By X. Mine-Boss. University of Mary Washington. 2019.
This is a transverse section through the wall of the esophagus at or near the junction of its upper and middle segments buy 160mg malegra fxt plus mastercard. For orientation purposes buy 160mg malegra fxt plus free shipping, identify the following successive layers in the esophageal wall: (1) an inner lining of non- keratinized stratified squamous epithelium cheap 160mg malegra fxt plus free shipping; (2) an adjacent loose connective tissue layer generic malegra fxt plus 160 mg on line; (3) a layer Skeletal muscle top, smooth muscle bottom formed by smooth muscle fibers (which have been cut in cross-section); (4) a subjacent connective tissue layer containing large blood vessels; (5) smooth and skeletal muscle fibers cut in longitudinal or oblique section; and (6) an outer layer rich in adipose cells and blood vessels. Using higher magnification, examine the muscle layers and notice that the musculature is skeletal mixed with bundles of smooth muscle fibers due to the level of the esophagus at which this section was taken. In cross-section note that the skeletal muscle fibers resemble rounded polygons separated by the endomysium with the nuclei clearly visible the periphery. Why do smooth muscle fibers in cross section have different diameters and why do some of these fail to show nuclei? During this lab, become familiar with the morphology of mature peripheral blood cells and study the stages of blood development. The cellular or formed elements of peripheral blood are classified according to the details of their appearance following staining with polychromic stains, e. After finding an area that is well smeared and well stained, use the highest magnification to examine the blood cells, particularly the leukocytes. This slide does not have basophils, which account for less than one percent of the total number of leukocytes. There are stem cells that are precursors of both the red and white blood cell series, however because their proportion in bone marrow is low it is unlikely that you will be able to recognize them in your slides. The student should bear in mind that the frequency of any given cell type or stage of differentiation in the marrow is a complex function related to the relative frequency of the cells in the blood, to the half life of the cell type in the circulation, and to the maturation time of the cells in the marrow. The most frequent precursor series is the erythroid cell series, followed closely by the neutrophilic series. Distinctions between the cells of the granulocytic series are based on nuclear morphology and the size and staining properties of the granules. Criteria for evaluating cell type and stage of maturation are as follows: Size of the cell and its nucleus: In general there is a gradual decrease in size of the cell and its nucleus with maturation. Appearance of the chromatin network in the nucleus: Immature cells have a delicate fine- meshed chromatin network. Presence or absence of nucleoli: Nucleoli are visible as pale blue circular areas within the chromatin network of immature cells. Cytoplasmic basophilia: Very immature cells have pale blue cytoplasm, due to the presence of only a few scattered ribosomes. Specialized cell products: Accumulation of hemoglobin in erythroid cells, and the appearance of granules and their type in granulocytes. Basophilic erythroblast - This cell is usually smaller and the nucleus, which is intensely heterochromatic, is centrally located. The cytoplasm is a deeper blue color than that of the proerythroblast, due to the mixture of abundant free ribosomes and the initiation of hemoglobin synthesis. Polychromatophilic erythroblast - The nucleus is intensely heterochromatic, and the cytoplasm is now a characteristic lilac color. The basophilia is due to the cytoplasmic ribosomes, and the acidophilia is due to the increase in the 38 amount of hemoglobin being synthesized by the ribosomes. Normoblast (orthochromatic erythroblast) - The nucleus has become pyknotic and therefore is very dark in appearance. Occasionally there is still some residual basophilia in the cytoplasm of these cells, due to the retention of some ribosomes. Such immature red cells are called reticulocytes because of the so-called reticulated pattern of cytoplasmic basophilia. Under normal conditions, a small percentage of reticulocytes enter the circulation before completing their maturation. However, when there is a great increase in erythrocyte production the percentage of reticulocytes entering the blood increases. The myeloblast is a large cell with a large ovoid pale-staining nucleus, 2 to 5 nucleoli, and lightly basophilic cytoplasm (due to a scattering of ribosomes). Promyelocyte: This large cell is very similar to a myeloblast, but can be distinguished by the presence of a few azurophilic granules (pink-purple, primary lysosomes) in its cytoplasm. Myelocyte: The promyelocyte in turn gives rise to eosinophilic, neutrophilic and basophilic myelocytes, which have both azurophilic and specific granules according to their respective cell line. These cells can be identified by the round nucleus and by the accumulation of specific granules in their cytoplasm. Metamyelocytes: This stage can be identified by the indented nucleus and the presence of their specific cytoplasmic granules. You may be able to identify the unstained image of the Golgi complex in the region where the nucleus is indented. Mature granulocytes: The mature cells can be recognized by their complex nuclear morphologies and their specific granules. Do not confuse the fine granules of the neutrophil (which may appear lightly acidophilic) for the coarser granules of eosinophils or basophils. The most immediately obvious cell type will be the enormous megakaryocyte which gives rise to blood platelets. Choose an area of this slide where the cells are not too closely smeared to study the cells of the erythroid and granulocyte series. You should be able to assign a well-fixed and well-stained cell to either the erythrocyte or granulocyte line of development. If a cell in the granulocyte line already has specific granules it should be further classified into the neutrophilic, eosinophilic, or basophilic series and based on its nuclear morphology, whether it is a myelocyte, metamyelocyte, or a mature cell. Be sure you know the biochemical composition of the cytoplasmic granules of neutrophils (polymorphonuclear leukocytes), eosinophils, and basophils. The cells of the erythroid and myeloid series tend to be grouped in small foci and that within each group the cells tend to be at the same stage of development. What is the functional significance of the cytoplasmic staining affinities of the basophilic erythroblast, polychromatophilic erythroblast, normoblast and erythrocyte? Know the structure and function of the lymphoid tissues and organs: (including afferent and efferent flow and specialized vasculature) a. B cells (as well as monocytes, erythrocytes, granulocytes, and megakaryoctyes) remain in the bone marrow as they mature. Lymphatic vessels carry lymph fluid, which contains particulate matter and protein that escape from blood capillaries as well as ingested fats, microorganisms, and other antigenic material that penetrate epithelial surfaces. Lymph is filtered in lymph nodes and then returned to the circulation via the thoracic duct and the right lymphatic duct. H & E The tonsillar ring is located near the entrance of the throat and consists of the palatine tonsil (commonly known as "the tonsil"), the pharyngeal tonsil (commonly known as "adenoids”), and the lingual tonsil (on the posterior surface of the tongue) This is a section through the palatine tonsil. Notice the stratified squamous non-keratinized epithelium covering the free oropharyngeal surface of the tonsil. In the underlying lamina propria identify simple and branched epithelial crypts sectioned in different planes and representing tubular invaginations of the surface epithelium. The lining epithelium of the crypts may show evidence of keratinization or erosion and can be obscured when heavily infiltrated with lymphocytes. Between the crypts identify the masses of lymphoid tissue containing numerous individual lymphoid nodules. Identify the connective tissue septa that extend at intervals between the crypts and Crypt Germinal center divide the tonsil into lobules, each with an 41 individual crypt as an axis. It occurs in three forms: diffuse lymphatic tissue, solitary lymphatic nodules, and aggregates of lymphatic nodules. The reticular fibers, stained black by the silver reticulum stain, are arranged in loose spidery meshworks. The connective tissue capsule stained red-brown by the counterstain and covered on its external surface by loose connective tissue in which there are fat cells, blood vessels and some afferent lymphatic vessels with delicate valves. Connective tissue trabeculae, stained red-brown and extending from the capsule into the cortical region. The medulla, characterized by lymphoid tissue arranged in branching and anastomosing medullary cords and medullary sinuses. An indented region, the hilum, which is surrounded by the medulla and contains connective tissue, a few fat cells, blood vessels, nerve bundles and large efferent lymphatic vessels with delicate valves to prevent the backup of lymph into the node. In the cortex examine the germinal centers and the dark surrounding zone within the lymphatic nodules. The dark zone surrounding the germinal center is composed of densely packed small and medium-sized lymphocytes, separated from each other by layers of flattened pale- staining reticular cells.
Before giving the drugs to make the patient sleep you should let him/her breathe 100% oxygen buy malegra fxt plus 160 mg visa, which will be used as a reserve during the time of intubation order malegra fxt plus visa. Induction can be performed: • With intravenous anesthetic agents: Ketamine + Atropine or Thiopentone • With inhalation agent (e buy 160mg malegra fxt plus mastercard. Halothane) After the patient is induced malegra fxt plus 160mg low cost, the anesthesia can be continued with intubation or with out (mask ventilation or spontaneous breathing). Endo tracheal intubation: It is a technique of passing an endotracheal tube into the trachea of the patient for securing the airway, and to make easier ventilation. For Intubation the patient should be adequately relaxed with inhalation agent or muscle relaxant. The relaxant used for intubation is Suxamethonium, which has fast onset of action and short effect. Monitoring: During anesthesia it is important to do strict monitoring of heart beat, blood pressure, respiration, temperature, fluid balance and urine output. The carrier gas for volatile anesthetic agent can be atmospheric air or oxygen from compressed source depending on the type of Anesthesia machine in use. Recovery and Extubation: During recovery phase the patient recovers from: • Inhalation agents by exhalation and/or metabolism • Ketamine by excretion and metabolism • Muscle relaxants by excretion and/or metabolism and/or reversal with neostigmine Before extubation • Be sure that the patient is breathing adequately (reversed from relaxant) • Suck oropharyngeal secretion • Deflate the cuff (which is used for adults) and remove the endotracheal tube Transportation and immediate postoperative care: • Transport in the recovery position • Check and observe closely the pulse rate, blood pressure, respiratory rate, urine output hourly, any abnormal and continuing blood loss and presence of pain. Because of these reasons it can be used alone for short procedures and surgery, which does not require relaxation and intubation. Dose and route of administration: Intramuscular: 5-10 mg/kg Intravenous: 1-2 mg/kg The effect of one single dose lasts for about 15 min. Treatment of systemic toxicity • The best treatment of systemic toxicity is prevention by meticulous attention to technique and recognition of intravascular injection. Commonly used local anesthetic drugs 118 Lidocaine (Xylocaine) 1%, 2% or 5% with or without Adrenaline in dose of: With Adrenaline: 7 mg/kg Without Adrenaline: 3 mg/kg • Bupivacaine (Carbosthesin, Marcain) 0. The level of lumbar puncture is at the rd th interspaces between the 3 and 4 lumbar vertebrae. Turn the patient to a supine position with pillow under the head in the case of heavy (hyperbaric) local anesthetic drug. Complications of spinal anesthesia and measures to take • Drop in blood pressure-due to high spinal block - Give Oxygen - Make faster the drip if that does not help. Commonly performed nerve blocks: o Digital nerve block o Axillary block of the brachial plexus o Wrist-block 122 C) Field block Field block is injection of local analgesic so as to create a zone of analgesia around the operative field. It can be used for: o Repair of an inguinal hernia o Caesarean section o Circumcision D) Infiltration Infiltration is direct injection of drugs into the area to be incised and between bone ends in fractures. E) Topical anesthesia This can be performed simply by applying 4% lidocaine to the mucus membrane, for minor surgery and instrumentation of: o Nose o Mouth o Eye o Pharynx and larynx o Urethral procedures 123 Review Questions 1. After evaluation by the surgeon, it is decided to take him to the operating theater. A 17 year old girl is brought to the Emergency department with polytrauma after a car accident. L Bartholomeusz: Safe Anesthesia: A Training manual, where facilities are limited. Outline management options for thyroid carcinomas Thyroid Enlargement: Goiter Goiter refers to a generalized enlargement of the thyroid gland which is normally impalpable. Inflammatory • Autoimmune (chronic lymphocyte thyroiditis, Hashimoto’s disease) • Infectious • Acute (bacterial thyroiditis, viral,) • Chronic (tuberculous, syphilitic) 126 Simple Goiter Patho-physiology: Simple Goiter is enlargement of the thyroid gland as a result of stimulation of the thyroid gland by high levels of circulating thyroid stimulating hormone. Defective hormone synthesis also cause goiter and it accounts for many sporadic goiters. In endemic goiter, it usually occurs at puberty when metabolic demands are high, this is reversible if stimulations cease. As a result of fluctuating stimulation of the thyroid gland, areas of active lobule and inactive lobules will develop. Active lobules become more vascular and hyperplasic until hemorrhage occurs causing necrosis. These necrotic lobules coalesce to form nodules filled with either iodine free colloid or inactive follicles. Secondary changes like cystic degeneration, hemorrhage and calcification occur at late stages. Diagnosis Clinical presentation: Discrete swelling in one lobe with no palpable abnormality else where is called solitary (isolated) nodule. The Goiter is painless and freely moves with swallowing and usually patients are euthyroid. Complications • Tracheal obstruction can occur due to gross lateral displacement or compression. Prevention and treatment Prevention In endemic areas the incidence of goiter can be significantly reduced by the introduction of iodized salt. In early stages, a hyper-plastic goiter may regress if thyroxin is given in a dose of 0. Operation might be indicated • On cosmetic grounds • Tracheal compression and • When malignancy cannot be excluded The options of surgical treatment are • Near total thyroidectomy • Subtotal thyroidectomy Toxic goiters Thyrotoxicosis - is a condition in which there is increased metabolic rate due to high level of circulating thyroid hormone. Clinical features The most significant symptoms are • Loss of weight in spite of good appetite, • A recent preference of cold • Palpitation. The most important clinical signs of thyrotoxicosis commonly seen are • excitability of the patient, • the presence of goiter, • hot and moist palms, • exophthalmus in primary type • tachycardia with cardiac arrhythmia 128 • Weakness of the proximal limb muscles • The goiter in primary thyrotoxicosis (Grave’s disease) is diffuse and vascular, it may be large or small, firm or soft and bruit may be present. Diffuse toxic goiter: Primary toxic goiter or Grave’s disease is a diffuse vascular goiter appearing at the same time as symptoms of hyperthyroidism. The hypertrophy and hyperplasia are due to abnormal thyroid stimulating antibodies Toxic nodular goiter: A simple nodular goiter is present for a long time before the hyperthyroidism, and hence termed secondary thyrotoxicosis. It is usually seen in middle aged or elderly people and less frequently associated with eye signs. In many cases of toxic nodular goiter, the nodules are inactive and it is the intermediate thyroid tissue that is involved in hyper secretion. Toxic nodule: This is a solitary hyperactive nodule which may be part of a generalized nodularity or a true toxic adenoma. It is autonomous and its hypertrophy and hyperplasia are not due to thyroid stimulating antibodies. Diagnosis of thyrotoxicosis • Most cases are easily diagnosed by the clinical picture. This helps to determine the functional activity relative to the surrounding gland according to isotope uptake. Treatment of thyrotoxicosis Treatment of thyrotoxicosis includes specific and non-specific measures. The specific measures are • the use of antithyroid drugs • surgery • radioiodine The nonspecific measures which include rest and sedation are not commonly recommended. But it should be clear that antithyroid drugs cannot cure a toxic nodule since the overactive thyroid tissue is autonomous and recurrence of the hyperthyroidism is certain when the drug is discontinued. Surgery: Surgery cures thyrotoxicosis by reducing the mass of overactive tissue below critical mass. Preoperatively, the patient must be prepared with antithyroid drugs so that the patient becomes euthyroid. Post-operative complications • Hemorrhage - a tension hematoma may develop deep to the cervical fascia – which is potentially life threatening • Respiratory obstruction - can occur due to laryngeal edema or secondary to tension hematoma. It occurs if a thyrotoxic patient has been inadequately prepared for thyroidectomy. Neoplasms of the thyroid Classification of thyroid neoplasm Benign: follicular adenoma Malignant: Primary - Follicular epithelial: follicular, papillary, anaplastic - Para follicular epithelium: medullary - Lymphoid cells: lymphoma Secondary -M etastatic - Local infiltrations 130 Benign tumors Follicular adenomas present as clinically solitary nodules and the distinction between a follicular carcinoma and an adenoma can only be made by histological examination. Malignant Tumors Clinical feature: The commonest presenting symptom is • thyroid swelling • Enlarged cervical lymph node may be the presentation of papillary carcinomas. Prognosis: Prognosis is influenced by histological type, age, extra thyroid spread, and size of tumor. With regard to age, males of more than 40 years of age and females over 50 years have worse prognosis. Local infiltration is an early feature of these tumors with spread by lymphatics and blood stream.
Early induced Proteins Early induced proteins are those that are not constitutively present in the body order malegra fxt plus 160mg, but are made as they are needed early during the innate immune response order 160 mg malegra fxt plus overnight delivery. Cells infected with viruses secrete interferons that travel to adjacent cells and induce them to make antiviral proteins buy genuine malegra fxt plus online. Other early induced proteins specific for bacterial cell wall components are mannose-binding protein and C-reactive protein cheap 160mg malegra fxt plus amex, made in the liver, which bind specifically to polysaccharide components of the bacterial cell wall. Phagocytes such as macrophages have receptors for these proteins, and they are thus able to recognize them as they are bound to the bacteria. This brings the phagocyte and bacterium into close proximity and enhances the phagocytosis of the bacterium by the process known as opsonization. Opsonization is the tagging of a pathogen for phagocytosis by the binding of an antibody or an antimicrobial protein. Complement System The complement system is a series of proteins constitutively found in the blood plasma. As such, these proteins are not considered part of the early induced immune response, even though they share features with some of the antibacterial proteins of this class. Made in the liver, they have a variety of functions in the innate immune response, using what is known as the “alternate pathway” of complement activation. Additionally, complement functions in the adaptive immune response as well, in what is called the classical pathway. The complement system consists of several proteins that enzymatically alter and fragment later proteins in a series, which is why it is termed cascade. Once activated, the series of reactions is irreversible, and releases fragments that have the following actions: • Bind to the cell membrane of the pathogen that activates it, labeling it for phagocytosis (opsonization) • Diffuse away from the pathogen and act as chemotactic agents to attract phagocytic cells to the site of inflammation • Form damaging pores in the plasma membrane of the pathogen Figure 21. In the alternate pathway, C3 is activated spontaneously and, after reacting with the molecules factor P, factor B, and factor D, splits apart. The larger fragment, C3b, binds to the surface of the pathogen and C3a, the smaller fragment, diffuses outward from the site of activation and attracts phagocytes to the site of infection. The classical pathway is similar, except the early stages of activation require the presence of antibody bound to antigen, and thus is dependent on the adaptive immune response. Phagocytic cells such as macrophages and neutrophils are attracted to an infection site by chemotactic attraction to smaller complement fragments. Additionally, once they arrive, their receptors for surface-bound C3b opsonize the pathogen for phagocytosis and destruction. Stub a toe, cut a finger, or do any activity that causes tissue damage and inflammation will result, with its four characteristics: heat, redness, pain, and swelling (“loss of function” is sometimes mentioned as a fifth characteristic). It is important to note that inflammation does not have to be initiated by an infection, but can also be caused by tissue injuries. The release of damaged cellular contents into the site of injury is enough to stimulate the response, even in the absence of breaks in physical barriers that would allow pathogens to enter (by hitting your thumb with a hammer, for example). The inflammatory reaction brings in phagocytic cells to the damaged area to clear cellular debris and to set the stage for wound repair (Figure 21. The process not only brings fluid and cells into the site to destroy the pathogen and remove it and debris from the site, but also helps to isolate the site, limiting the spread of the pathogen. If the cause of the inflammation is not resolved, however, it can lead to chronic inflammation, which is associated with major tissue destruction and fibrosis. It can be caused by foreign bodies, persistent pathogens, and autoimmune diseases such as rheumatoid arthritis. The released contents of injured cells stimulate the release of mast cell granules and their potent inflammatory mediators such as histamine, leukotrienes, and prostaglandins. Histamine increases the diameter of local blood vessels (vasodilation), causing an increase in blood flow. Histamine also increases the permeability of local capillaries, causing plasma to leak out and form interstitial fluid. Additionally, injured cells, phagocytes, and basophils are sources of inflammatory mediators, including prostaglandins and leukotrienes. Prostaglandins cause vasodilation by relaxing vascular smooth muscle and are a major cause of the pain associated with inflammation. Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen relieve pain by inhibiting prostaglandin production. Many inflammatory mediators such as histamine are vasodilators that increase the diameters of local capillaries. At the same time, inflammatory mediators increase the permeability of the local vasculature, causing leakage of fluid into the interstitial space, resulting in the swelling, or edema, associated with inflammation. Leukotrienes are particularly good at attracting neutrophils from the blood to the site of infection by chemotaxis. Following an early neutrophil infiltrate stimulated by macrophage cytokines, more macrophages are recruited to clean up the debris left over at the site. When local infections are severe, neutrophils are attracted to the sites of infections in large numbers, and as they phagocytose the pathogens and subsequently die, their 996 Chapter 21 | The Lymphatic and Immune System accumulated cellular remains are visible as pus at the infection site. Not only are the pathogens killed and debris removed, but the increase in vascular permeability encourages the entry of clotting factors, the first step towards wound repair. Inflammation also facilitates the transport of antigen to lymph nodes by dendritic cells for the development of the adaptive immune response. However, they slow pathogen growth and allow time for the adaptive immune response to strengthen and either control or eliminate the pathogen. The innate immune system also sends signals to the cells of the adaptive immune system, guiding them in how to attack the pathogen. The Benefits of the Adaptive Immune Response The specificity of the adaptive immune response—its ability to specifically recognize and make a response against a wide variety of pathogens—is its great strength. Antigens, the small chemical groups often associated with pathogens, are recognized by receptors on the surface of B and T lymphocytes. The adaptive immune response to these antigens is so versatile that it can respond to nearly any pathogen. This increase in specificity comes because the adaptive immune 11 response has a unique way to develop as many as 10 , or 100 trillion, different receptors to recognize nearly every conceivable pathogen. The mechanism was finally worked out in the 1970s and 1980s using the new tools of molecular genetics Primary Disease and Immunological Memory The immune system’s first exposure to a pathogen is called a primary adaptive response. Symptoms of a first infection, called primary disease, are always relatively severe because it takes time for an initial adaptive immune response to a pathogen to become effective. Upon re-exposure to the same pathogen, a secondary adaptive immune response is generated, which is stronger and faster that the primary response. The secondary adaptive response often eliminates a pathogen before it can cause significant tissue damage or any symptoms. This secondary response is the basis of immunological memory, which protects us from getting diseases repeatedly from the same pathogen. By this mechanism, an individual’s exposure to pathogens early in life spares the person from these diseases later in life. Self Recognition A third important feature of the adaptive immune response is its ability to distinguish between self-antigens, those that are normally present in the body, and foreign antigens, those that might be on a potential pathogen. As T and B cells mature, there are mechanisms in place that prevent them from recognizing self-antigen, preventing a damaging immune response against the body. These mechanisms are not 100 percent effective, however, and their breakdown leads to autoimmune diseases, which will be discussed later in this chapter. T Cell-Mediated Immune Responses The primary cells that control the adaptive immune response are the lymphocytes, the T and B cells. T cells are particularly important, as they not only control a multitude of immune responses directly, but also control B cell immune responses in many cases as well. Thus, many of the decisions about how to attack a pathogen are made at the T cell level, and knowledge This OpenStax book is available for free at http://cnx. The variable region domain is furthest away from the T cell membrane and is so named because its amino acid sequence varies between receptors. The differences in the amino acid sequences of the variable domains are the molecular basis of the diversity of antigens the receptor can recognize. Thus, the antigen-binding site of the receptor consists of the terminal ends of both receptor chains, and the amino acid sequences of those two areas combine to determine its antigenic specificity. Antigens Antigens on pathogens are usually large and complex, and consist of many antigenic determinants. An antigenic determinant (epitope) is one of the small regions within an antigen to which a receptor can bind, and antigenic determinants are limited by the size of the receptor itself. They usually consist of six or fewer amino acid residues in a protein, or one or two sugar moieties in a carbohydrate antigen.
Hair Color Similar to the skin buy malegra fxt plus 160mg line, hair gets its color from the pigment melanin generic 160 mg malegra fxt plus, produced by melanocytes in the hair papilla generic malegra fxt plus 160 mg with visa. Different hair color results from differences in the type of melanin cheap malegra fxt plus 160 mg online, which is genetically determined. As a person ages, the melanin production decreases, and hair tends to lose its color and becomes gray and/or white. Nails The nail bed is a specialized structure of the epidermis that is found at the tips of our fingers and toes. The nail body is formed on the nail bed, and protects the tips of our fingers and toes as they are the farthest extremities and the parts of the body that experience the maximum mechanical stress (Figure 5. The nail body forms at the nail root, which has a matrix of proliferating cells from the stratum basale that enables the nail to grow continuously. The nail fold that meets the proximal end of the nail body forms the nail cuticle, also called the eponychium. The nail bed is rich in blood vessels, making it appear pink, except at the base, where a thick layer of epithelium over the nail matrix forms a crescent-shaped region called the lunula (the “little moon”). Sweat glands develop from epidermal projections into the dermis and are classified as merocrine glands; that is, the secretions are excreted by exocytosis through a duct without affecting the cells of the gland. These glands are found all over the skin’s surface, but are especially abundant on the palms of the hand, the soles of the feet, and the forehead (Figure 5. They are coiled glands lying deep in the dermis, with the duct rising up to a pore on the skin surface, where the sweat is released. This type of sweat, released by exocytosis, is hypotonic and composed mostly of water, with some salt, antibodies, traces of metabolic waste, and dermicidin, an antimicrobial peptide. Eccrine glands are a primary component of thermoregulation in humans and thus help to maintain homeostasis. An apocrine sweat gland is usually associated with hair follicles in densely hairy areas, such as armpits and genital regions. Apocrine sweat glands are larger than eccrine sweat glands and lie deeper in the dermis, sometimes even reaching the hypodermis, with the duct normally emptying into the hair follicle. In addition to water and salts, apocrine sweat includes organic compounds that make the sweat thicker and subject to bacterial decomposition and subsequent smell. The release of this sweat is under both nervous and hormonal control, and plays a role in the poorly understood human pheromone response. Most commercial antiperspirants use an aluminum-based compound as their primary active ingredient to stop sweat. When the antiperspirant enters the sweat gland duct, the aluminum-based compounds precipitate due to a change in pH and form a physical block in the duct, which prevents sweat from coming out of the pore. Sebaceous Glands A sebaceous gland is a type of oil gland that is found all over the body and helps to lubricate and waterproof the skin and hair. They generate and excrete sebum, a mixture of lipids, onto the skin surface, thereby naturally lubricating the dry and dead layer of keratinized cells of the stratum corneum, keeping it pliable. The fatty acids of sebum also have antibacterial properties, and prevent water loss from the skin in low-humidity environments. The underlying hypodermis has important roles in storing fats, forming a “cushion” over underlying structures, and providing insulation from cold temperatures. It acts as a protective barrier against water loss, due to the presence of layers of keratin and glycolipids in the stratum corneum. It also is the first line of defense against abrasive activity due to contact with grit, microbes, or harmful chemicals. Sweat excreted from sweat glands deters microbes from over-colonizing the skin surface by generating dermicidin, which has antibiotic properties. It provides a barrier between your vital, life-sustaining organs and the influence of outside elements that could potentially damage them. The skin can be breached when a child skins a knee or an adult has blood drawn—one is accidental and the other medically necessary. However, you also breach this barrier when you choose to “accessorize” your skin with a tattoo or body piercing. Because the needles involved in producing body art and piercings must penetrate the skin, there are dangers associated with the practice. These include allergic reactions; skin infections; blood-borne diseases, such as tetanus, hepatitis C, and hepatitis D; and the growth of scar tissue. Despite the risk, the practice of piercing the skin for decorative purposes has become increasingly popular. According to the American Academy of Dermatology, 24 percent of people from ages 18 to 50 have a tattoo. Sensory Function The fact that you can feel an ant crawling on your skin, allowing you to flick it off before it bites, is because the skin, and especially the hairs projecting from hair follicles in the skin, can sense changes in the environment. The hair root plexus surrounding the base of the hair follicle senses a disturbance, and then transmits the information to the central nervous system (brain and spinal cord), which can then respond by activating the skeletal muscles of your eyes to see the ant and the skeletal muscles of the body to act against the ant. The skin acts as a sense organ because the epidermis, dermis, and the hypodermis contain specialized sensory nerve structures that detect touch, surface temperature, and pain. These receptors are more concentrated on the tips of the fingers, which are most sensitive to touch, especially the Meissner corpuscle (tactile corpuscle) (Figure 5. In addition to these specialized receptors, there are sensory nerves connected to each hair follicle, pain and temperature receptors scattered throughout the skin, and motor nerves innervate the arrector pili muscles and glands. The sympathetic nervous system is continuously monitoring body temperature and initiating appropriate motor responses. Recall that sweat glands, accessory structures to the skin, secrete water, salt, and other substances to cool the body when it becomes warm. Even when the body does not appear to be noticeably sweating, approximately 500 mL of sweat (insensible perspiration) are secreted a day. In addition to sweating, arterioles in the dermis dilate so that excess heat carried by the blood can dissipate through the skin and into the surrounding environment (Figure 5. In contrast, the dermal blood vessels constrict to minimize heat loss in response to low temperatures (b). Although the temperature of the skin drops as a result, passive heat loss is prevented, and internal organs and structures remain warm. If the temperature of the skin drops too much (such as environmental temperatures below freezing), the conservation of body core heat can result in the skin actually freezing, a condition called frostbite. Among these changes are reductions in cell division, metabolic activity, blood circulation, hormonal levels, and muscle strength (Figure 5. In the skin, these changes are reflected in decreased mitosis in the stratum basale, leading to a thinner epidermis. The dermis, which is responsible for the elasticity and resilience of the skin, exhibits a reduced ability to regenerate, which leads to slower wound healing. The hypodermis, with its fat stores, loses structure due to the reduction and redistribution of fat, which in turn contributes to the thinning and sagging of skin. Other cells in the skin, such as melanocytes and dendritic cells, also become less active, leading to a paler skin tone and lowered immunity. Wrinkling of the skin occurs due to breakdown of its structure, which results from decreased collagen and elastin production in the dermis, weakening of muscles lying under the skin, and the inability of the skin to retain adequate moisture. In general, these products try to rehydrate the skin and thereby fill out the wrinkles, and some stimulate skin growth using hormones and growth factors. In the presence of sunlight, a form of vitamin D called cholecalciferol is synthesized from a derivative of the steroid cholesterol in the skin. The liver3 converts cholecalciferol to calcidiol, which is then converted to calcitriol (the active chemical form of the vitamin) in the kidneys. Vitamin D is essential for normal absorption of calcium and phosphorous, which are required for healthy bones. The absence of sun exposure can lead to a lack of vitamin D in the body, leading to a condition called rickets, a painful condition in children where the bones are misshapen due to a lack of calcium, causing bowleggedness. Elderly individuals who suffer from vitamin D deficiency can develop a condition called osteomalacia, a softening of the bones. In present day society, vitamin D is added as a supplement to many foods, including milk and orange juice, compensating for the need for sun exposure. These range from annoying but relatively benign bacterial or fungal infections that are categorized as disorders, to skin cancer and severe burns, which can be fatal. Cancer is a broad term that describes diseases caused by abnormal cells in the body dividing uncontrollably. The Skin Cancer Foundation reports that one in five Americans will experience some type of skin cancer in their lifetime. These mutations can result in cell populations that do not die when they should and uncontrolled cell proliferation that leads to tumors.
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