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keywords: description:digital medical library love is medicine digital medical library love is medicineCellular and Molecular Biology of the Kidney
Introduction
The kidney is one of the most highly differentiated organs in the body. At the conclusion of embryologic development, nearly 30 different cell types form a multitude of filtering capillaries and segmented nephrons enveloped by a dynamic interstitium. This cellular diversity modulates a variety of complex physiologic processes. Endocrine functions, the regulation of blood pressure and intraglomerular hemodynamics, solute and water transport, acid-base balance, and removal of drug metabolites are all accomplished by intricate mechanisms of renal response. This breadth of physiology hinges on the clever ingenuity of nephron architecture that evolved as complex organisms came out of water to live on land.
layers
Embryologic Development
Kidneys develop from intermediate mesoderm under the timed or sequential control of a growing number of genes
please see this page
http://www.ivumed.org/video/80
Determinants and Regulation of Glomerular Filtration
Renal blood flow normally drains approximately 20% of the cardiac output, or 1000 mL/min. Blood reaches each nephron through the afferent arteriole leading into a glomerular capillary where large amounts of fluid and solutes are filtered to form the tubular fluid. The distal ends of the glomerular capillaries coalesce to form an efferent arteriole leading to the first segment of a second capillary network (cortical peritubular capillaries or medullary vasa recta) surrounding the tubules. Thus, nephrons have two capillary beds arranged in a series separated by the efferent arteriole that regulates the hydrostatic pressure in both capillary beds. The distal capillaries empty into small venous branches that coalesce into larger veins to eventually form the renal vein.
The hydrostatic pressure gradient across the glomerular capillary wall is the primary driving force for glomerular filtration. Oncotic pressure within the capillary lumen, determined by the concentration of unfiltered plasma proteins, partially offsets the hydrostatic pressure gradient and opposes filtration. As the oncotic pressure rises along the length of the glomerular capillary, the driving force for filtration falls to zero on reaching the efferent arteriole. Approximately 20% of the renal plasma flow is filtered into Bowman's space, and the ratio of glomerular filtration rate (GFR) to renal plasma flow determines the filtration fraction. Several factors, mostly hemodynamic, contribute tothe regulation of filtration under physiologic conditions.
Although glomerular filtration is affected by renal artery pressure, this relationship is not linear across the range of physiologic blood pressures due to autoregulation of GFR. Autoregulation of glomerular filtration is the result of three major factors that modulate either afferent or efferent arteriolar tone:
these include
an autonomous vasoreactive (myogenic) reflex in the afferent arteriole
tubuloglomerular feedback
angiotensin II–mediated vasoconstriction of the efferent arteriole.
The myogenic reflex is a first line of defense against fluctuations in renal blood flow. Acute changes in renal perfusion pressure evoke reflex constriction or dilatation of the afferent arteriole in response to increased or decreased pressure, respectively. This phenomenon helps protect the glomerular capillary from sudden changes in systolic pressure.
Tubuloglomerular feedback changes the rate of filtration and tubular flow by reflex vasoconstriction or dilatation of the afferent arteriole. Tubuloglomerular feedback is mediated by specialized cells in the thick ascending limb of the loop of Henle called the macula densa that act as sensors of solute concentration and tubular flow rate. With high tubular flow rates, a proxy for an inappropriately high filtration rate, there is increased solute delivery to the macula densa that evokes vasoconstriction of the afferent arteriole causing GFR to return toward normal. One component of the soluble signal from the macula densa is adenosine triphosphate (ATP) released by the cells during increased NaCl reabsorption. ATP is metabolized in the extracellular space to generate adenosine, a potent vasoconstrictor of the afferent arteriole. During conditions associated with a fall in filtration rate, reduced solute delivery to the macula densa attenuates the tubuloglomerular response, allowing afferent arteriolar dilatation and restoring glomerular filtration to normal levels. Angiotensin II and reactive oxygen species enhance, while nitric oxide (NO) blunts, tubuloglomerular feedback.
The third component underlying autoregulation of GFR involves angiotensin II. During states of reduced renal blood flow, renin is released from granular cells within the wall of the afferent arteriole near the macula densa in a region called the juxtaglomerular apparatus Renin, a proteolyticenzyme, catalyzes the conversion of angiotensinogen to angiotensin I, that is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE) Angiotensin II evokes vasoconstriction of the efferent arteriole, and the resulting increased glomerular hydrostaticpressure elevates filtration to normal levels
Direction of PressureCause of pressureHow much pressure does it provide?Special circumstances for this pressure in the kidneyOut of the blood(into the capsule)Blood pressure(hydrostatic pressure of blood)60 mm Hg
Marieb says the same
1. The afferent arteriole has a wider diameter than the efferent arteriole. This causes some additional pressure.2. The afferent arteriole is a larger arteriole than usually supplies capillaries, so it has a higher pressure.
Into the blood(out of the capsule)Osmotic pressure32 mm Hg
Marieb says 28 mm Hg
nothing really...Capsular hydrostatic pressure18 mm HgMarieb says 15 mm Hg
We haven't seen this before. This occurs when fluid backs up into the glomerular capsule.You see, as fluid leaves the blood, it enters a defined volume of space within the capsule. If that is already full, it resists getting more fluid. That resistance is capsular hydrostatic pressure.
Mechanisms of Renal Tubular Transport
The renal tubules are composed of highly differentiated epithelia that vary dramatically in morphology and function along the nephron. The cells lining the various tubular segments form monolayers connected to one another by a specialized region of the adjacent lateral membranes called the tight junction. Tight junctions form an occlusive barrier that separates the lumen of the tubule from the interstitial spaces surrounding the tubule and also apportions the cell membrane into discrete domains: the apical membrane facing the tubular lumen and the basolateral membrane facing the interstitium. This regionalization allows cells to allocate membrane proteins and lipids asymmetrically. Owing to this feature, renal epithelial cells are said to be polarized. The asymmetric assignment of membrane proteins, especially proteins mediating transport processes, provides the machinery for directional movement of fluid and solutes by the nephron.
Epithelial Solute Transport
There are two types of epithelial transport. Movement of fluid and solutes sequentially across the apical and basolateral cell membranes (or vice versa) mediated by transporters, channels, or pumps is called cellular transport. By contrast, movement of fluid and solutes through the narrow passageway between adjacent cells is called paracellular transport. Paracellular transport occurs through tight junctions, indicating that they are not completely "tight." Indeed, some epithelial cell layers allow rather robust paracellular transport to occur (leaky epithelia), whereas other epithelia have more effective tight junctions (tight epithelia). In addition, because the ability of ions to flow through the paracellular pathway determines the electrical resistance across the epithelial monolayer, leaky and tight epithelia are also referred to as low or high-resistance epithelia, respectively. The proximal tubule contains leaky epithelia, whereas distal nephron segments such as the collecting duct, contain tight epithelia. Leaky epithelia are most well suited for bulk fluid reabsorption, whereas tight epithelia allow for more refined control and regulation of transport.
Membrane Transport
Cell membranes are composed of hydrophobic lipids that repel water and aqueous solutes. The movement of solutes and water across cell membranes is made possible by discrete classes of integral membrane proteins, including channels, pumps, and transporters. These different mechanisms mediate specific types of transport activities, including active transport (pumps), passive transport (channels), facilitated diffusion (transporters), and secondary active transport (cotransporters). Active transport requires metabolic energy generated by the hydrolysis of ATP. Active transport pumps are ion-translocating ATPases, including the ubiquitous Na+/K+-ATPase, the H+-ATPases, and Ca
backgaround
Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity (allergy) resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity. This allergic reaction causes inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation.
The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis. Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin and by specific sensitivity in the case of allergic contact dermatitis.
A detailed history, both before and after patch testing, is crucial in evaluating individuals with allergic contact dermatitis. Before patch testing, the history identifies potential causes of allergic contact dermatitis and the materials to which individuals are exposed that should be included in patch testing. After patch testing, the history determines the clinical significance of the findings
pathophysiology
Approximately 3000 chemicals are well documented as specific causes of allergic contact dermatitis. Most of the chemicals able to provoke allergic contact dermatitis are small molecules (< 500 d). These molecules must bind to carrier proteins on Langerhans cells, which are situated within the suprabasilar layer of the epidermis.
Langerhans cells are the antigen-presenting cells within the skin. Langerhans cells interact with CD4+ T cells (helper T cells). Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation. In contrast, only allergenic compounds induce CD1a+ CD83+ Langerhans cell migration with partial maturation at subtoxic concentrations
Cytokines also play an important role in allergic contact dermatitis because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating allergic contact dermatitis, not irritant contact dermatitis.
Langerhans cells can migrate from the epidermis to the regional draining lymph nodes. Sensitization to a chemical requires intact lymphatic pathways.
The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such as poison ivy. Some individuals develop specific sensitivity to allergens following years of chronic low-grade exposure; for example, sensitivity to chromate in cement can eventually develop in individuals with chronic irritant contact dermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, allergic contact dermatitis develops within hours to several days of exposure.
CD4+ CCR10+ memory T cells persist in the dermis after clinical resolution of allergic contact dermatitis.
Filaggrin barrier defects that predispose individuals to atopic dermatitis might also predispose them to allergic contact dermatitis by allowing greater penetration of chemical haptens
etiology
Approximately 25 chemicals appear to be responsible for as many as one half of all cases of allergic contact dermatitis. These include nickel, preservatives, dyes, and fragrances.
Poison ivyPoison ivy (Toxicodendron radicans) is the classic example of acute allergic contact dermatitis in North America. Allergic contact dermatitis from poison ivy is characterized by linear streaks of acute dermatitis that develop where plant parts have been in direct contact with the skin.
NickelNickel is the leading cause of allergic contact dermatitis in the world. The incidence of nickel allergic contact dermatitis in North America is increasing; in contrast, new regulations in Europe have resulted in a decreasing prevalence of nickel allergy in young and middle-aged women
Allergic contact dermatitis to nickel typically is manifested by dermatitis at the sites where earrings or necklaces (see the image below) containing nickel are worn or where metal objects (including the keypads of some cell phones) containing nickel are in contact with the skin.
Nickel may be considered a possible occupational allergen. Workers in whom nickel may be an occupational allergen primarily include hairdressers, retail clerks, caterers, domestic cleaners, and metalworkers. Individuals allergic to nickel occasionally may develop vesicles on the sides of the fingers (dyshidrotic hand eczema or pompholyx) from nickel in the diet.
Allergic contact dermatitis to nickel in a necklace.Rubber glovesAllergy to 1 or more chemicals in rubber gloves is suggested in any individual with chronic hand dermatitis who wears them, unless patch testing demonstrates otherwise. Allergic contact dermatitis to chemicals in rubber gloves typically occurs maximally on the dorsal aspects of the hand. Usually, a cutoff of dermatitis occurs on the forearms where skin is no longer in contact with the gloves. Individuals allergic to chemicals in rubber gloves may develop dermatitis from other exposures to the chemicals (eg, under elastic waistbands).
Hair dye and temporary tattoosp-Phenylenediamine (PPD) is a frequent component of and sensitizer in permanent hair dye products and temporary henna tattoos ; exposure in to it in hair dye products may cause acute dermatitis with severe facial edema. Severe local reactions from PPD may occur in black henna tattoos in adults and children. Epidemiologic data indicate that the median prevalence of positive patch test reactions to PPD among dermatitis patients is 4.3% (increasing) in Asia, 4% (plateau) in Europe, and 6.2% (decreasing) in North America.[7]
TextilesIndividuals allergic to dyes and permanent press and wash-and-wear chemicals added to textiles typically develop dermatitis on the trunk, which occurs maximally on the lateral sides of the trunk but spares the vault of the axillae. Primary lesions may be small follicular papules or may be extensive plaques.
Individuals in whom this allergic contact dermatitis is suspected should be tested with a series of textile chemicals, particularly if routine patch testing reveals no allergy to formaldehyde. New clothing is most likely to provoke allergic contact dermatitis, since most allergens decrease in concentration in clothing following repeated washings.
PreservativesPreservative chemicals added to cosmetics, moisturizers, and topical medications are major causes of allergic contact dermatitis (see the image below). The risk of allergic contact dermatitis appears to be highest to quaternium-15, followed by allergic contact dermatitis to isothiazolinones (Kathon CG). Although parabens are among the most widely used preservatives, they are not a frequent cause of allergic contact dermatitis.
Severe allergic contact dermatitis resulting from preservatives in sunscreen. Patch testing was negative to the active ingredients in the sunscreen.Schnuch et al estimated that preservatives found in leave-on topical products varied over 2 orders of magnitude in relative sensitization risk.
Formaldehyde is a major cause of allergic contact dermatitis (see the image below). Certain preservative chemicals widely used in shampoos, lotions, other moisturizers, and cosmetics are termed formaldehyde releasers (ie, quaternium-15 [Dowicil 200], imidazolidinyl urea [Germall 115], and isothiazolinones
Onycholysis developing from allergic contact dermatitis to formaldehyde used to harden nails.FragrancesIndividuals may develop allergy to fragrances. Fragrances are found not only in perfumes, colognes, aftershaves, deodorants, and soaps, but also in numerous other products, often as a mask to camouflage an unpleasant odor. Unscented products may contain fragrance chemicals used as a component of the product and not labeled as fragrance.
Individuals allergic to fragrances should use fragrance-free products. Unfortunately, the exact chemicals responsible for a fragrance in a product are not labeled. Four thousand different fragrance molecules are available to formulate perfumes. The fragrance industry is not required to release the names of ingredients used to compose a fragrance in the United States, even when individuals develop allergic contact dermatitis to fragrances found in topical medications.
Deodorants may be the most common cause of allergic contact dermatitis to fragrances because they are applied to occlude skin that is often abraded by shaving in women.
Massage and physical therapists and geriatric nurses are at higher risk of occupational allergic contact dermatitis to fragrances.
CorticosteroidsIn the last decade, it has become clear that some individuals with chronic dermatitis develop allergy to topical corticosteroids. Most affected individuals can be treated with some topical corticosteroids, but an individual can be allergic to all topical and systemic corticosteroids. Budesonide and tixocortol pivalate are useful patch test corticosteroids for identifying individuals allergic to topical corticosteroids.
NeomycinThe risk of allergy to neomycin is related directly to the extent of its use in a population. The risk of allergy to neomycin is much higher when it is used to treat chronic stasis dermatitis and venous ulcers than when it is used as a topical antibiotic on cuts and abrasions in children. Assume that individuals allergic to neomycin are allergic to chemically related aminoglycoside antibiotics (eg, gentamicin, tobramycin).Avoid these drugs both topically and systemically in individuals allergic to neomycin.
BenzocaineAvoid topical use of benzocaine. Benzocaine is included in most standard patch test trays. Individuals allergic to benzocaine may safely use or be injected with lidocaine (Xylocaine), which does not cross-react with benzocaine.
Many individuals complain of adverse reactions to sunscreens, but many of these individuals are not allergic to the sunscreen materials. They may be allergic to preservatives in these products or may have nonspecific cutaneous irritation from these products.
PhotoallergyOccasionally, individuals develop photoallergic contact dermatitis. Allergic contact dermatitis may be accentuated by ultraviolet (UV) light, or patients may develop an allergic reaction only when a chemical is present on the skin and when the skin is exposed sufficiently to ultraviolet light A (UV-A; 320-400 nm).
epidemiology
No racial predilection exists for allergic contact dermatitis. Allergic contact dermatitis is more common in women than in men. This predominantly is a result of allergy to nickel, which is much more common in women than in men in most countries.
Allergic contact dermatitis may occur in neonates. In elderly individuals, the development of allergic contact dermatitis may be delayed somewhat, but the dermatitis may be more persistent once developed. Contact allergy to topical medicaments is more common in persons older than 70 years
prognosis
Individuals with allergic contact dermatitis may have persistent or relapsing dermatitis, particularly if the material(s) to which they are allergic is not identified or if they continue to practice skin care that is no longer appropriate (ie, they continue to use harsh chemicals to wash their skin, they do not apply creams with ceramides or bland emollients to protect their skin).
The longer an individual has severe dermatitis, the longer it is believed it will take the dermatitis to resolve once the cause is identified.
Some individuals have persistent dermatitis following allergic contact dermatitis, which appears to be true especially in individuals allergic to chrome.
A particular problem is neurodermatitis (lichen simplex chronicus), in which individuals repeatedly rub or scratch an area initially affected by allergic contact dermatitis.
MortalityDeath from allergic contact dermatitis is rare in the United States. Allergic contact dermatitis to the weed wild feverfew caused deaths in India when the seeds contaminated wheat shipments to India. This plant then became widespread and a primary cause of severe airborne allergic contact dermatitis.
history
A detailed history, both before and after patch testing, is crucial in evaluating individuals with allergic contact dermatitis. Potential causes of allergic contact dermatitis and the materials to which individuals are exposed should be included in patch testing. Evaluation of allergic contact dermatitis requires a much more detailed history than most other dermatologic disorders.
History is equally important after patch testing. Only history and questioning can determine whether the materials to which a patient is allergic are partly or wholly responsible for the current dermatitis. A positive patch reaction may indicate only a sensitivity and not the cause of current dermatitis.
Preexisting skin diseases
Individuals with stasis dermatitis are at high risk for developing allergic contact dermatitis to materials and agents applied to the areas of stasis dermatitis and leg ulcers. Neomycin is an important cause of allergic contact dermatitis in these individuals because it is used frequently despite the lack of documentation of its efficacy in the treatment of stasis ulcers.
Individuals with otitis externa frequently are allergic to topical neomycin and topical corticosteroids.
Individuals with pruritus ani and pruritus vulvae may become sensitized to benzocaine and other medications applied to chronic pruritic processes.
Women with lichen sclerosus et atrophicus frequently develop allergic contact dermatitis, complicating the severe chronic vulvar dermatosis. Patch testing these patients may provide important information that can help in the management of recalcitrant and difficult-to-manage dermatosis.
Atopic dermatitis
Patients with a history of atopic dermatitis are at increased risk for developing nonspecific hand dermatitis and irritant contact dermatitis. However, they do not appear to be at an increased risk for allergic contact dermatitis, despite the wide range of topical medications and moisturizers used by individuals with chronic atopic dermatitis. They are at lower risk of allergic contact dermatitis to poison ivy. Some European studies indicate that patients with atopic dermatitis may have increased incidence of allergic contact dermatitis to nickel.
Onset of symptoms
Individuals with allergic contact dermatitis typically develop dermatitis, within a few days of exposure, in areas that were exposed directly to the allergen. Certain allergens (eg, neomycin) penetrate intact skin poorly, and the onset of dermatitis may be delayed up to a week following exposure.
A minimum of 10 days is required for individuals to develop specific sensitivity to a new contactant. For example, an individual who never has been sensitized to poison ivy may develop only a mild dermatitis 2 weeks following the initial exposure but typically develops severe dermatitis within 1-2 days of the second and subsequent exposures.
Remember that removing the poison ivy allergen from the skin is difficult, and unless an individual washes exposed skin within 30 minutes of exposure, allergic contact dermatitis will develop. The hallmark of the diagnosis of poison ivy is linear dermatitic lesions. The possibility of an external cause of dermatitis always must be considered if the dermatitis is linear or sharply defined.
The immediate onset of dermatitis following initial exposure to material suggests either a cross-sensitization reaction, prior forgotten exposure to the substance, or nonspecific irritant contact dermatitis provoked by the agent in question.
Eyelid dermatitis
Individuals may develop dermatitis on eyelids and other exposed skin following exposure to airborne allergens or allergens transferred to that site by the fingers. Contact dermatitis may also result from allergy to eyelid makeup.
Contact urticaria
Immediate reactions, ie, visible lesions developing less than 30 minutes after exposure, indicate contact urticaria (not allergic contact dermatitis). This is particularly true if the lesions are urticarial in appearance and if the skin reaction is associated with other symptoms, such as distant urticaria, wheezing, ophthalmedema, rhinorrhea, or anaphylaxis.
Latex
Rubber latex currently is the most important source of allergic contact urticaria (see Latex Allergy). The term hypoallergenic may refer to gloves that do not contain sensitizing chemicals added to rubber latex but may not indicate whether the gloves are rubber latex free.
Some individuals may have delayed specific contact sensitivity to rubber latex, but contact urticaria to rubber latex is much more common than allergic contact dermatitis to latex. Individuals with hand dermatitis, hospital workers, children with spina bifida, and atopic individuals are at increased risk of developing contact urticaria to rubber latex. Individuals may have allergic contact dermatitis to chemicals added to rubber gloves and have contact urticaria to latex. Individuals wearing rubber gloves should be evaluated carefully for both possibilities.
Rare reports exist of immediate anaphylactic reactions to topical antibiotics (eg, bacitracin).
Occupational dermatitis
Contact dermatitis is 1 of the 10 leading occupational illnesses. It may prevent individuals from working. The hands are the sites exposed most intensely to contact allergens and irritants, both at work and at home. Allergic contact dermatitis in response to workplace materials may improve initially on weekends and during holidays, but individuals with chronic dermatitis may not demonstrate the classic history of weekend and holiday improvement.
Irritant contact dermatitis is more likely if multiple workers are affected in the workplace. Most allergens rarely sensitize a high percentage of the population.
Hobbies
Hobbies may be the source of allergic contact dermatitis. Examples include woodworking with exotic tropical woods or processing film using color-developing chemicals that may provoke cutaneous lesions of lichen planus from direct skin exposure.
Medications
Medications (both self-prescribed and physician-prescribed) are important causes of allergic contact dermatitis. The workplace nurse may dispense ineffective and sensitizing topical preparations, such as thimerosal (Merthiolate), which may change a simple abrasion into a severe case of allergic contact dermatitis. Individuals may develop allergy to preservatives in medications and/or to the active ingredients in topical medications, especially neomycin and topical corticosteroids.[11, 12]
Patients with dermatitis that did not clear with topical corticosteroid treatment should be considered for patch testing with a corticosteroid series and the commercial preparations of corticosteroids and their vehicles.
physical examination
Acute allergic contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base. Lichenified pruritic plaques may indicate chronic allergic contact dermatitis. Occasionally, allergic contact dermatitis may affect the entire integument (ie, erythroderma, exfoliative dermatitis). The initial site of dermatitis often provides the best clue regarding the potential cause of allergic contact dermatitis. Note the following.
HandsHands are an important site of allergic contact dermatitis, particularly in the workplace. Common causes of allergic dermatitis on the hands include the chemicals in rubber gloves.
Topical medication sitesAllergic contact dermatitis is frequent in the perianal area as a result of the use of sensitizing medications and remedies (eg, topical benzocaine). Topical medications are also important causes of allergic contact dermatitis in cases of otitis externa. Allergy to chemicals in ophthalmologic preparations may provoke dermatitis around the eyes.
Airborne allergic contact dermatitisChemicals in the air may produce airborne allergic contact dermatitis. This dermatitis usually occurs maximally on the eyelids, but it may affect other areas exposed to chemicals in the air, particularly the head and the neck.
Hair dyesHair dye—in particular, the component p-phenylenediamine (PPD)—may trigger allergic contact dermatitis. Individuals allergic to hair dyes typically develop the most severe dermatitis on the ears and adjoining face rather than on the scalp.
Stasis dermatitis and stasis ulcersIndividuals with stasis dermatitis and stasis ulcers are at high risk for developing allergic contact dermatitis to topical medications applied to inflamed or ulcerated skin (see the image below). The chronicity of this condition and the frequent occlusion of applied medications contribute to the high risk of allergic contact dermatitis to medicament (eg, neomycin) in these patients.
Individuals may develop widespread dermatitis from topical medications applied to leg ulcers or from cross-reacting systemic medications administered intravenously. For example, a patient allergic to neomycin may develop systemic contact dermatitis if treated with intravenous gentamicin.
Chronic stasis dermatitis with allergic contact dermatitis to quaternium-15, a preservative in moisturizer. Allergic contact dermatitis produces areas of erythema in areas of atrophie blanche and varicose veins.Erythema multiformeErythema multiforme (EM) is a severe cutaneous reaction with targetoid lesions that occurs primarily after exposure to certain medications or is triggered by infection, most commonly by herpes simplex virus. Rare cases of EM have been reported after allergic contact dermatitis resulting from exposure to poison ivy,[13]tropical woods, nickel, and hair dye (see the image below).
Erythema multiformelike reaction that developed acutely following hair dying.Intraoral metal contact allergy may result in mucositis that mimics lichen planus, which has an association with intraoral squamous cell carcinoma. Intraoral squamous cell carcinoma adjacent to a dental restoration containing a metal to which the patient was allergic has been reported.[14]
Allergic contact dermatitis may be a direct trigger for skin ulceration in patients with venous insufficiency. Early diagnosis and treatment of allergic contact dermatitis may prevent the development of venous ulcers.
ComplicationsDarkly pigmented individuals may develop areas of hyperpigmentation or hypopigmentation from allergic contact dermatitis. Occasionally, they may develop depigmentation at sites of allergic contact dermatitis to certain chemicals.
Occasionally, allergic contact dermatitis is complicated by secondary bacterial infection, which may be treated by the appropriate systemic antibiotic.
DDx
Asteatotic EczemaContact Dermatitis, IrritantDrug-Induced Bullous DisordersDrug-Induced PhotosensitivityNummular DermatitisOnycholysisPerioral DermatitisPhytophotodermatitisPrurigo NodularisSeborrheic DermatitisTinea CorporisTransient Acantholytic DermatosisUrticaria, Contact Syndromelab studies
Potassium hydroxide preparation and/or fungal culture to exclude tinea are often indicated for dermatitis of the hands and feet. This will identify disorders such astinea pedis.
histologic finding
The histology of allergic contact dermatitis is similar to that found in other forms of eczematous dermatitis. A pattern of subacute chronic dermatitis or acute dermatitis may be seen. The inflammatory infiltrate in the dermis predominately contains lymphocytes and other mononuclear cells.
Epidermal edema (ie, spongiosis and microvesicle formation) may be seen, but these changes may be absent in long-standing dermatitis in which thickening of the epidermis (acanthosis) with hyperkeratosis and parakeratosis may be seen in the epidermis and stratum corneum. Allergic contact dermatitis may provoke atypical T-cell infiltrates, simulating mycosis fungoides.
background
Asteatotic eczema of the lower extremities in elderly persons secondary to aging, dehydrated skin, and malnutrition
Cracked erythema secondary to irritant contact dermatitis from soaps or detergents
Eczema craquelé in areas in which corticosteroid therapy was discontinued
Asteatotic eczema in neurologic disorders
pathophysiology
Initially, excess water loss from the epidermis results in dehydration of the stratum corneum with upward curling of corneocytes. The outer keratin layers require 10-20% water concentration to maintain their integrity. A significant decrease in free fatty acids in the stratum corneum is present in people with asteatotic dermatitis. Stratum corneum lipids act as water modulators, and cutaneous loss of these lipids can increase transepidermal water loss to 75 times that of healthy skin.Elderly persons with decreased sebaceous and sweat gland activity, patients on antiandrogen therapy, people using degreasing agents, and people bathing without replacing natural skin emollients lost to bath water are at risk for asteatotic eczema.
When the stratum corneum loses water, the cells shrink. A significantly decreased cellular volume can stress the skin's elasticity, creating fissures. Edema in the dermis leads to additional stretch on the overlying epidermis. Fissures rupture dermal capillaries, causing clinical bleeding. The disruption of cutaneous integrity can result in inflammation with risk of infection. Transepidermal absorption of allergens and irritants is increased as the epidermis is damaged, increasing susceptibility to allergic contact dermatitis and irritant contact dermatitis.Allergic contact dermatitis and irritant contact dermatitis may cause a persistent and possibly more extensive dermatitis despite therapy. Furthermore, low environmental humidity contributes to xerosis, creating a clinical picture of asteatotic dermatitis in some dermatologic conditions, such as atopic dermatitis.
epidemiology
Men older than 60 years develop asteatotic dermatitis more commonly than women
symptom of asteatotic eczema
Fissured skin lesionsSore skin lesionsItchy skin lesionsRed skin lesionsFine cracks in skinhistory
The typical presenting picture is an elderly patient complaining of itchy, dry skin in the winter. Younger age groups and even children can, however, be affected. The classical distribution is on the legs, although hands, arms and trunk can also be affected. The appearance is of slightly scaly fissured skin, which has been described as crazy paving or cracked porcelain (see Document reference 2 for a picture). Areas of excoriation, erythema and bleeding may be evident, due to rubbing or scratching. Most patients have a localised condition, but a more severe generalised form is sometimes seen.
. Sometimes, the dysesthesia may be described as a pinprick or biting sensation.
_ Asking the patient about pertinent controllable factors, such as the following, is important:
Frequency of bathing, showering, and cleansing, and which soaps and cleansers are in contact with the skinTypes of skin lubricants used, and method and frequency of applicationDietMedicationsTypes of clothing worn (Wool may cause irritation.)The source, the type, and the temperature of heat that may alter the humidity of the environmentIf the eruption persists despite therapy, behavioral changes, and treatment compliance, allergic contact dermatitis and irritant contact dermatitis and internal malignancy may require investigation.
physicalPrimary lesions: Slightly scaly, inflamed, curvilinearly cracked and/or fissured skin most commonly involves the pretibial areas, but it may also occur on the thighs, on the hands, and on the trunk .Asteatotic dermatitis on the lower extremity.Secondary lesions:Excoriated, erythematous, edematous patches may result from rubbing or scratching.Bleeding fissures secondary to the disruption of dermal capillaries have been described in exaggerated eczema craquelé, which begins as superficial cracks in the epidermis.Generalized lesions: Generalized or extensive asteatotic dermatitis presents with primary lesions and secondary excoriations Asteatotic dermatitis on the lower extremity.Asteatotic dermatitis on the lower extremity.
causesXerosis and frictionxerosis: excessive dryness Frequent or prolonged bathing in hot water, use of soap on the involved site, and infrequent use of emollients for water retention in the stratum corneumDegreasing agentsSolventsCleansersDecreased sebaceous and sweat gland activity in elderly personsDecreased keratin synthesis in elderly personsLow environmental humidity and cold winds that increase the loss of water by convectionRadiationLong-term malabsorption of essential fatty acids, including linoleic acid and linolenic acidNutritional deficienciesZinc deficiencyEssential fatty acid deficiency, such as linoleic acid deficiency or linolenic acid deficiencyAtopy Ichthyosis: hereditary skin disease characterized by flaky and scaly skin
Thyroid disease - Myxedema and other thyroid diseases with diminished sweat and sebaceous gland activityNeurologic disorders - Decreased sweating in denervated areasDrugs - Antiandrogen therapy and diuretic therapyMalignancies - Malignant lymphoma gastric adenocarcinoma, glucagonoma, angioimmunoblastic lymphadenopathy, breast cancer, large-cell lung carcinoma, and colorectal carcinoma
DDx Cellulitis fever not seen in eczema Contact Dermatitis, AllergicContact Dermatitis, IrritantStasis DermatitisThrombophlebitis
histologic finding
Spongiosis and a varying amount of inflammatory dermal infiltrate similar to that of mild, . subacute eczema are seen
inflammation of derm is assosiated with secondary infection
treatment and management
Patients should follow the methods listed below to improve the condition.
Take short baths with decreased water temperature.Eliminate or reduce the use of soap on the involved areas.Avoid harsh skin cleansers.Apply petrolatum-based emollients following bathing, and use moisturizing agents liberally.Apply topical steroid ointments with or without polyethylene occlusion. Note that steroids can thin the cutaneous barrier and lower the threshold for further insults that lead to dermatitis, especially in elderly patients.Use humidifiers.Symptoms can be alleviated by moisturizing and steroid creams. Antibiotics may be needed if secondary infection developsSteps for Managing Eczema:Make lifestyle changes to avoid temperature, humidity extremes and other exacerbating factorsBathe only once every 1-2 days - over-bathing can dry the skin.Use bath oil to help moisturise skin e.g. Dermaveen, Hamilton's Alpha Ker or QVKeep the nails short and wear a covering over the hands (gloves or socks) to avoid night-time scratching as the patient is often unaware that they are scratchingUsing low-allergenic washing powdersWear cotton clothing as other materials increase sweating and rubbing on the skinMoisturise twice a day. It may take some experimentation to find a cream that doesn't irritate the skin. Avoid creams with mineral oils. Commonly used brands include: Alpha Keri, Cetaphil, QV, Dermaveen and HamiltonsOils such as olive oil (extra-virgin) may be used as a moisturizerA topical cream called Pimecrolimus may be used to treat eczema - it is non-steroidal and doesn't cause thinning of the skin. Strong steroid-based topical creams may be needed for more resistant patches.Very red dry skin may benefit from using QV Flare Up Bath OilUse topical antibacterial cream for infected eczema - oral antibiotics may be recommended in more severe cases.Avoid environments that are excessively hot, cold or dry as they can exacerbate skin symptoms
Topical immunomodulators - Pimecrolimus and Tacrolimus - may be used as an alternative to topical steroidsmedication summary
Topical steroid ointments with 24- to 48-hour occlusion with polyethylene or Unna boots are the treatment of choice for the rapid resolution of asteatotic dermatitis. Many patients heal with mild topical steroids (class III-VI) alone, depending on the severity of the dermatitis, the patient's compliance with treatment, and the reduction in the use of soap and hot water to the involved areas. Several studies have reported on the successful use of pimecrolimus or tacrolimus cream in conditions other than atopic dermatitis, including seborrheic dermatitis and asteatotic eczema, among others. 4
The liberal use of moisturizers, especially petrolatum-based preparations, alone or in combination with topical steroids for mild cases of asteatotic dermatitis is recommended.
The soak-and-smear method of hydrating the skin by bathing or soaking the affected area followed by immediate application of steroid ointment once daily has been shown to clear more that 90% of patients in 4-14 days. This is best performed at night
Note that steroids can thin the cutaneous barrier and lower the threshold for further insults that lead to dermatitis, especially in elderly patients.
Use topical antibacterial cream for infected eczema - oral antibiotics may be recommended in more severe casesAvoid environments that are excessively hot, cold or dry as they can exacerbate skin symptomscomplication
Allergy to topical steroidsSecondary infectionprognosis
Asteatotic dermatitis responds well to therapy; however, if the causative factors are not eliminated, recurrences are common.
+ نوشته شده در ۱۳۹۱/۰۶/۲۵ ساعت 21:42 توسط mary | آناتومی اجزای دستگاه تنفس: ادامه شش چپ در ریه چپ ۲ لوب داریم . شامل:Left Upper Lobe (LUL)
Left Lower Lobe (LLL)
و یک فیشور به اسم:
Major Fissure
The Left Upper Lobe (LUL)
+ نوشته شده در ۱۳۹۱/۰۳/۱۹ ساعت 14:3 توسط mary | آناتومی اجزای دستگاه تنفس: شش راست و بخشی از شش چپ
The Left Lower Lobe
شش پايه اي ترين ارگان تنفسي است كه از نظر آناتوميكي در راست و چپ كمي با هم متفاوتن طوري كه در راست 3 لوب و در چپ 2 لوب دارد. حالا بقيه شو تو شكل ببينين كه از هر نوشته اي واضح تره!
پس ریه راست ۳ تا لوب داره . شامل:
+ نوشته شده در ۱۳۹۱/۰۳/۱۹ ساعت 13:50 توسط mary | آناتومي اجزاي دستگاه تنفس: برونش و برونشیولRight Upper Lobe (RUL)
Right Middle Lobe (RML)
Right Lower Lobe (RLL)و ۲ تا فیشر داریم:
Major Fissure (aka oblique fissure)
minor fissure (horizontal fissure
The Right Upper Lobe
The Right Middle Lobe
The Right Lower Lobe
درخت برونشي :
ناي به 2 تا برونش اصلي تقسيم ميشه كه در ناف ريه وارد ريه ميشن كه در اين محل شريان و و ريد و لنف هم وارد ميشن و اطراف اونا رو بافت هم بندب احاطه كرده كه بهش مي گن : pulmonary root
لوبول هاي يوي ساختمان هاي هرمي شكلي اند كه رأسشان به طرف ناف ريه است.
اپيتليوم برونشيول هاي انتهايي حاوي سلول هاي كلارا (clara) ست . اين سلول ها حاوي گرانول هاي ترشحي اند كه پروتئين هايي ترشح ميكنند كه برونشيول را در برابر مواد اكسيداتيو و التهاب حفاظت مب كنند.
برونشيول هم چنين اجسام نورواپيتليالي دارن كه حاوي گرانول هاي ترشحي اند كه به تغييرات تركيب گاز هاي درون مجرا واكنش نشان مي دهد . كه البته به نظر مي رسد كه در روند ترميمي سلول ها هم نقش دارد.
برونشيول هاي تنفسي :
در ديواره آن ها آلوئول قرار گرفته اند كه هر چه به انتها مي رويم به تعداد اونا افزوده ميشه . ديواره بين آلوئوله ها از جنس مكعبي مژه دار است اما در فضاي الوئول مژه وجود ندارد.
آلوئول ها مسئول ساختمان اسفنجي ريه ها هستند. آلوئول ها شبيه پاكت هاي كوچكي اند كه كه از يك طرف باز اند مثل حفره هاي لانه زنبور.
Blood-air barrier: شامل 2 لايه اپيتلويم سنگفرشي 2 آلوئول است و مويرگ ها و بافت هم بند بين آن ها ( interstitial tissue)
رشته هاي الاستيك و رتيكولار درون بافت هم بند طوري قرار ميگيرند كه بتونن راحت انقباض و انبساط آلوئول ها را تنظيم كنند. علاوه بر اين اين رشته ها از مويرگ هاي ريوي هم حمايت ميكنند.
پوشش آلوئول ها 2 نوع سلول دارد: 1. نوموسيت۱ : ۹۷٪ سطح آلوئول ها را مي پوشاند
2. نوموسيت II : در بين نوع I پراكنده شده اند كه 2 وظيفه دارند :
1. ترشح سورفاكتانت: به وسيله اجسام تيغه ای موجود در آن ها (lamellar body)
اين اجسام در هفته هاي آخر حاملگي به وجود ميان
2. ميتوز و ايجاد نوموسيت I
برونش ها انشعاباتي از تراشه اند كه در محاذاتT5 از آن جدا ميشن. دو برونش اصلي راست و چپ داريم: (Left Main Bronchus (LMB و Right Main Bronchus (RMB) كه اين دو تفاوت هايي از نظر ساختاري با هم دارن به طوري كه RMB نسبت به LMB كوتاه تر ، گشاد تر و با زاويه كمتري نسبت به ناي قرار دارد.
طول برونش ها با غضروف هاي O شكل پوشيده ميشه ( اگه يادتون باشه در ناي C شكل بود). و از نظر هيستولوژي از سلول هاي سنگفرشي مژك دار پوشيده ميشه كه سلول هاي گابلت هم بين آن ها قرار گرفتن كه موكوس تشح مي كنن.
حواستون باشه كه در اين محل هم تبادل گاز نداريم و صرفأ اين جا محلي ست براي عبور گاز!
بذارین یه نکته ی دیگه هم بگم یه وقت جا نیفته!!
RMB به 3 قسمت تقسیم میشه که بهشون میگن lobar bronchi و LMB به 2 lobar bronchi تقسیم میشه . این lobar bronchi ها خودشون تبدیل میشن به tertiary bronchi یا همون segmental bronchi . حالا هر کدوم از این segmental ها خودشون به primary bronchioles ها تبدیل میشن که اونا هم با تقسیمشون میشن terminal bronchioles. این terminal ها با تقسیم های متعدد respiratory bronchiol ها رو ایجاد میکنن. Respiratory bronchioles ها به alveolar duct ها تبدیل میشن و آن ها هم در انتها alveolar sac ها را ایجاد میکنند.
از نظر عملکردی تا مقطع respiratory bronchioles ها ما تبادل گازی نداریم و این بخش ها همگی باعث انتقال گاز میشن.
از نظر هیستولوژی هم برونشیول ها تا سطح respiratory از سلول های استوانه ای بدون مژک پوشیده شدن و برعکس بروش ها هیچ گونه غضروفی ندارن. Respiratory bronchioles که شروع تبادل گاز از همین محل هست از سلول های سنگفرشی تک لایه و بدون مژک پوشیده شدن که غضروف هم ندارن. البته که همه ی این ساختار ها با کاری که هر قسمت انجام میده متناسبه.
+ نوشته شده در ۱۳۹۱/۰۳/۱۸ ساعت 12:49 توسط mary | آناتومي اجزاي دستگاه تنفس: نایناي (trachea)
تراشه يا windpipe لوله ايست به طول حدود 10 تا 12 سانتي متر و عرض 16 تا 18 ميلي متر داره كه از مهره C6 شروع شده و تا حدود T6 در حالت ايستاده و تا مهره T4-5در حالت خوابيده ادامه دارد كه اين محل به دو برونش اصلي راست و چپ تقسيم ميشه. يه سري غضروف هاي نعلي شكل( يا c-shape) به تعداد 16 تا 20 تا طولش را احاطه كردن.
از نظر بافت شناسي حاوي از سلول هاي استوانه اي مژك داري پوشيده شده و همچنين در آن سلول هاي گابلت هم وجود دارد كه موكوس ترشح ميكنن.
به قسمت قدامي تراشه convex ميگن كه در پشت تيروئيد است. تراشه از خلف هم با مري esophagus)) مجاورت داره.
عملكرد اصلي ناي انتقال هواست اما در cleaning و moistening هوا هم نقش داره
انقباض عضله و تنگ شدن مجراي ناي ناشي از ناي در رفلكس سرفه نقش دارد .
كاهش قطر ناي كه بعد از انقباض عضله رخ مي دهد باعث افزايش سرعت هواي بازدمي مي شود كه همين مسأله باعث پاك شدن راه هوايي مي شود.
+ نوشته شده در ۱۳۹۱/۰۳/۱۷ ساعت 23:27 توسط mary | آناتومي اجزاي دستگاه تنفس: حلق
حلق ( pharynx)
بخشي از گلو (throat) ست كه به 3 قسمت تقسيم ميشه:
· nasopharynx (epipharynx)
· oropharynx (mesopharynx)
· laryngopharynx (hypopharynx)
كه ديگه با جزئيات هر كدوم كاري نداريم ( البته اگه اونا هم با ما كاري نداشته باشن!)
+ نوشته شده در ۱۳۹۱/۰۳/۱۷ ساعت 22:29 توسط mary | آناتونی اجزای دستگاه تنفس: بيني
حفره بيني
شامل: 1. دهليز (vestibule) در خارج ← پوشش خارجي بيني وارد سوراخ ها يا پره هاي بيني (narse) ميشه
اطراف سطح داخلي پره ها غدد سباسه و عرق متعدد + موهاي ضخيم و كوتاه ( vibrissae) قرار دارد.
نكته : در داخل وستيبول اپيتليوم ماهيت شاخي خود را از دست مي دهد و قبل از آن كه وارد حفرات بيني شود به تدريج به صورت اپيتليوم مشخص تنفسي در مياد.
2. حفرات بيني ( nasal fossae ) در داخل ← دو محفظه غاري ( covernous chamber ) داريم كه با septum از هم جدا ميشن.
در ديواره جانبي اين حفرات 3 برامدگي به نام شاخك ( conchae) داريم كه شامل:
1. شاخك فوقاني : پوشيده شده با اپيتليوم بويايي
2. شاخك مياني : پوشيده شده با اپيتليوم تنفسي
3. شاخك تحتاني: پوشيده شده با اپيتليوم تنفسي
در نتيجه تماس هوا با اپيتليوم موكوسي هوا گرم و مرطوب ميشه كه بعدأ توضيح داده ميشه .( warm and moisten).
نكته : دورن لامينا پروپرياي شاخك ها شبكه وريدي به نام swell body وجود داره كه گاهي در يك طرف از خون پر شده و باعث اتساع مخاط شاخك ها و كاهش هم زمان هوا ميشه كه در اين حالت هوا از طريق حفره ديگر منتقل ميشه.
خب فايده اين كار چيه؟ جريان هوا در اين حالت كم ميشه و باعث جلوگيري از خشك شدن اپيتليوم تنفسي ميشه.
گرم شدن هوا چه جوري صورت ميگيرد؟ حفره ي بيني سيستم عروقي غني دارد كه در نزديكي ضريع شبكه اي ايجاد ميكنند كه از آن شاخه هاي قوس دار به طرف سطح ميرن . در اين عروق قوس دار خون از عقب به طرف جلو ( در خلاف جهت حركت هواي دمي) ميره كه همين موضوع ( countercurrent) هوا رو گرم ميكنه.
بويايي
اپيتليوم بويايي شامل : 1. سل هاي پشتيبان ( supporting) : محتوي يك رنگدانه به رنگ زرد روشن است كه رنگ مخاط بويايي را مي وجودد.
2. سل هاي بويايي : نورون هاي دوقطبي اند كه توليد پتانسيل به بودار واكنش نشان مي دهد.
نكته : لامينا پروپرياي اپيتليوم بويايي داراي غدد بومن اند كه با يك مايع باعث پاك سازي مژه هاي بويايي دسترسي آن ها به مواد بودار ميشه
3. سل هاي قاعده اي
بيني 2 سوراخ داره كه بهشون ميگن nostrils
در سقف بيني olfactory epithelium قرار دارد كه در آن رسپتور هاي مخصوصي ست كه به انواع مولكول هاي بو حساس اند كه هر كدام از اين رسپتورا بوي خاصي رو ميگيرن. حالا.... وقتي اين رسپتورا تحريك شدن سشگنال رو از طريق عصب بويايي ميفرستن به olfactory bulb و بعد از اونجا به مغز ميره و درك ميشه. كاراي ديگه ي بيني:
كمك به چشايي ( taste)
کمک به تولید صدا ( voice):
The air resonating in nose assists in giving the voice its particular sound
حالا... یه نگاه کلی بهش بنداز .....
خب حالا یه کم ریز تر واردش میشیم:
Figure 1: Frontal
1 - glabella
2 - nasion
3 - tip-defining points
4 - alar-sidewall
5 - supra-alar crease
6 - philtrum
Figure 2: Base
1 – infratip lobule
2 - columella
3 – alar sidewall
4 – facet, or soft-tissue triangle
5 - nostril sill
6 - columella-labial angle or junction
7 - alar-facial groove or junction
8 - tip defining points
Figure 3: Lateral
1 - glabella
2 - nasion, nasofrontal angle
3 – rhinion (osseocartilaginous junction)
4 - supratip
5 - tip-defining points
6 - infratip lobule
7 - columella
8 - columella-labial angle or junction
9 - alar-facial groove or junction
Figure 4: Oblique
1 - glabella
2 - nasion, nasofrontal angle
3 - rhinion
4 - alar sidewall
5 - alar-facial groove or junction
6 - supratip
7 - tip-defining point
8 – philtrum
Figures 5-7 show the internal anatomy, beneath the skin.
Figure 5: Oblique
1 - nasal bone
2 - nasion (nasofrontal suture line)
3 - internasal suture line
4 - nasomaxillary suture line
5 - ascending process of maxilla
6 - rhinion (osseocartilaginous junction)
7 - upper lateral cartilage
8 - caudal edge of upper lateral cartilage
9 - anterior septal angle
10 - lower lateral cartilage - lateral crus
11 - medial crural footplate
12 - intermediate crus
13 - sesamoid cartilage
14 - pyriform aperture
Figure 6: Lateral
1 - nasal bone
2 - nasion (nasofrontal
suture line)
3 - internasal suture line
4 - nasomaxillary suture
line
5 - ascending process of
maxilla
6 - rhinion
(osseocartilaginous
junction)
7 - upper lateral cartilage
8 - caudal edge of upper
lateral cartilage
9 - anterior septal angle
10 - lower lateral cartilage
lateral crus
11 - medial crural footplate
12 - intermediate crus
13 - sesamoid cartilage
14 - pyriform aperture
Figure 7: Base
1 - tip-defining point
2 - intermediate crus
3 - medial crus
4 - medial crural footplate
5 - caudal septum
6 - lateral crus
7 - naris
8 - nostril floor
9 - nostril sill
10 - alar lobule
11 - alar-facial groove or
junction
12 - nasal spine
The septum is the midline structure inside your nose that divides your nose into left and right. The septum is an important structure in septorhinoplasty. Its anatomy is shown here.
Figure 8: Septum
1 – quadrangular caratilage
2 – nasal spine
3 – posterior septal angle
4 – middle septal angle
5 – anterior septal angle
6 – vomer
7 – perpendicular plate of
ethmoid bone
8 – maxillary crest,
maxillary component
9 – maxillary crest –
palatine component
Figures 9-10 are not as important for the web viewer, but they highlight the important fact that the skin over the nose has muscles and blood vessels. This may seem obvious, but it is important because if the surgeon does not fully recognize the importance of this fact, they may operate in the incorrect tissue planes, which can result in violation of the muscle and blood vessels and subsequent abnormal scarring.
Figure 9: Musculature
A: Elevator muscles -
1. Procerus
2. Levator labii alaequae
nasi
3. Anomalous nasi
B: Depressor muscles -
4. Alar nasalis
5. Depressor septi nasi
C: Compressor muscles -
6. Transverse nasalis
7. Compressor narium
minor
D: Minor dilator muscles -
8. Dilator naris anterior
E: Other -
9. Orbicularis oris
10. Corrugator
Figure 10: Vasculature
1 – dorsal nasal artery
2 – lateral nasal artery
3 - angular vessels
4 - columellar artery
دستگاه تنفس (respiratory system):
سلام
فك كردم با يه مطلب علمي شروع كنم بهتره ولي دلم نيومد تعارفات روزمره ي مخصوص ايراني ها رو كنار بذارم و حالو احوال پرسي نكنمو يه بيت شعر مشت هم نذارم!!
مهربان
آنقدر شاعرم امشب که فقط ،
سایه مهرتورا کم دارم
باتو هستم
ای سراپا احساس
خون تو در رگ من هم جاریست ،
جنس ما جنس بلد بودن کانون گل است
.............
از نظر آناتومیکی دستگاه تنفسی دو بخش میشه:
Upper respiratory tract (URT): از بيني شروع ميشه تا اون قسمتي از ناي كه هنوز وارد قفسه سينه نشده
Lower respiratory tract (URT): از اون قسمتي از ناي كه وارد قفسه سينه ميشه شروع ميشه تا آلوئول ها.
حالا اگه بخوايم جزیی تر بگيم داريم:
تقسيم بندي از نظر آناتوميكي:
1. ريه
2. مجاري هوايي : شامل ← 1. Conducting : بيني
حلق
حنجره
ناي
برونش
برونشيول
2. respiratory = آسينوس : برونشيول تنفسي
مجراي آلوئولي
كيسه آلوئولي
تقسيم بندي از نظر عملكردي:
1. conducting: مسيري براي حركت هوا
مطبوع كردن هوا ( conditioning of air): گرم و مرطوب و پاك سازي هوا
2. respiratory: محلي براي تبادل هوا ( gas exchange)
تقسيم بندي از نظر هيستولوژي:
1. conducting: ناي ← اپيتليوم تنفسي
5 لايه دارد: 1. سل هاي استوانه اي مژك دار
2. سل هاي قاعده اي يا كوتاه ( basal or short) : اين سلول ها قابليت تبديل به انواع ديگر سلول را هم دارن
3. سل هاي جامي موكوسي ( mucous gablet cells)
4. سل هاي برسي ( brush cells) : حاوي ميكروويلوس هاي زيادي اند كه در قاعده خود به اعصاب حسي آوران ميرسند و گويي سلول هاي حسي به حساب ميان.
۵. سل هاي دانه اي كوچك ( small granul): اين سلول ها بخشي از جمعيت سلول هاي نورواندوكرين منتشر اند
nasal cavity (حفره بيني) ← pharynx (حلق) شامل nasopharynx, oropharynx, laryngopharynx ← larynx
Trachea(ناي) ← bronchi (نايژه) ← bronchioles terminal (نايژك) ← respiratory bronchioles )1)←
← (2) alveolar duct alveolar sac (3)
(1) و (2) و (3) ← آسينوس
+ نوشته شده در ۱۳۹۱/۰۳/۱۷ ساعت 0:58 توسط mary | dokhtar che karesh be pesar!!!
ادامه نوشته + نوشته شده در ۱۳۹۰/۱۰/۰۶ ساعت 22:12 توسط mary | maryam namazi
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ادامه نوشته + نوشته شده در ۱۳۹۰/۱۰/۰۶ ساعت 20:49 توسط mary | InflammationFrom Wikipedia, the free encyclopediaJump to: navigation, search Toes inflamed by Chilblains
Inflammation (Latin, inflammare, to set on fire) is part of the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants.[1] Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process. Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection. Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen.Without inflammation, wounds and infections would never heal. Similarly, progressive destruction of the tissue would compromise the survival of the organism. However, chronic inflammation can also lead to a host of diseases, such as hay fever, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). It is for that reason that inflammation is normally closely regulated by the body.Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes ) from the blood into the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.Contents[hide]1 Causes 2 Types 2.1 Cardinal signs 2.2 Process of acute inflammation 3 Exudative component 3.1 Vascular changes 3.2 Plasma cascade systems 3.3 Plasma derived mediators 4 Cellular component 4.1 Leukocyte extravasation 4.2 Cell derived mediators 5 Morphologic patterns 6 Inflammatory disorders 6.1 Atherosclerosis 6.2 Allergies 6.3 Myopathies 6.4 Leukocyte defects 6.5 Pharmacological 6.6 Cancer 6.7 Resolution of inflammation 7 Systemic effects 7.1 Acute-phase proteins 7.2 Leukocyte numbers 7.3 Systemic inflammation and obesity 7.4 Systemic inflammation and overeating 8 Outcomes 9 Examples 10 Exercise and Inflammation 10.1 Exercise-induced acute inflammation 10.2 Post-inflammatory muscle growth and repair 10.3 Chronic inflammation and muscle loss 10.4 Exercise as a treatment for inflammation 10.5 Signal-to-noise theory 11 See also 12 References 13 External links [edit] CausesBurns Chemical irritants Frostbite Toxins Infection by pathogens Physical injury, blunt or penetrating Immune reactions due to hypersensitivity Ionizing radiation Foreign bodies, including splinters, dirt and debris Trauma [edit] TypesComparison between acute and chronic inflammation:AcuteChronicCausative agentPathogens, injured tissuesPersistent acute inflammation due to non-degradable pathogens, persistent foreign bodies, or autoimmune reactionsMajor cells involvedNeutrophils, mononuclear cells (monocytes, macrophages)Mononuclear cells (monocytes, macrophages, lymphocytes, plasma cells), fibroblastsPrimary mediatorsVasoactive amines, eicosanoidsIFN-γ and other cytokines, growth factors, reactive oxygen species, hydrolytic enzymesOnsetImmediateDelayedDurationFew daysUp to many months, or yearsOutcomesResolution, abscess formation, chronic inflammationTissue destruction, fibrosis, necrosis[edit] Cardinal signsThe classic signs and symptoms of acute inflammation:EnglishLatinRednessRubor*SwellingTumor*HeatCalor*PainDolor*Loss of functionFunctio laesa**All the above signs may be observed in specific instances, but no single sign must, as a matter of course, be present.[2] These are the original, or "cardinal signs" of inflammation.[2]*Functio laesa is an apocryphal notion, as it is not unique to inflammation and is a characteristic of many disease states.[3]** Infected ingrown toenail showing the characteristic redness and swelling associated with acute inflammationAcute inflammation is a short-term process, usually appearing within a few minutes or hours and ceasing upon the removal of the injurious stimulus.[4] It is characterized by five cardinal signs:[5]The acronym that may be used for this is "PRISH" for Pain, Redness, Immobility (loss of function), Swelling and Heat.The traditional names for signs of inflammation come from Latin:Dolor (pain) Calor (heat) Rubor (redness) Tumor (swelling) Functio laesa (loss of function)[6] The first four (classical signs) were described by Celsus (ca 30 BC–38 AD),[7] while loss of function was added later by Galen[8] even though the attribution is disputed and the origination of the fifth sign has also been ascribed to Thomas Sydenham[9] and Virchow.[4][5]Redness and heat are due to increased blood flow at body core temperature to the inflamed site; swelling is caused by accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings. Loss of function has multiple causes.[5]These five signs appear when acute inflammation occurs on the body's surface, whereas acute inflammation of internal organs may not result in the full set. Pain only happens where the appropriate sensory nerve endings exist in the inflamed area — e.g., acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings.[5][edit] Process of acute inflammation Micrograph showing acute inflammation of the prostate gland with the characteristic neutrophilic infiltrate. H a process that appears accentuated by eccentric exercise, in which large forces are distributed over relatively small cross-sectional area of the muscle.[edit] Post-inflammatory muscle growth and repairThere is a known relationship between inflammation and muscle growth.[39] For instance, high doses of anti-inflammatory medicines (e.g., NSAIDs) are able to blunt muscle growth.[40][41]It has been further theorized that the acute localized inflammatory responses to muscular contraction during exercise, as described above, are a necessary precursor to muscle growth.[42] As a response to muscular contractions, the acute inflammatory response initiates the breakdown and removal of damaged muscle tissue.[43] Muscles can synthesize cytokines in response to contractions,[44][45][46] such that the cytokines Interleukin-1 beta (IL-1β), TNF-α, and IL-6 are expressed in skeletal muscle up to 5 days after exercise.[43]In particular, the increase in levels of IL-6 can reach up to one hundred times that of resting levels.[46] Depending on volume, intensity, and other training factors, the IL-6 increase associated with training initiates about 4 hours after resistance training and remains elevated for up to 24 hours.[47][48][49]These acute increases in cytokines, as a response to muscle contractions, help initiate the process of muscle repair and growth by activating satellite cells within the inflamed muscle. Satellite cells are crucial for skeletal muscle adaption to exercise.[50] They contribute to hypertrophy by providing new myonuclei and repair damaged segments of mature myofibers for successful regeneration following injury- or exercise-induced muscle damage;[51][52][53] high-level powerlifters can have up to 100% more satellite cells than untrained controls.[54][55]A rapid and transient localization of the IL-6 receptor and increased IL-6 expression occurs in satellite cells following contractions.[47] IL-6 has been shown to mediate hypertrophic muscle growth both in vitro and in vivo.[50] Unaccustomed exercise can increase IL-6 by up to sixfold at 5 hours post-exercise and threefold 8 days after exercise.[56] Also telling is the fact that NSAIDs can decrease satellite cell response to exercise[40], thereby reducing exercise-induced protein synthesis.[41]The increase in cytokines after resistance exercise coincides with the decrease in levels of myostatin, a protein that inhibits muscle differentiation and growth.[49] The cytokine response to resistance exercise and moderate-intensity running occur differently, with the latter causing a more prolonged response, especially at the 12-24 hour mark.[49][edit] Chronic inflammation and muscle lossBoth chronic and extreme inflammation are associated with disruptions of anabolic signals initiating muscle growth. Chronic inflammation has been implicated as part of the cause of the muscle loss that occurs with aging.[39][57] Increased protein levels of myostatin have been described in patients with diseases characterized by chronic low-grade inflammation.[58] Increased levels of TNF-α can suppress the AKT/mTOR pathway, a crucial pathway for regulating skeletal muscle hypertrophy,[59] thereby increasing muscle catabolism.[60][61][62] Cytokines may antagonize the anabolic effects of Insulin-like growth factor 1 (IGF-1).[63][64] In the case of sepsis, an extreme whole body inflammatory state, the synthesis of both myofibrillar and sarcoplasmic proteins are inhibited, with the inhibition taking place preferentially in fast-twitch muscle fibers.[65][63] Sepsis is also able to prevent leucine from stimulating muscle protein synthesis.[44] In animal models, when inflammation is created, mTOR loses its ability to be stimulated by muscle growth.[66][edit] Exercise as a treatment for inflammationRegular physical activity is reported to decrease markers of inflammation[quantify],[67][68][69] although the correlation is imperfect and seems to reveal differing results contingent upon training intensity. For instance, while baseline measurements of circulating inflammatory markers do not seem to differ greatly between healthy trained and untrained adults,[70][71] long-term chronic training may help reduce chronic low-grade inflammation.[72] On the other hand, levels of inflammatory markers (IL-6) remained elevated longer into the recovery period following an acute bout of exercise in patients with inflammatory diseases, relative to the recovery of healthy controls.[72] It may well be that low-intensity training can reduce resting pro-inflammatory markers (CRP, IL-6), while moderate-intensity training has milder and less-established anti-inflammatory benefits.[70][73][74][75] There is a strong relationship between exhaustive exercise and chronic low-grade inflammation.[76] Marathon running may enhance IL-6 levels as much as 100 times over normal and increases total leuckocyte count and neturophil mobilization.[76] As such, individuals pursuing exercise as a means to treat the other factors behind chronic inflammation may wish to balance their exercise protocol with bouts of low-intensity training, while striving to avoid chronic over-exertion.[edit] Signal-to-noise theoryGiven that localized acute inflammation is a necessary component for muscle growth, and that chronic low-grade inflammation is associated with a disruption of anabolic signals initiating muscle growth, it has been theorized that a signal-to-noise model may best describe the relationship between inflammation and muscle growth.[77] By keeping the "noise" of chronic inflammation to a minimum, the localized acute inflammatory response signals a stronger anabolic response than could be achieved with higher levels of chronic inflammation. + نوشته شده در ۱۳۹۰/۰۴/۲۳ ساعت 9:16 توسط mary | + نوشته شده در ۱۳۹۰/۰۴/۲۳ ساعت 9:15 توسط mary | The two lung abscesses seen here are examples of liquefactive necrosis in which there is a liquid center in an area of tissue injury. One abscess appears in the upper lobe and one in the lower lobe. Liquefactive necrosis is typical of organs in which the tissues have a lot of lipid (such as brain) or when there is an abscess with lots of acute inflammatory cells whose release of proteolytic enzymes destroys the surrounding tissues.
The liver shows a small abscess here filled with many neutrophils. This abscess is an example of localized liquefactive necrosis
This is liquefactive necrosis in the brain in a patient who suffered a "stroke" with focal loss of blood supply to a portion of cerebrum. This type of infarction is marked by loss of neurons and neuroglial cells and the formation of a clear space at the center left.
At high magnification, liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris. The job description of a macrophage includes janitorial services such as this, particularly when there is lipid.
Grossly, the cerebral infarction at the upper left here demonstrates liquefactive necrosis. Eventually, the removal of the dead tissue leaves behind a cavity
As this infarct in the brain is organizing and being resolved, the liquefactive necrosis leads to resolution with cystic spaces.
This is fat necrosis of the pancreas. Cellular injury to the pancreatic acini leads to release of powerful enzymes which damage fat by the production of soaps, and these appear grossly as the soft, chalky white areas seen here on the cut surfaces.
Microscopically, fat necrosis adjacent to pancreas is seen here. There are some remaining steatocytes at the left which are not necrotic. The necrotic fat cells at the right have vague cellular outlines, have lost their peripheral nuclei, and their cytoplasm has become a pink amorphous mass of necrotic material.
This is the gross appearance of caseous necrosis in a hilar lymph node infected with tuberculosis. The node has a cheesy tan to white appearance. Caseous necrosis is really just a combination of coagulative and liquefactive necrosis that is most characteristic of granulomatous inflammation
This is more extensive caseous necrosis, with confluent cheesy tan granulomas in the upper portion of this lung in a patient with tuberculosis. The tissue destruction is so extensive that there are areas of cavitation (cystic spaces) being formed as the necrotic (mainly liquefied) debris drains out via the bronchi.
Microscopically, caseous necrosis is characterized by acellular pink areas of necrosis, as seen here at the upper right, surrounded by a granulomatous inflammatory process
This is gangrene, or necrosis of many tissues in a body part. In this case, the toes were involved in a frostbite injury. This is an example of "dry" gangrene in which there is mainly coagulative necrosis from the anoxic injury
This is gangrene of the lower extremity. In this case the term "wet" gangrene is more applicable because of the liquefactive component from superimposed infection in addition to the coagulative necrosis from loss of blood supply. This patient had diabetes mellitus
Gangrenous necrosis involves the tissues of a body part. The inflammation seen here is extending beneath the skin of a toe to involve soft tissue (fat and connective tissue) and bone. Because multiple tissues are non-viable, amputation of such areas is necessary
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 10:21 توسط mary |When many cells undergo necrosis at once, then definable patterns of necrosis are produced, depending upon the nature of the injury, the type of tissue, and the length of time. This is an example of coagulative necrosis. This is the typical pattern with ischemia and infarction (loss of blood supply and resultant tissue anoxia). Here, there is a wedge-shaped pale area of coagulative necrosis (infarction) in the renal cortex of the kidney.
Microscopically, the renal cortex has undergone anoxic injury at the left so that the cells appear pale and ghost-like. There is a hemorrhagic zone in the middle where the cells are dying or have not quite died, and then normal renal parenchyma at the far right. This is an example of coagulative necrosis
The contrast between normal adrenal cortex and the small pale infarct is good. The area just under the capsule is spared because of blood supply from capsular arterial branches. This is an odd place for an infarct, but it illustrates the shape and appearance of an ischemic (pale) infarct well
Two large infarctions (areas of coagulative necrosis) are seen in this sectioned spleen. Since the etiology of coagulative necrosis is usually vascular with loss of blood supply, the infarct occurs in a vascular distribution. Thus, infarcts are often wedge-shaped with a base on the organ capsule
The small intestine is infarcted. The dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom. Some organs such as bowel with anastomosing blood supplies, or liver with a dual blood suppy, are hard to infarct. This bowel was caught in a hernia and the mesenteric blood supply was constricted by the small opening to the hernia sac
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 10:3 توسط mary |
The testis at the right has undergone atrophy and is much smaller than the normal testis at the left.
This is cerebral atrophy in a patient with Alzheimer disease. The gyri are narrowed and the intervening sulci widened, particularly pronounced toward the frontal lobe region
Here is the centrilobular portion of liver next to a central vein. The cells have reduced in size or been lost from hypoxia. The pale brown-yellow pigment is lipochrome that has accumulated as the atrophic and dying cells undergo autophagocytosis.
This is cardiac hypertrophy involving the left ventricle. The number of myocardial fibers does not increase, but their size can increase in response to an increased workload, leading to the marked thickening of the left ventricle in this patient with systemic hypertension
The prominent folds of endometrium in this uterus opened to reveal the endometrial cavity are an example of hyperplasia. Cells forming both the endometrial glands and the stroma have increased in number. As a result, the size of the endometrium has increased. This increase is physiologic with a normal menstrual cycle.
This is an example of prostatic hyperplasia. The normal adult male prostate is about 3 to 4 cm in diameter. The number of prostatic glands, as well as the stroma, has increased in this enlarged prostate seen in cross section. The pattern of increase here is not uniform, but nodular. This increase is in response to hormonal manipulation, but in this case is not a normal physiologic process
Here is one of the nodules of hyperplastic prostate, with many glands along with some intervening stroma. The cells making up the glands are normal in appearance, but there are just too many of them
Metaplasia of laryngeal respiratory epithelium has occurred here in a smoker. The chronic irritation has led to an exchanging of one type of epithelium (the normal respiratory epithelium at the right) for another (the more resilient squamous epithelium at the left). Metaplasia is not a normal physiologic process and may be the first step toward neoplasia
Metaplasia of the normal esophageal squamous mucosa has occurred here, with the appearance of gastric type columnar mucosa
This is cellular dysplasia in the uterine cervix. The normal cervical squamous epithelium has become transformed to a more disorderly growth pattern, or dysplastic epithelium. This is farther down the road toward neoplasia, but dysplasia is still a potentially reversible process.
Apoptosis is a more orderly process of cell death. Apoptosis is individual cell necrosis, not simultaneous localized necrosis of large numbers of cells. In this example, hepatocytes are dying individually (arrows) from injury through infection by viral hepatitis. The apoptotic cells are enlarged, pink from loss of cytoplasmic detail, and without nuclei. The cell nucleus and cytoplasm become fragmented as enzymes such as caspases destroy cellular components
In this fetal thymus there is involution of thymic lymphocytes by the mechanism of apoptosis. In this case, it is an orderly process and part of normal immune system maturation. Individual cells fragment and are consumed by phagocytes to give the appearance of clear spaces filled with cellular debris. Apoptosis is controlled by many mechanisms. Genes such as BCL-2 are turned off and Bax genes turned on. Intracellular proteolytic enzymes called caspases produce much cellular breakdown
When there is marked cellular injury, there is cell death and necrosis. This microscopic appearance of myocardium shown here is a mess because so many cells have died that the tissue is not recognizable. Many nuclei have become pyknotic (shrunken and dark) and have then undergone karorrhexis (fragmentation) and karyolysis (dissolution). The cytoplasm and cell borders are no longer recognizable. In this case, loss of the blood supply from a major coronary artery led to ischemia and cell death
Here is myocardium in which the cells are dying as a result of ischemic injury from coronary artery occlusion. This is early in the process of necrosis. The nuclei of the myocardial fibers are being lost. The cytoplasm is losing its structure, because no well-defined cross-striations are seen
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 10:2 توسط mary |Some of these skeletal muscle fibers here show atrophy, compared to normal fibers. The number of cells is the same as before the atrophy occurred, but the size of some fibers is reduced. This is a response to injury by "downsizing" to conserve the cell. In this case, innervation to the small, atrophic fibers was lost. (This is a trichrome stain.)
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 9:54 توسط mary |
Cells are connected by various components that form junctions.
The zonula occludens toward the apical margin, acts as an "O" ring to provide a tight seal so there is no leakage, and movement of fluids, ions, and small molecules is rigorously controlled. Key proteins include occludin and claudin as well as several zonula occludens (ZO) proteins. Actin filaments extend out into the cytoplasm.
The zonula adherens provides cellular attachment similar to caulking. Key proteins include catenins just inside the cell membranes and E-cadherin with calcium between the membranes. Actin filaments extend out into the cytoplasm.
The macula adherens, or desmosome provides cellular attachment similar to a rivet, with desmoglein and desmocollin proteins with calcium between the cell membranes linking two plaque regions with plakoglobin and desmoplakin proteins just inside the cell membrane. Intermediate filaments extend into the cytoplasm for anchoring.
The hemidesmosome attaches the cell to the basement membrane.
Connexons with connexin protein provide conduits for fluid, ions, and molecules passing between cells
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 9:53 توسط mary |
Cellular structure and function are determined by various cellular components. Glandular epithelial cells, such as the lining of the small intestine with a brush border, have microvilli. Glandular epithelial cells may have cytoplasmic mucin vacuoles. Epithelial cells are characterized by the presence of desmosomes that connect them. Many types of cells have cytoskeletal proteins. Squamous epithelial cells may have cytoskeletal elements such as tonofilaments. Cells with neuroendocrine differentiation tend to be rounded and may have cytoplasmic neurosecretory granules.
The extracellular matrix (ECM) is composed of a variety of components. An adhesion complex in the cell links to integrin that extends outward. Seen here is a basement membrane. An important component of basement membrane is laminin, which acts as a "lag bolt" to connect cells via integrin to the ECM. Collagen (type IV in basement membrane and types V and VI as fine fibrils) comprises the structural component of ECM that provides shape and stability. Fibronectin is an adhesive protein that acts as a "glue" to hold the various components together
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 9:52 توسط mary |A basic cell is bounded by a cell membrane. Within the cell is a nucleus containing chromatin, often condensed at the periphery, along with larger clumps called chromocenters, and in some cells a nucleolus into which RNA is concentrated. The cytoplasm contains the cytosol and a variety of organelles, including mitochondria that power the cell via production of ATP, endoplasmic reticulum and ribosomes that synthesize new materials, a Golgi apparatus, and lysosomes.
+ نوشته شده در ۱۳۹۰/۰۴/۲۱ ساعت 9:50 توسط mary |Clinical Summary
This 68-year-old man with a 7-year history of prostatic carcinoma developed metastases to the bones of the pelvis and lumbar spine which produced significant pain and discomfort. He was treated with androgen deprivation therapy to slow the growth of the tumor and decrease the size of the tumor metastases in order to help relieve his bone pain. The androgen deprivation therapy did reduce his pain; however, two months after starting the androgen deprivation therapy, the patient experienced an acute myocardial infarction and died suddenly.
Autopsy Findings
At autopsy the patient's myocardial infarction was found to have resulted from the thrombotic occlusion of the proximal left anterior descending coronary artery. There was evidence of cancer in the peripheral region of the prostate gland and there were metastases present in the pelvis and lumbar spine. The patient also had moderate testicular atrophy.
Images
Clinical Summary
This 70-year-old man was admitted to the hospital with a history of upper abdominal pain, anorexia, nausea, and general malaise, all of approximately three weeks' duration. His hospital stay was characterized by fever and severe respiratory distress. There were multiple densities in the patient's chest x-ray consistent with pneumonia and examination of a stained sputum specimen showed acid fast bacilli. Despite intensive therapy, the patient progressively deteriorated and died 14 days after admission.
Autopsy Findings
It was determined at autopsy that the patient suffered from pulmonary tuberculosis with widespread dissemination throughout the body. The left lung weighed 620 grams and the right lung 1230 grams. These were characterized by marked congestion and edema. In addition, multiple gray-white nodules ranging from pinpoint size up to 1 cm were diffusely distributed throughout the lung parenchyma.
Images
Clinical Summary
This was a 37-year-old female with chronic renal failure that necessitated a renal transplant. Following transplantation, the patient developed a herpes simplex virus (HSV) infection in her nasal cavity, oral candidiasis, pneumonia, hematuria, pyuria, and gastrointestinal bleeding. Subsequently, the patient became septic and died.
Autopsy Findings
Major findings at autopsy included extensive hemorrhagic bronchopneumonia (Pseudomonas aeruginosa) and multiple ulcers affecting the stomach and esophagus. There was also evidence of disseminated intravascular coagulation (DIC) with multiple hemorrhages present. Firm, whitish foci of necrotic tissue were found in the fat around the pancreas.
Images
Clinical Summary
This 67-year-old male with advanced colon cancer developed obstruction of the bowel and underwent palliative surgery to remove an 8-cm portion of colon containing the obstruction. During the surgery the patient had several episodes of hypotension. After surgery he did not regain consciousness and required ventilator support. Four days after surgery, the patient developed a fever and his white blood cell count was found to be 15,256 cells/cmm. Thus, he was started on broad-spectrum antibiotics. A chest x-ray demonstrated infiltrates in both lungs, which worsened over the next several days. His overall condition continued to deteriorate and he died 12 days after surgery.
Autopsy Findings
At autopsy, metastatic colon cancer was found throughout the abdominal cavity and invading into the liver. The lungs were markedly consolidated and had several focal abscesses that were 2 to 4 cm in diameter. Liquefied material poured out from inside these abscesses when the lungs were sliced.
Images
Clinical Summary
This was a 57-year-old male whose hospital course following abdominal surgery was characterized by progressive deterioration and hypotension. Four days post-operatively, the patient sustained an anterior myocardial infarction and died the next day.
Autopsy Findings
The patient's heart weighed 410 grams. Examination of the coronary arteries revealed marked atherosclerotic narrowing of all three vessels with focal occlusion by a thrombus of the left anterior descending artery. Fresh necrosis of the anterior wall of the left ventricle and anterior portion of the septum was present, extending from the endocardium to the inner half of the ventricular wall.
Images
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