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Jennifer McCann, PharmD, BCPS, BCCCP

• Assistant Professor of Pharmacy Practice, Butler University College of Pharmacy and Health Sciences, Indianapolis, Indiana

The importance of interleukin 18 erectile dysfunction vacuum pump reviews discount vardenafil express, glutathione peroxidase erectile dysfunction in the military buy genuine vardenafil on line, and selenium concentration changes in acute pancreatitis erectile dysfunction doctors in fresno ca discount 10 mg vardenafil otc. The first histological demonstration of pancreatic oxidative stress in human acute pancreatitis erectile dysfunction blue pill cheap vardenafil line. Relationship of carotenoid and vitamins A and E with the acute inflammatory response in acute pancreatitis. Role of oxidative stress in the pathogenesis of caerulein-induced acute pancreatitis. Assessment of total antioxidant status in acute pancreatitis and prognostic Significance Int J Biol Med Res. Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis. Serum profiles of E-selectin, interleukin-10, and interleukin-6 and oxidative stress parameters in patients with acute pancreatitis and nonpancreatic acute abdominal pain. Association of antioxidant enzyme gene polymorphisms and glutathione status with severe acute pancreatitis. Intravenous n acetylcysteine, ascorbic acid and selenium-based anti-oxidant therapy in severe acute pancreatitis. The dynamics of the oxidant-antioxidant balance in the early phase of human acute biliary pancreatitis. Introduction In acute pancreatitis, reductions in blood flow and alterations of microvascular integrity resulting in impaired tissue oxygenation play an important part in the progression and possibly the initiation of the disease. Independently of the initial noxa, the intra-pancreatic activation of trypsinogen to trypsin is the crucial trigger of acute pancreatitis. The central events for the further course are the release of local mediators (cytokines, vasoactive substances, free oxygen radicals) and subsequently the development of microcirculatory disturbances and the activation of leukocytes and their infiltration into the tissue. At present, the deterioration of microcirculation is seen as the most important pacemaker in the progression to a necrotizing pancreatitis. In addition to its potentiatory role, severe pancreatic ischemia can play a pathogenetic role in the initiation of acute pancreatitis. The acute edematous pancreatitis is characterized by an increased and homogeneous microperfusion. The experimental necrotizing pancreatitis shows a progredient decrease of capillary perfusion despite stable macrohemodynamics. There is increasing evidence that ischemia alone may be the primary cause of pancreatitis or may be the exacerbating promotor for the progression from edematous to necrotizing pancreatitis. In clinical studies there was evidence, that ischemia during cardiopulmonary bypass triggered acute pancreatitis and acute pancreatitis was found in up to 25% of autopsies of patients dying after shock. In animal models severe pancreatitis could be induced by obstruction of terminal pancreatic arterioles. The hypothesis, that the manifestation of microvascular injury in acute pancreatitis involves ischemia/reperfusion(I/R)-associated events, is supported by the study of Menger et al. In this investigation, post-ischemic reperfusion was characterized by a significant reduction of functional capillary density (no reflow) and by a marked increase of the permanently adherent leukocytes in postcapillary venules (reflow paradox) (Fig. In addition, the functional and histomorphological alterations in this study were similar to the alteration seen in edematous pancreatitis. Postischemic activation of leukocytes has been reported to determine the outcome of I/R injury. Increased leukocyte endothelial cell interactions in postcapillary venules mimicking the I/R event were observed during vasodilation. The concept of I/R-induced pancreatitis is mostly reflected in the clinical situation of post-transplant pancreatitis. Experimental studies using the model of syngeneic pancreas transplantation in rats show microcirculatory disturbances and cellular damages similar to those seen in the beginning of an acute pancreatitis [4]. Pancreatitis after hemorrhagic shock or hypotension with hypoxia, but not complete ischemia/anoxia may also involve pathomechanisms associated with ischemia/reperfusion. A recent study demonstrates, that hemorrhagic hypotension in rats induces intermittent capillary perfusion, which is characterized by periods of normal blood flow followed by periods of complete cessation of blood flow [5]. This type of regional ischemia and reperfusion may contribute to the manifestation of pancreatitis, independent of the etiology. In-vivo microscopic image of sticking platelets in a postcapillary venule of a post ischemic rat pancreas. This interaction takes place in three parts: a weak adhesion of the neutrophils to the endothelium, followed by a stronger adhesion and, finally, the neutrophil migration (Fig. Three families of adhesion molecules are implicated: selectins, b2-integrins and immunoglobulins (Table 1). The L-selectin, expressed by the endothelial cells and the neutrophils, plays a part at the beginning of reperfusion. A more important stowing of neutrophils in the endothelium utilizes other leukocyte and endothelium proteins that have a stronger affinity for each other. This interaction fastens the neutrophil to the surface of the endothelial cell and allows the next stage. Arriving at the interstitium, the activated neutrophil will cause considerable damage to a tissue, which has already suffered from hypoxia. The neutrophilic granules, filled with proteases, collagenases, elastases, lipooxygenases, phospholipases and myeloperoxidases, will digest and disorganize the protein network of extracellular matrix (Table 2). The proteic network of extracellular matrix is important in healing while being used to guide tissue formation. The inflammation induced by reperfusion is a major cause of the lesions observed after restoration of blood flow in an ischemic organ. The massive production of cytokines, the activation of the complement and a complex choreography of the neutrophils are the key factors and are therefore being examined in research to modulate the inflammatory reaction. Therefore, platelets can potentially contribute to the manifestation of 146 Acute Pancreatitis pancreatitis after normothermic I/R injury. Activation products released by leukocytes and platelets that may impair endothelial barrier function. Platelet activation was accompanied by leukocyte activation in a study of Hackert et al. An interaction between these two cell types has been demonstrated by different authors in the past [26-28]. Among others, P-selectin seems to be one of the most important adhesion molecules, which links the inflammatory and procoagulatory cascades and has the potency to activate leukocytes and platelets as the cellular elements of either pathway [27-30]. Besides their adherence to endothelial cells, activated platelets form stable aggregates with leukocytes. This results in a combined inflammatory and coagulatory contribution to thrombus formation and is also mediated by P-selectin and beta-integrins [31, 32]. Especially, the formation of microthrombotic vessel occlusion with microcirculatory perfusion failure and consequent ischemia, hypoxia, and tissue necrosis promote organ damage. Evidence is mounting on the importance of T cells in mediating both short and long-term damage during I/R injury, which in turn could explain why I/R contributes to poor late allograft function [37, 38]. The adherence of lymphocytes in hepatic sinusoids occurs early duringreperfusion and impairs liver function following prolonged cold ischemic times [44]. Adhesion molecules A variety of adhesion molecules are implicated in the progression of disease. Under normal circumstances, it will not be expressed or just with low expression in most vessels. However, when its expression increased, it can interact with integrin on the surface of granular cells. Therefore, it can cause leukocyte migration through capillary endothelial barriers to inflammatory regions, and then cause excessive architectonic inflammatory response [47]. This upregulation is mirrored by increased tissue infiltration of leukocytes and increased endothelium-leukocyte interaction. I/R leads to fibrinogen deposition on microvascular endothelial cells and a corresponding accumulation of firmly adherent platelets. In I/R models of platelet adhesion, it appears that those models that elicit a rapid adhesion response in both venules and arterioles are entirely Microcirculatory Disturbances in the Pathogenesis of Acute Pancreatitis 149 dependent on endothelial P-selectin [56], while I/R models exhibiting slow, time-dependent platelet adhesion only in venules involve both platelet and endothelial cell P-selectin [57]. Therapeutic approaches to prevent or treat microcirculatory disturbances in acute pancreatitis.

In advanced cases with severe corneal complications impotence qigong purchase vardenafil pills in toronto, corneal transplantation may be needed to improve the visual acuity impotence juice recipe effective 10mg vardenafil. It is probably a basophil-rich delayed hypersensitivity disorder (Jones-Mote hypersensitivity) insulin pump erectile dysfunction buy vardenafil once a day, perhaps with an IgE humoral component impotence fonctionnelle purchase vardenafil us. Use of glass instead of plastic for prostheses and spectacle lenses instead of contact lenses is curative. If the goal is to maintain contact lens wear, additional therapy will be required. Hydrogen peroxide disinfection and enzymatic cleaning of contact lenses may also help. Alternatively, changing to a weekly disposable or daily disposable contact lens system may be beneficial. If these treatments are unsuccessful, use of contact lenses should be discontinued. Until recently, by far the most frequent cause of phlyctenulosis in the United States was delayed hypersensitivity to the protein of the human tubercle bacillus. This is still the most common cause in regions where tuberculosis is still prevalent. In the United States, however, most cases 232 are now associated with delayed hypersensitivity to S aureus. Mild limbal phlyctenule probably secondary to Staphylococcus marginal disease in a 30-year-old female that improved with corticosteroid treatment. Consistent with this difference is the fact that scars form on the corneal side of the limbal lesion and not on the conjunctival side. Phlyctenulosis is often triggered by active blepharitis, acute bacterial conjunctivitis, and dietary deficiencies. Phlyctenulosis induced by tuberculoprotein and the proteins of other systemic infections responds dramatically to topical corticosteroids. A major reduction of symptoms occurs within 24 hours and disappearance of the lesion in another 24 hours. Topical antibiotics should be added for active staphylococcal blepharoconjunctivitis. Treatment should be aimed at the underlying disease, and corticosteroids, when effective, should be used only to control acute symptoms and persistent corneal scarring. Examination of Giemsa-stained scrapings often discloses only a few degenerated epithelial cells, a few polymorphonuclear and mononuclear cells, and no eosinophils. Treatment should be directed toward finding the offending agent and 234 eliminating it. The contact blepharitis may clear rapidly with topical corticosteroids, but their use should be limited. Long-term use of corticosteroids on the lids may lead to steroid glaucoma and to skin atrophy with disfiguring telangiectasis. When associated with a generalized autoimmune disease, usually rheumatoid arthritis, it is known as secondary rather than primary Sjogren syndrome. The syndrome is overwhelmingly more common in women at or beyond menopause than in other groups, although men and younger women may also be affected. The lacrimal gland is infiltrated with lymphocytes and occasionally with plasma cells, leading to atrophy and destruction of the glandular structures. Dry eye syndrome is characterized by bulbar conjunctival hyperemia (especially in the palpebral aperture) and symptoms of irritation that are out of proportion to the mild inflammatory sign, with pain increasing by the afternoon and evening but being absent or only slight in the morning. Rose bengal or lissamine green staining of the cornea and conjunctiva in the palpebral aperture is a helpful diagnostic test. Demonstration with fluorescein staining of punctuate epithelial erosions found in dry eye syndrome due to Sjogren syndrome, with greater distribution of epithelial lesions inferiorly. Treatment is directed toward preserving and improving the quality of the tear film with artificial tears, obliteration of the puncta, and side shields, moisture chambers, and Buller shields. The conjunctiva may be affected alone or, as indicated by its name, in combination with the mouth, nose, esophagus, vulva, and skin. The cornea is affected only secondarily as a result of trichiasis 236 and lack of the precorneal tear film. The disease is often more severe in women than in men and typically occurs in middle life, very rarely before age 45. In women, it may progress to blindness in a year or less; in men, progress is slower, and spontaneous remission sometimes occurs. Conjunctival biopsies may contain eosinophils, and the basement membrane will stain positively with certain immunofluorescent stains (IgG, IgM, IgA complement). The secondary consequences, such as tear deficiency, trichiais, and ocular toxicity need to be recognized and treated appropriately. Generally, the course is long and the prognosis poor, with blindness due to complete symblepharon and corneal desiccation. Silver nitrate instilled into the conjunctival sac at birth (Crede prophylaxis) is a frequent cause of mild chemical conjunctivitis. If tear production is reduced by continual irritation, the conjunctiva can be further damaged by the lack of dilution of the noxious agent as it is instilled into the conjunctival sac. Conjunctival scrapings often contain keratinized epithelial cells, a few polymorphonuclear neutrophils, and an occasional oddly shaped cell. Treatment consists of stopping the offending agent and using bland drops or none at all. Often the conjunctival reaction persists for weeks or months after its cause has been eliminated. Some common irritants are fertilizers, soaps, deodorants, hair sprays, tobacco, makeup preparations (mascara, etc), and various acids and alkalies. In certain areas, smog has become the most common cause of mild chemical conjunctivitis. The specific irritant in smog has not been positively identified, and treatment is nonspecific. There are no permanent ocular effects, but affected eyes are frequently chronically red and irritated. In acid burns, the acids denature the tissue proteins and the effect is immediate. Alkalies do not denature the proteins, but tend to penetrate the tissues deeply and rapidly and to linger in the conjunctival tissue. Once in contact with the ocular surface, alkalies saponify fatty acids and continue to inflict damage for hours or days, depending on the molar concentration of the alkali and the amount introduced. Adhesions between the bulbar and palpebral conjunctiva (symblepharon) and corneal scarring are more likely to occur if the offending agent is an alkali. In either event, pain, injection, photophobia, and blepharospasm are the principal symptoms of caustic burns. Immediate and profuse irrigation of the conjunctival sac with water or saline solution is of great importance, and any solid material should be removed mechanically. Further treatment may involve intensive topical steroids, ascorbate and citrate eye drops, cycloplegics, 238 antiglaucoma treatment as necessary, cold compresses, and systemic analgesics (see Chapter 19). Corneal involvement may require amniotic membrane graft, limbal stem cell transplantation, or corneal transplantation.

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The receptor is believed to exist in two inter changeable states: Ra (active) and Ri (inactive) which are in equilibrium erectile dysfunction among young adults discount 20 mg vardenafil. The inverse agonist (D) has high affinity known to be capable of adopting not just two erectile dysfunction treatment old age cheap vardenafil 20mg with mastercard, for the Ri state (Fig erectile dysfunction ayurvedic drugs purchase vardenafil without prescription. Molecular cloning has also helped in obtaining the delineation of multiple types and subtypes the receptor protein in larger quantity to study of receptors for signal molecules has played an its structure and properties impotence due to diabetes cheap vardenafil 10mg overnight delivery, and in subclassifying important role in the development of a number receptors. Multiple of the four major families of receptors (described subtypes of receptors for practically all later) have a well defined common structural motif, transmitters, autacoids, hormones, etc. Majority of receptor cases, receptor classification has provided sound molecules are made up of several non-identical explanation for differences observed in the actions subunits (heteropolymeric), and agonist binding of closely related drugs. Pharmacological criteria Classification is based on receptor move apart opening a centrally located relative potencies of selective agonists and antagonists. This is the classical and oldest approach with direct clinical bearing; was used in delineating M and N Many drugs act upon physiological receptors cholinergic, and adrenergic, H1 and H2 histaminergic which mediate responses to transmitters, hormo receptors, etc. Tissue distribution the relative organ/tissue distri molecules; examples are cholinergic, adrenergic, bution is the basis for designating the subtype. Ligand binding Measurement of specific binding of there are no known physiological ligands. Autoradiography has Receptors subserve two essential functions, helped in mapping distribution of receptor subtypes in viz, recognition of the specific ligand molecule the brain and other organs. Transducer pathway Receptor subtypes may be Accordingly, the receptor molecule has a ligand distinguished by the mechanism through which their activation is linked to the response. M cholinergic binding domain(spatially and energetically suitable receptor acts through G-proteins, while N cholinergic for binding the specific ligand) and an effector receptor gates influx of Na+ ions; adrenergic receptor domain (Fig. Molecular cloning the receptor protein is cloned and variously translated into the response. The sequen its detailed amino acid sequence as well as three tial relationship between drug action, transducer dimentional structure is worked out. The functional significance of many of these subtypes/ Considerable progress has been made in the isoforms is dubious. Even receptors without known understanding of transducer mechanisms which ligands (orphan receptors) have been described. However, a consensus received extra and intra-cellular signals at each receptor classification is now decided on a step. Silent receptors these are sites which bind specific the transducer mechanisms can be grouped into drugs but no pharmacological response is elicited. To avoid homology, and belong to one super-family of confusion, the term receptor should be restricted to those regulatory binding sites which are capable of generating a receptors. All such receptors have a common drug with its receptor resulting in a conforma pattern of structural organization (Fig. In case of nicotinic cholinergic receptor, the molecule (8 nm in diameter) is composed of 5 subunits (2 + + + ) enclosing a transmembrane ion channel within the subunit. When two molecules of acetylcholine bind to the two subunits (B), all subunits move apart opening the central pore to 0. Anions are blocked from passage through the channel by positive charges lining it. In other cases, K+, Ca2+ or Cl ions move through the channel depending on its ion selectivity. The G proteins float in the membrane with their exposed domain lying in the cytosol, and are heterotri meric in composition (, and subunits). The diamer has also been shown to activate receptor-operated K+ channels, to inhibit voltage gated Ca2+ channels Fig. The intervening A number of G proteins distinguished by their segments connecting the helices form 3 loops on either subunits have been described. The amino terminus of the chain ones with their action on the effector are: lies on the extracellular face, while the carboxy terminus Gs : Adenylyl cyclase activation, Ca2+ is on the cytosolic side. The onset time of response through this on the type of effector cell) and mediates various type of receptors is also in seconds. So that it can serve There are three major effector pathways (Table signaling functions, the cytosolic concentration 4. The diamer of Gi activates membrane K+ channels causing hyperpolarization which depresses impulse generation. Thus, the same intracellular messenger can trigger different inhibitory G-protein when directionally opposite responses depending on the nature and strength of the responses would be expected. Cytosolic Ca2+ is recycled by uptake into the endoplasmic reticulum as well as effluxed by membrane Ca2+ pump. Hormone binding induces these cell surface receptors, also called ligand dimerization of receptor molecules, brings about gated ion channels, enclose ion selective channels conformation changes which activate the kinase (for Na+, K+, Ca2+ or Cl) within their molecules. These are then changes in cytosolic ionic composition, depending phosphorylated and released to carry forward the on the ion that flows through. The receptor is usually a pentameric protein; all subunits, in addition to large intra and extracellular segments, generally have four membrane spanning helical domains. The subunits are mostly arranged round the channel like a rosette and the subunits usually bear the agonist binding sites. Certain receptor-operated (or ligand-gated) ion channels also have secondary ligands which bind to an allosteric site and modulate the gating of the channel by the primary ligand. Thus, in these receptors the agonist directly operates ion channels, without the intervention Fig. The linked receptor: On binding the peptide hormone to the extracellular onset and offset of responses through this class domains, the monomeric receptors move laterally in the of receptors is the fastest (in milliseconds). The phosphorylated substrate proteins then peptide hormones, and are made up of a large perform downstream signaling function. Many cytokines, growth phosphorylate tyrosine residues on the receptor which then hormone, prolactin, interferons, etc. Receptors regulating gene expression nucleus to regulate transcription of target genes. Thus, by controlling these are intracellular (cytoplasmic or nuclear) phosphorylation of key enzymes, ion channels, soluble proteins which respond to lipid soluble transporters, etc. The receptor protein (specific for each reactions, cell growth and differentiation. The liganded receptor internalization, degradation in lysosomes and diamer moves to the nucleus and binds other co down regulation if activation is fast enough. A dimerization region that overlaps the steroid binding domain is exposed, promoting dimerization of the occupied receptor. The expression of these genes is consequently altered resulting in promotion (or suppression) of their transcription. The mechanisms involved may be unmasking rone), thyroxine, vit D and vit A function in this of receptors or their proliferation (up regulation) manner. Different steroidal hormones affect or accentuation of signal amplification by the different target cells and produce different effects transducer. This can be easily will be bound is provided by the hormone binding demonstrated experimentally (Fig. Different ligands of the same parkinsonian patients treated with high doses of nuclear receptor have been found to induce ligand levodopa gradually become less reponsive. The specific conformations of the receptor so that changes may be brought about by: different combinations of co-activators and co repressors may be bound in different target tissues, (i) Masking or internalization of the receptor (it. Chimeric receptors have also been produced which respond to one hormone, but produce the effects of the other hormone. This transduction mechanism is the slowest in its time course of action (takes hours) because adequate quantity of the effector protein will have to be produced before the response occurs. The effects also generally out last the signal (hormone), because majority of the generated effector proteins have slow turnover, and persist in the body even after the hormone has been eliminated. Regulation of receptors Receptors exist in a dynamic state; their density and efficacy to elicit the response is subject to regulation by the level of on-going activity, feedback from their own signal output and other Fig. The sensitivity of uterus to con high (100 fold) dose of the agonist, the response is tractile action of oxytocin increases progressively markedly attenuated, but is regained if sufficient time is during the third trimester of pregnancy, especially allowed to elapse.

The enuresis may have been present from birth or it may have arisen following a period of acquired bladder control erectile dysfunction doctors in cincinnati best 20mg vardenafil. The enuresis may or may not be associated with a more widespread emotional or behavioural disorder age related erectile dysfunction causes discount 20mg vardenafil visa. The condition may represent an abnormal continuation of normal infantile incontinence erectile dysfunction premature ejaculation treatment buy discount vardenafil 10mg line, it may involve a loss of continence following the acquisition of bowel control erectile dysfunction typical age buy vardenafil now, or it may involve the deliberate deposition of faeces in inappropriate places in spite of normal physiological bowel control. The condition may occur as a monosymptomatic disorder, or it may form part of a wider disorder, especially an emotional disorder (F93. Includes: Functional encopresis Incontinence of faeces of nonorganic origin Psychogenic encopresis Use additional code to identify the cause of any coexisting constipation. It generally involves food refusal and extreme faddiness in the presence of an adequate food supply, a reasonably competent caregiver, and the absence of organic disease. There may or may not be associated rumination (repeated regurgitation without nausea or gastrointestinal illness). Includes: Rumination disorder of infancy Excludes: anorexia nervosa and other eating disorders (F50. It may occur as one of many symptoms that are part of a more widespread psychiatric disorder (such as autism), or as a relatively isolated psychopathological behaviour; only the latter is classified here. The phenomenon is most common in mentally retarded children and, if mental retardation is also present, F70-F79 should be selected as the main diagnosis. When such movements occur as symptoms of some other disorder, only the overall disorder should be recorded. The movements that are of a non self-injurious variety include: body-rocking, head-rocking, hair plucking, hair-twisting, finger-flicking mannerisms, and hand-flapping. Stereotyped self injurious behaviour includes repetitive head-banging, face-slapping, eye-poking, and biting of hands, lips or other body parts. All the stereotyped movement disorders occur most frequently in association with mental retardation (when this is the case, both should be recorded). If eye poking occurs in a child with visual impairment, both should be coded: eye-poking under this category and the visual condition under the appropriate somatic disorder code. Includes: Stereotype/habit disorder Excludes: abnormal involuntary movements (R25. It should be classified as a disorder only if its severity is such as to markedly disturb the fluency of speech. The "sequelae" include conditions specified as such or as late effects, or those present one year or more after onset of the causal condition. For use of this category reference should be made to the relevant morbidity and mortality coding rules and guidelines. Excludes: epileptic seizure related to psychoactive substance withdrawal (F10-F19 with common fourth characters. The category is also for use in multiple coding to identify these types of hemiplegia resulting from any cause. The category is also for use in multiple coding to identify these conditions resulting from any cause. Includes: with mention of hypertension (I10-I15) Use additional code to identify presence of hypertension. I20 Angina pectoris Use additional code from category (E10-E14) with fourth and fifth characters. J09 Influenza due to certain identified influenza virus Note: Influenza caused by influenza virus strains of special epidemiological importance with an animal-human or inter-human transmission limited to the inclusions. Includes: Influenza A/H1N1 pandemic 2009 [swine flu] Influenza A/H5N1 epidemic [avian influenza] Use additional code to identify pneumonia or other manifestations. Complicated haemorrhoids include those with additional signs of strangulation, thrombosis, necrosis and/or ulceration. Includes: bedsore plaster ulcer Use additional code from category (E10-E14) with fourth and fifth characters. Includes: Decubitus [pressure] ulcer limited to erythema [redness] only, without skin breakdown L89. Distinction is made between the following types of etiological relationship a) direct infection of joint, where organisms invade synovial tissue and microbial antigen is present in the joint; b) indirect infection, which may be of two types: a reactive arthropathy, where microbial infection of the body is established but neither organisms nor antigens can be identified in the joint, and a postinfective arthropathy, where microbial antigen is present but recovery of an organism is inconstant and evidence of local multiplication is lacking. M00 Pyogenic arthritis Excludes: infection and inflammatory reaction due to internal joint prosthesis (T84. The term primary has been used with its customary clinical meaning of no underlying or determining condition identified. M99 the following fifth characters represent the following sites of involvement 0 Head region occipitocervical 1 Cervical region cervicothoracic 2 Thoracic region thoracolumbar 3 Lumbar region lumbosacral 4 Sacral region sacrococcygeal, sacroiliac 5 Pelvic region hip, pubic 6 Lower extremity 7 Upper extremity acromioclavicular,sternoclavicular 8 Rib cage costochondral, costovertebral, sternochondral 9 Abdomen and other M99. Use additional codes to identify any associated hypertensive renal disease (I12) or hypertensive heart and renal disease (I13). Excludes: erosion and ectropion of cervix without cervicitis (N86) N73 Other female pelvic inflammatory diseases Use additional code (B95-B97) to identify infectious agent. N77* Vulvovaginal ulceration and inflammation in diseases classified elsewhere N77. O03 Spontaneous abortion Note: Incomplete abortion includes retained products of conception following abortion. For use of this category reference should be made to the morbidity coding rules and guidelines. O08 O08 Complications following abortion Ectopic Hydatidiform Spontaneous Medical Other Unspecified and ectopic and molar pregnancy pregnancy mole and abortion abortion abortion type of other abortion, abnormal subsequent products of episode of conception care only O08. O94 Sequelae of complication of pregnancy, childbirth and the puerperium Note: Category O94 is to be used for morbidity coding only to indicate previous episodes of conditions in categories (O00-O75 and O85-O92) as the cause of sequelae, which are themselves classified elsewhere. Not to be used for chronic complications of pregnancy, childbirth and the puerperium. Excludes: that resulting in death (O96, O97) O95 Obstetric death of unspecified cause Includes: maternal death from unspecified cause occurring during pregnancy, labour and delivery, or the puerperium O95. Includes: the listed conditions, without further specification, as the cause of mortality, morbidity or additional care, in newborn Excludes: low birth weight due to slow fetal growth and fetal malnutrition (P05. Usually implies a birth weight>90th percentile for gestational age or 4000g or more at term Excludes: birth weight of 4500g or more (P08. In general, categories in this chapter include the less well-defined conditions and symptoms that, without the necessary study of the case to establish a final diagnosis, point perhaps equally to two or more diseases or to two or more systems of the body. Practically all categories in the chapter could be designated "not otherwise specified", "unknown etiology" or "transient". The Alphabetical Index should be consulted to determine which symptoms and signs are to be allocated here and which to other chapters. The category is for use in multiple coding to identify this condition resulting from any cause. Where multiple sites of injury are specified in the titles, the word "with" indicates involvement of both sites, and the word "and" indicates involvement of either or both sites. The principle of multiple coding of injuries should be followed wherever possible. Combination categories for multiple injuries is provided for use when there are insufficient detail as to the nature of the individual conditions, or for primary tabulation purposes when it is more convenient to record single code; otherwise, the component injuries should be coded separately.