitrogen goes up another 11.6 pounds per square inch. As the pressure due to nitrogen increases, more nitrogen dissolves into the tissues. The longer a diver remains at depth, the more nitrogen dissolves. Unlike the oxygen in the air tank a diver uses to swim underwater, the nitrogen gas is not utilized by the body and builds up over time in body tissues. The underlying cause of symptoms throughout the body is due mainly to nitrogen bubbles being released when the diver returns to sea level and blocking blood flow and disrupting blood vessels and nerves by stretching or tearing them. They may also cause emboli, blood coagulation and the release of vasoactive compounds.
A clear example to illustrate this bubble formation process is that of a bottle of carbonated soda. A bottle of carbonated soda is filled with gas (carbon dioxide), which cannot be seen because it is dissolved in solution under pressure. When the bottle is opened, the pressure is released and the gas leaves the solution in the form of bubbles. A diver returning to the surface is similar to opening the bottle of soda. As a diver swims to the surface, the pressure decreases. The nitrogen, which has dissolved in tissues, wants again to leave, because the body can hold only a certain amount based on that nitrogen pressure.
- If a diver surfaces too fast, the excess nitrogen will come out rapidly as gas bubbles. Depending on which organs are involved, these bubbles produce the symptoms of decompression sickness.
- The risk of decompression illness is directly related to the depth of the dive, the amount of time under pressure, and the rate of ascent. Dive tables, such as the U.S. Navy Dive Tables, provide general guidelines as to what depths and dive times are less risky for the development of decompression sickness.
Symptoms of the Bends
The nervous and musculoskeletal system are most often affected. If divers are going to develop symptoms, they will show within 48 hours in all cases. Most have symptoms within 6 hours, while some develop them within the first hour of surfacing from a dive.
DCS is often categorized into two types. Type I indicating mild symptoms and Type II with neurologic and other serious symptoms.
Symptoms of the bends include the following:
Musculoskeletal Symptoms (most common symptoms)
- Pain in and around major joints with the shoulder and elbows being the most commonly affected in divers, but any joint can be involved due to nitrogen being released into the joints and muscles.
- Rashes that are red or marbled may occur. They can be very itchy also.
- It is rare to have skin findings with DCS.
Itching (also known as "the creeps")
- Seen more commonly during decompression in hyperbaric chamber workers (see media photos)
- Very itchy reaction on the skin that is exposed to pressures of the dive (i.e. not covered up by a wet suit)
- This is due to gas from the chamber dissolving into the skin and forming bubbles under the skin.
- The creeps do not occur in divers.
The Chokes (pulmonary or lung decompression sickness)
- Rare but if it occurs can be very serious
- A burning pain in the chest that is usually worse with breathing in (inspiration).
- Other symptoms include cough, difficulty breathing, and cyanosis (blue lips and skin).
- Divers with the chokes can progress to shock rapidly.
Neurologic Decompression Sickness (these symptoms may be the only DCS signs)
- The most common area affected in divers is the spinal cord.
- Symptoms classically include low back pain, "heaviness" of the legs, paralysis and/or numbness of the legs, and even loss of control of the sphincter (or valve) that controls urine and stool resulting in incontinence.
- Other symptoms may include fatigue, weak or numb upper extremities, chest or abdominal pains.
- DCS involving the brain can present with dizziness, confusion, decreased awareness, loss of consciousness, loss or limited vision and even difficulty with balance and/or walking.
Lymph nodes (glands)
The lymph glands can be swollen and painful.
Pain can occur at the head, neck, or torso. Pain at these sites versus the arms or legs carries a worse prognosis.
Occasionally someone with decompression illness may have symptoms suggesting an inner ear problem, such as a spinning sensation, deafness, ringing in the ears, or vomiting. This group of symptoms is called the "staggers."
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When to Seek Medical Care
Anyone reporting signs or symptoms of decompression illness that began within 48 hours of scuba diving should be seen by a doctor at an emergency care facility immediately.
The doctor will likely presume that a victim reporting symptoms within 48 hours of surfacing from a scuba dive to have decompression illness. It is important to inform the doctor of your recent diving experience and of your symptoms.
The Bends Self-Care at Home
Rescue the diver from the water and provide emergency care within the limits of your training.
- Dry and rewarm the diver with blankets if hypothermia (drop in body temperature) develops.
- If you have access to oxygen, a mask should be applied to deliver high-flow oxygen to the individual with symptoms.
- You can visit the Divers Alert Network website or call them in the United States at (919) 684-9111 to determine where the nearest hyperbaric chamber is located.
- Transport the person in a supine position (horizontal, lying on his or her back) to an emergency care facility. If a hyperbaric chamber is available, you may coordinate to transport directly to that facility for definitive care.
- If air transport is used, attempt to find an air frame that can transport the diver below 1,000 feet or is able to be pressurized to sea level pressure. Use high-flow oxygen if it is available during transport.
Treatment for the Bends
The bends are treated in a hyperbaric recompression chamber.
The Bends Medical Treatment
The doctor will first treat immediate life threats, such as breathing problems or shock, if present.
- The diver will need high-flow oxygen and IV fluids. Blood and urine will be sent for laboratory tests to assess any blood clotting problems and hydration status.
- The diver will likely need to go to a hyperbaric chamber for recompression. During recompression, the chamber becomes pressurized with air and oxygen based on prearranged protocols to simulate pressure depths of 30 to 60 feet. The duration of "the dive" within the chamber varies, but can be up to 12 hours and sometimes longer. At this depth or chamber pressure, bubbles are reduced in size or reabsorbed to ensure adequate blood flow. Recompression prevents further bubble formation and provides high amounts of oxygen to the injured tissues. Further treatments depend on how the diver responds to the initial treatment.
- Often the person is admitted to the hospital to monitor medical condition and to ensure that there is no recurrence of symptoms.
The Bends Follow-Up
Follow up immediately for any further signs or symptoms of decompression illness within the next 7 days. After suffering decompression sickness, individuals should not dive again until cleared by a doctor. Depending on the severity of symptoms, and if the person has suffered decompression sickness before, the doctor will likely recommend not to dive again or to avoid diving for some amount of time.
The Bends Prevention
Decompression illness or the bends and other types of barotrauma (decompression sickness) may be prevented by following guidelines for diving taught in professional diving courses.
The following actions increase risk of developing decompression illness:
- Diving outside dive table recommendations
- Flying within 18 hours after diving: Most experts consider it reasonably safe to fly 12 hours after the last dive if the person only dove once, dove easily within the dive tables, and no decompression stop was required. For more complicated diving, waits of 48 hours have been recommended. In general, the longer a person waits to fly after diving, the lower the risk of developing decompression sickness. Even long waits, however, do not reduce the risk all the way to zero. Data collected by DAN (Divers Alert Network) from 1987 to 1999, showed that 17% of divers in the DAN injury database had their first symptoms of DCS either during or after flying.
- Diving in cold water (nitrogen is lipid-soluble)
- Recent alcohol intoxication
- Vigorous exertion while diving
- Multiple repetitive dives
- Jogging or other heavy exercise within 6 hours of a dive
The Bends Prognosis
Prognosis or outlook of people who develop the bends varies with the following factors:
Mycobacterium marinum (M. marinum) is a slow-growing atypical mycobacterium that is commonly found in bodies of fresh or saltwater in many parts of the world. Skin infections with Mycobacterium marinum in humans are relatively uncommon and are usually acquired from contact with contents of aquariums or fish. Most infections occur following skin exposure to the bacteria through a small cut or skin scrape. The first signs of infection with M. marinum include a reddish or tan skin bump called a granuloma. Less commonly, a string or batch of the small reddish bumps crop up on the exposed body area in a classic pattern called sporotrichotic lymphangitis.
It is somewhat rare to acquire this infection from well-maintained swimming pools because of protection afforded by proper chlorination. Mycobacterium marinum does not typically grow at normal body temperature, which is why it remains localized to the cooler skin surface. Overall, diagnosis and treatment of this unusual skin infection is often delayed because of a lack of suspicion for this atypical mycobacterium versus more common bacteria like Staphylococcus .
What are other names for Mycobacterium marinum infections?
Some synonyms for Mycobacterium marinum skin infections include tropical fish granuloma, fish tank granuloma and fish tank granuloma.
How common is Mycobacterium marinum?
Although rare, infections can occur worldwide, most commonly in individuals with occupational and recreational exposure to fresh or saltwater. In the United States, infections caused by M. marinum are rare. The infection is very rare in children and is typically a disease of adults, although any person, regardless of age, may become infected.
Mycobacterium marinum Symptoms & Signs
Bumps on the Skin
People often describe localized swollen areas on, or under, the skin as lumps or bumps. While bumps on, or under, the skin may result from conditions that give rise to a skin rash, many other conditions can result in solitary raised lumps on the skin. Infections, tumors, and the body's response to trauma or injury can all lead to lumps or bumps that appear to be located on or underneath the skin.
How does a person get infected with Mycobacterium marinum?
Human infections with M. marinum under normal circumstances are rare. People are prone to this infection when there is minor trauma to an extremity like the forearm before or during contact with marine animals like fish or turtles, or just an aquarium, saltwater or freshwater.
However, people who have minor breaks in the skin such as small cuts or scrapes are at increased risk
- when in contact with water from an aquarium or fish tank,
- when handling, cleaning, or processing fish,
- while swimming or working in fresh or salt water, or
- while standing in contaminated water.
One form of the infection, known as "swimming pool granuloma," can occur when there is inadequate chlorination of swimming pools. However, in the U.S., most human infections with this bacteria have been associated with contact with fish tanks.
Are Mycobacterium marinum infections contagious?
M. marinum infection is not contagious it is not spread from person to person. It is also not transmitted in hospitals like other common bacteria.
Who is at risk for Mycobacterium marinum infection?
People at highest risk include home-aquarium hobbyists, swimmers, aquarium workers, marine-life handlers, anglers, and oyster workers. Overall, anyone with frequent or persistent saltwater or freshwater exposure is at potential risk. Here is a list of at risk people:
- personal home-aquarium owners
- professionals who clean aquariums
- marine biologists
- fishermen and workers exposed to saltwater fish
- immunocompromised patients (HIV/AIDS)
What are the symptoms of Mycobacterium marinum infection?
Typically, patients may initially notice a small red bump or non-healing red sore on their skin a few weeks after a history of exposure to non-chlorinated water. Ninety percent of the cases involve the arms (upper extremities). They may remember getting a scratch, scrape, or puncture wound several weeks before while in the water. Many people may easily overlook the early signs and try over-the-counter antibiotic creams and disinfectants on their own in an attempt to make the bump or sore go away. Often, patients may not decide to go to their physician until they can't get rid of the bump for weeks or months, when they see more bumps, or when they see spreading bumps in a "line" pattern up their arm or leg.
Some patients may feel no pain or itch while others commonly have some localized pain and firmness at the site of the infection. Most otherwise healthy people overall feel well during the infection and do not have fever or chills.
Patients in poor health or those with other health issues like an impaired immune system or other serious illnesses may experience fever, enlarged localized lymph nodes, and systemic infection.
When M. marinum infects the skin, it causes localized microscopic nodules to form. These nodules are called granulomas. They occur at sites of skin trauma where there are scratches, cuts, and the like.
The granulomas slowly increase in size usually become visible within two to three weeks of exposure. Some reported cases have developed two to four months or more after exposure to M. marinum because of the very slow-growing nature of this bacterium.
The most frequent sign is a slowly developing nodule (raised bump) at the site the bacteria entered the body. Frequently, the nodule is on the hand or upper arm. Later the nodule can become an enlarging sore (an ulcer). Swelling of nearby lymph nodes occurs. Multiple granulomas may form in a line along the lymphatic vessel that drains the site. These lesions will usually spontaneously heal in several months. This infection can also involve the joints (septic arthritis) and bones (osteomyelitis).
A health-care provider should be consulted if a skin nodule or reddened sore (ulcer) develops following direct skin contact with fresh or saltwater or after handling or processing fish.
For people with compromise of the immune system, M. marinum infection can be especially serious and involve disseminated (widespread) disease. If an infection is suspected under such circumstances, a health-care provider should be promptly consulted.
The skin covers the entire external surface of the human body and is the principal site of interaction with the surrounding world. It serves as a protective barrier that prevents internal tissues from exposure to trauma, ultraviolet (UV) radiation, temperature extremes, toxins, and bacteria. Other important functions include sensory perception, immunologic surveillance, thermoregulation, and control of insensible fluid loss.
The integument consists of 2 mutually dependent layers, the epidermis and dermis, which rest on a fatty subcutaneous layer, the panniculus adiposus. The epidermis is derived primarily from surface ectoderm but is colonized by pigment-containing melanocytes of neural crest origin, antigen-processing Langerhans cells of bone marrow origin, and pressure-sensing Merkel cells of neural crest origin. The dermis is derived primarily from mesoderm and contains collagen, elastic fibers, blood vessels, sensory structures, and fibroblasts.  See the image below.
During the fourth week of embryologic development, the single cell thick ectoderm and underlying mesoderm begin to proliferate and differentiate. The specialized structures formed by the skin, including teeth, hair, hair follicles, fingernails, toenails, sebaceous glands, sweat glands, apocrine glands, and mammary glands also begin to appear during this period in development. Teeth, hair, and hair follicles are formed by the epidermis and dermis in concert, while fingernails and toenails are formed by the epidermis alone. Hair follicles, sebaceous glands, sweat glands, apocrine glands, and mammary glands are considered epidermal glands or epidermal appendages, because they develop as downgrowths or diverticula of the epidermis into the dermis. [1, 2]
The definitive multi-layered skin is present at birth, but skin is a dynamic organ that undergoes continuous changes throughout life as outer layers are shed and replaced by inner layers. Skin also varies in thickness among anatomic location, sex, and age of the individual. This varying thickness primarily represents a difference in dermal thickness, as epidermal thickness is rather constant throughout life and from one anatomic location to another. Skin is thickest on the palms and soles of the feet (1.5 mm thick), while the thinnest skin is found on the eyelids and in the postauricular region (0.05 mm thick).
Male skin is characteristically thicker than female skin in all anatomic locations. Children have relatively thin skin, which progressively thickens until the fourth or fifth decade of life when it begins to thin. This thinning is also primarily a dermal change, with loss of elastic fibers, epithelial appendages, and ground substance.