Z. Runak. United States Naval Academy.
Inflammation - Inflammation may be a primary phenomenon or a secondary phenomenon and plays a role in the development of acne comedones buy cefpodoxime 200mg with mastercard, papules buy generic cefpodoxime on-line, pustules buy cefpodoxime 200mg on-line, and nodules in a sebaceous distribution characterize acne vulgaris discount cefpodoxime 200 mg. The face may be the only involved skin surface, but the chest, the back, and the upper arms are often involved 5. Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrine disorders with excess androgens may trigger the development of acne vulgaris. The grade and the severity of the acne help in determining, which of the following treatments, alone or in combination, is most appropriate. The development of resistance is lessened if topical antibiotics are used in combination with benzoyl peroxide. They cause epidermal differentiation and, thus, normalize follicular hyperproliferation and hyperkeratinization. Systemic treatment Tetracycline, (minocycline, docycyline and tetracycline, erythromycin 1g daily for one month then 250 bid for 4-6 moths). Trimethoprim, alone or in combination with sulfamethoxazole, are systemic antibiotics and anti-inflammatory. Isotretinoin is a systemic retinoid that is highly effective in the treatment of severe, recalcitrant acne vulgaris 47 Patients with moderate to severe inflammatory acne may be treated with prescription of topical or oral medicines, alone or in combination. Psoriasis Psoriasis is a chronic inflammatory and proliferative disorder of the skin clinically manifested as well-circumscribed, erythematous papules and plaques covered with silvery scales typically located over the extensor surfaces and scalp. While specific systemic and environmental factors are known to influence the disease, it has unpredictable course with spontaneous improvement and exacerbations of lesions. Immune system dysfunction in the background of a genetic predisposition is believed to be at the core of the disease process. The Male and female ratio is 1 to 1 and the peak age of onset is in the 20s Etiology and Pathogenesis Despite being the subject of intensive research over the years, the precise etiology of psoriasis still remains unknown. Genetic factors can be implicated on the basis of population surveys, twin studies (65% concordant in monozygotic twins) and analysis of pedigrees. Trauma - All types of trauma can lead to the development of plaque psoriasis (eg, physical, chemical, surgical, infective, and inflammatory). Alcohol - Alcohol is considered a risk factor for psoriasis, particularly in young to middle-aged males. Accelerated epidermal cell proliferation results from recruitment of a large proportion of resting cells into the proliferative cycle. The pathology of psoriasis reflects the underlying immune-mediated inflammation and cellular hyperproliferation. Types of presentations: the patients may present in a variety of ways with overlapping features being not uncommon. The commonest type of psoriasis, presenting with typical plaques of psoriasis of the extensors surfaces like knee, pretibial area elbows and trunk, back and scalp. Flexural psoriasis (psoriasis inversa): lesions are present over the flexors and intertriginous areas (axilla, groin, umbilical region, inframammary folds) the lesions may be moist and lack the typical scaling. Generalized pustular psoriasis may occur as an explosive eruption of generalized pustules with systemic disturbances. Localized pustular psoriasis usually presents with persistent pustular eruptions of the hands and feet. The commonest type is asymmetrical oligoarthritis, other types are: symmetrical seronegative rheumatoid- like disease , distal interphalangeal involvement( most characteristic, but relatively rare), axial skeletal involvement, and a destructive mutilating form (arthritis mutilans) The typical lesions of psoriasis have the following features; The lesions are very well marginated with distinct border and are raised above the surface. The lesions are covered with silvery white, mica-like, loosely adherent scales which, on removal may reveal punctate bleeding points (Auspitz sign) Symmetry: the lesions are symmetrically disposed on extensor surfaces of the body. Management of psoriasis Topical therapy is generally indicated when psoriasis is limited to less than 20% of the body surface. Either alone or in combination with coal tar or topical corticosteroids, salicylic acid (2% to 10%) helps to soften and remove psoriatic scale. Coal tar 5-10% Ultraviolet Radiation although coal tar has been used to treat psoriasis for decades, its mechanism of action is still not well understood. Moisturizer (Emollients) help to hydrate, soften, and loosen psoriatic plaques A strong topical steroid once or twice daily, cover with salicylic acid 2- 10 if necessary. Vitamin D3 analogues: Calcitriol and Calcipotriol, act by regulating keratinocyte proliferation and maturation. Therapy usually is given 2-3 times per week on an outpatient basis, with maintenance treatments every 2-4 weeks until remission. Systemic corticosteroids are generally contraindicated, and they can exacerbate a very severe type of psoriasis called pustular psoriasis, which has a high rate of mortality 3. In the acute and sub acute phases, there is rapid onset of generalized vivid red erythema and fine branny scales; the patient feels hot and cold, shivers, and has fever. There is a loss of scalp and body hair, the nails become thickened and separated from the nail bed (onycholysis), and there may be hyperpigmentation or patchy loss of pigment in patients whose normal skin color is brown or black. The most frequent preexisting skin disorders are (in order of frequency) psoriasis, eczematous dermatitis (atopic, allergic contact, seborrheic), adverse cutaneous drug reaction, lymphoma, and pityriasis rubra pilaris. Drugs most commonly implicated in erythroderma are found In 10 to 20% of patients it is not possible to identify the cause by history or histology. Large amounts of warm blood are present in the skin due to the dilatation of capillaries, and there is considerable heat dissipation through insensible fluid loss and by convection. Also, there may be high output cardiac failure; the loss of scales through exfoliation can be considerable, up to 9 g/m2 of body surface per day, and this may contribute to the reduction in serum albumin and the edema of the lower extremities so often noted in these patients. Thickening leads to exaggerated skin folds; scaling may be fine and branny, and may be barely perceptible or large, up to 5 cm, and lamellar. Palms and Soles Usually involved, with massive hyperkeratosis and deep fissures in pityriasisrubra pilaris, Sézary’s syndrome, and psoriasis. General Examination Lymph nodes generalized, rubbery, and usually small; enlarged in Sézary’s syndrome. Despite the best attention to all details, patients may succumb to infections or, if they have cardiac problems, to cardiac failure (“high output” failure) or to the effects of the prolonged glucocorticoid therapy that may be required. Management This is an important medical problem that should be dealt with in a modern inpatient dermatology facility with experienced personnel. The patient should be hospitalized in a single room, at least for the beginning workup and during the development of a therapeutic program. The hospital room conditions (heat and cold) should be adjusted to the patient’s needs; most often these patients need a warm room with many blankets. Presenting with atypical presentation, more disseminated disease, or being resistant to conventional therapies and patient having related disorders eg candidiasis, H. The eruption, which is characterized by widespread inflammatory and hyperkeratotic lesions in seborrhoeic areas, may progress to erythroderma in some patients. In some instances, pre-existing psoriasis may become more severe with disseminated plaques and pustules. It manifests as small, itchy, red or skin-colored papules on the head, the neck, and the upper part of the trunk. Oral hairy leukoplakia has no malignant potential, but it may be the initial sign of progressive immunosuppression. Systemic coccidioidomycosis may disseminate to the skin, usually as hemorrhagic papules or nodules Cutaneous drug eruptions 10% Sulfonamides may cause urticaria; erythema multiforme; toxic epidermal necrolysis; and systemic reactions, including fever, leukopenia, thrombocytopenia, hepatitis, and 59 nephritis. B: Regarding Leprosy you are advised to refer the Manual prepared by disease prevention and control department, Ministry of Health, Ethiopia, 2002. Purpose and use of this satellite module This module is intended to be used by midlevel Nurses and is believed to equip them with basic and adequate information that are not discussed in the core module. Besides, it helps the health worker to appreciate common skin infectious disease by focusing on bacterial, fungal, viral and parasitic skin problems including non- infectious skin disease 4. All are possible causes of skin diseases, except a) Chemical agent b) Physical agent c) Irritant substances d) None of the above 5. All can be practical measures to prevent skin disease except a) By keeping cleanliness of the skin b) By early identification c) By removing the predisposing factors d) By treating all skin diseases with antibiotics 6. It is the disease associated with poor personal hygiene and low living condition a) Scabies b) Acne c) Carbuncle d) Leprosy 8. Nurse can manage a disease called scabies in the health center by ordering a) Benzyl benzoate lotion b) White filed ointment c) Procaine penicillin 600. All are true statements about cutaneous Leshimaniasis except, a) Single or multiple lesion that can be changed to ulcer b) Mucocutaneous lesion will involve in nasopharyngeal tissue c) Animals are consider as source of infection d) All of the above e) None of the above 12. The role of nurse who is working in primary health care unit, for the patient who is admitted and developed bedsore will be all, except a) Clean and dress the wound b) Encourage the patient to take balanced diet c) Maintain skin integrity d) Refer the patient to nearest hospital e) None of the above 64 4.
The three-carbon pyruvate molecule generated during glycolysis moves from the cytoplasm into the mitochondrial matrix generic cefpodoxime 200mg with visa, where it is converted by the enzyme pyruvate dehydrogenase into a two-carbon acetyl coenzyme A (acetyl CoA) molecule purchase 100 mg cefpodoxime. Acetyl CoA enters the Krebs cycle by combining with a four-carbon molecule buy cheap cefpodoxime line, oxaloacetate purchase cefpodoxime 200mg line, to form the six-carbon molecule citrate, or citric acid, at the same time releasing the coenzyme A molecule. The six-carbon citrate molecule is systematically converted to a five-carbon molecule and then a four-carbon molecule, ending with oxaloacetate, the beginning of the cycle. In addition, the Krebs cycle supplies the starting materials to process and break down proteins and fats. To start the Krebs cycle, citrate synthase combines acetyl CoA and oxaloacetate to form a six-carbon citrate molecule; CoA is subsequently released and can combine with another pyruvate molecule to begin the cycle again. Oxaloacetate is then ready to combine with the next acetyl CoA to start the Krebs cycle again (see Figure 24. Each of these reactions releases a small amount + of energy, which is used to pump H ions across the inner membrane. The accumulation of these protons in the space between the membranes creates a proton gradient with respect to the mitochondrial matrix. Effectively, + it is a turbine that is powered by the flow of H ions across the inner membrane down a gradient and into the mitochondrial + matrix. This process takes place primarily in the liver during periods of low glucose, that is, under conditions of fasting, starvation, and low carbohydrate diets. So, the question can be raised as to why the body would create something it has just spent a fair amount of effort to break down? Certain key organs, including the brain, can use only glucose as an energy source; therefore, it is essential that the body maintain a minimum blood glucose concentration. When the blood glucose concentration falls below that certain point, new glucose is synthesized by the liver to raise the blood concentration to normal. Then, 3-phosphoglycerate is converted into 1,3 bisphosphoglycerate and then into glyceraldehyde-3-phosphate. Two molecules of glyceraldehyde-3-phosphate then combine to form fructose-1-6-bisphosphate, which is converted into fructose 6-phosphate and then into glucose-6-phosphate. In gluconeogenesis (as compared to glycolysis), the enzyme hexokinase is replaced by glucose-6-phosphatase, and the enzyme phosphofructokinase-1 is replaced by fructose-1,6-bisphosphatase. Body’s Metabolic Rate The human body’s metabolic rate decreases nearly 2 percent per decade after age 30. Changes in body composition, including reduced lean muscle mass, are mostly responsible for this decrease. The most dramatic loss of muscle mass, and consequential decline in metabolic rate, occurs between 50 and 70 years of age. Loss of muscle mass is the equivalent of reduced strength, which tends to inhibit seniors from engaging in sufficient physical activity. This results in a positive-feedback system where the reduced physical activity leads to even more muscle loss, further reducing metabolism. There are several things that can be done to help prevent general declines in metabolism and to fight back against the cyclic nature of these declines. These include eating breakfast, eating small meals frequently, consuming plenty of lean protein, drinking water to remain hydrated, exercising (including strength training), and getting enough sleep. These measures can help keep energy levels from dropping and curb the urge for increased calorie consumption from excessive snacking. While these strategies are not guaranteed to maintain metabolism, they do help prevent muscle loss and may increase energy levels. Because stress activates cortisol release, and cortisol slows metabolism, avoiding stress, or at least practicing relaxation techniques, can also help. Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids. Lipid metabolism begins in the intestine where ingested triglycerides are broken down into smaller chain fatty acids and subsequently into monoglyceride molecules (see Figure 24. Within the intestinal cells, these triglycerides are packaged along with cholesterol molecules in phospholipid vesicles called chylomicrons (Figure 24. The chylomicrons enable fats and cholesterol to move within the aqueous environment of your lymphatic and circulatory systems. Chylomicrons leave the enterocytes by exocytosis and enter the lymphatic system via lacteals in the villi of the intestine. Once in the circulation, they can either go to the liver or be stored in fat cells (adipocytes) that comprise adipose (fat) tissue found throughout the body. They function to carry these water-insoluble molecules from the intestine, through the lymphatic system, and into the bloodstream, which carries the lipids to adipose tissue for storage. Lipolysis To obtain energy from fat, triglycerides must first be broken down by hydrolysis into their two principal components, fatty acids and glycerol. The resulting fatty acids are oxidized by β- oxidation into acetyl CoA, which is used by the Krebs cycle. Because one triglyceride molecule yields three fatty acid molecules with as much as 16 or more carbons in each one, fat molecules yield more energy than carbohydrates and are an important source of energy for the human body. Triglycerides yield more than twice the energy per unit mass when compared to carbohydrates and proteins. The breakdown of fatty acids, called fatty acid oxidation or beta (β)-oxidation, begins in the cytoplasm, where fatty acids are converted into fatty acyl CoA molecules. This fatty acyl CoA combines with carnitine to create a fatty acyl carnitine molecule, which helps to transport the fatty acid across the mitochondrial membrane. Once inside the mitochondrial matrix, the fatty acyl carnitine molecule is converted back into fatty acyl CoA and then into acetyl CoA (Figure 24. Ketogenesis If excessive acetyl CoA is created from the oxidation of fatty acids and the Krebs cycle is overloaded and cannot handle it, the acetyl CoA is diverted to create ketone bodies. Ketones serve as fuel in times of prolonged starvation or when patients suffer from uncontrolled diabetes and cannot utilize most of the circulating glucose. In both cases, fat stores are liberated to generate energy through the Krebs cycle and will generate ketone bodies when too much acetyl CoA accumulates. Ketone Body Oxidation Organs that have classically been thought to be dependent solely on glucose, such as the brain, can actually use ketones as an alternative energy source. The carbon dioxide produced can acidify the blood, leading to diabetic ketoacidosis, a dangerous condition in diabetics. The carbon within the acetoacetyl CoA that is not bonded to the CoA then detaches, splitting the molecule in two. These two acetyl CoA molecules are then processed through the Krebs cycle to generate energy (Figure 24. Lipogenesis When glucose levels are plentiful, the excess acetyl CoA generated by glycolysis can be converted into fatty acids, triglycerides, cholesterol, steroids, and bile salts. This process, called lipogenesis, creates lipids (fat) from the acetyl CoA and takes place in the cytoplasm of adipocytes (fat cells) and hepatocytes (liver cells). When you eat more glucose or carbohydrates than your body needs, your system uses acetyl CoA to turn the excess into fat. Although there are several metabolic sources of acetyl CoA, it is most commonly derived from glycolysis. Lipogenesis begins with acetyl CoA and advances by the subsequent addition of two carbon atoms from another acetyl CoA; this process is repeated until fatty acids are the appropriate length. However, the creation of triglycerides and lipids is an efficient way of storing the energy available in carbohydrates. Although lipogenesis occurs in the cytoplasm, the necessary acetyl CoA is created in the mitochondria and cannot be transported across the mitochondrial membrane. Oxaloacetate forms via the action of pyruvate carboxylase, whereas the action of pyruvate dehydrogenase creates acetyl CoA. Oxaloacetate and acetyl CoA combine to form citrate, which can cross the mitochondrial membrane and enter the cytoplasm. There is protein in bones (collagen), muscles, and tendons; the hemoglobin that transports oxygen; and enzymes that catalyze all biochemical reactions. Amid all these necessary functions, proteins also hold the potential to This OpenStax book is available for free at http://cnx. Proteins are not stored for later use, so excess proteins must be converted into glucose or triglycerides, and used to supply energy or build energy reserves. Although the body can synthesize proteins from amino acids, food is an important source of those amino acids, especially because humans cannot synthesize all of the 20 amino acids used to build proteins.
These include: Female Gender Hormonal Factors Age Benign Breast Disease Personal history of cancer Obesity and Dietary Fat Family history of cancer and Radiation exposure genetics Female Gender Breast cancer accounts for over 32% of all invasive cancers in women and only 1% in men order 200mg cefpodoxime free shipping. Age The risk of breast cancer increases with age buy 200 mg cefpodoxime free shipping, with breast cancer extremely rare in those under 20 years cheap cefpodoxime 100mg amex, however incidence rates increase sharply and become substantial before 50 years buy 200mg cefpodoxime visa. Personal History of Cancer Previously diagnosed breast cancer increases the risk by 4 times of breast cancer in the opposite breast. Previous ovarian, endometrial or colon cancer have been associated with a 1- 2 times increased risk over the general population. Hormonal Factors Early menarche (before 12), late menopause (after 55) and greater total duration of regular menses are associated with an increased risk of breast cancer. Radiation Exposure Women exposed to ionizing radiation of the chest have been shown to be at an increased risk of developing breast cancer. Obesity and Dietary Fat 16 Obesity occurs in approximately 60% of patients at diagnosis of breast cancer and a further 60-75% gain weight during treatment. The majority of studies indicate that being obese is a poor prognostic factor and are associated with less favourable nodal status as well as increased risk of contralateral disease, recurrence, co-morbid disease and overall mortality (Doyle et al, 2006). Obesity is associated with higher levels of insulin and other hormones in both pre and post menopausal women. Insulin and related proteins have been shown to increase the risk of cancer diagnosis and increase risk of cancer recurrence two-fold. Other metabolic hormones play a role between obesity and breast cancer recurrence. Physical Examination The physical breast examination is a step by step process that should be carried out by an experienced practitioner, examining each breast, nipple and regional nodes through observation and palpation in both the erect and supine position. Skin oedema of the breast erythema (skin reddening) or a palpable breast mass, nipple retraction, asymmetry or changes of the character of the skin and regional node presence, size and character should all be noted. Other causes of breast masses Presentation Diagnosis Treatment Cystic Mass Firm/rubbery, Direct Ultrasound/ Aspiration, Follow-Up in Aspiration 6-8 weeks, Excisional Biopsy (if aspiration bloody) Fibroadenomas Non-tender, round, Triple Test Evaluation Observation/follow-up (Common in women macrolobulated masses (Physical Exam, studies, complete under 40 years) that are firm/ rubbery. Mammography and Fine surgical excision Needle Aspiration) Hematoma Ecchymosis (blood below Breast Imaging- Supportive garments, subcutaneous tissue) mammography analgesics and needle painful tender mass. During a mammography each breast is placed between two plates and compressed so that a clear image is obtained. During a screening mammography 2 X-Rays are taken of each breast of asymptomatic women to detect change at a preclinical stage, this is the primary role of mammography. After analyzing mammographic images, radiologists classify findings into five categories (see table). American Cancer Society and American College of Radiology guidelines for screening for breast cancer and appropriate use of mammography state: Asymptomatic Women Women of 20 years of age or older should perform Breast Screening Examination monthly. Symptomatic Women Any women experiencing signs or symptoms of breast cancer or unusual changes to the breasts should have a thorough breast examination including mammography and ultrasound despite age, to determine whether cancer is present. A diagnostic mammography includes additional views such as spot compression or magnification views for a more detailed report. Its sensitivity is 65-98% and specificity is 34-100% in diagnosing breast lesions (Irish Cancer Society, 2011). The palpable breast mass is trapped and a fine needle is slowly inserted into the mass. After several advances within the mass along multiple planes the needle is withdrawn and the specimen is placed on a slide for investigation. Excisional Biopsy Excisional Biopsy is the complete surgical removal of a palpable breast lesion and is indicated if Needle biopsy is not feasible or if it is non-diagnostic or discordant with imaging results. Depending on the likelihood of malignancy, a rim of surrounding normal breast tissue can be removed. The patient is usually under local anaesthetic and 21 sedation with placement of the incision determined by both oncologic and cosmetic considerations. Langer’s lines are natural lines of skin tension and creasing and incisions along them produce optimal cosmetic results. The breast lesion is removed and the biopsy cavity is examined for further abnormality or suspect lesions. Non-invasive or invasive breast cancer Cells Non-invasive breast cancers stay within the ducts/lobules. Cell Grade A 1-3 Grade Scale with Gr 1 cells slightly different to normal cells and Gr 3 cells appearing very different to normal cells and growing in a rapid and disorganised pattern. Tumour Necrosis (Cell death) This is often a sign of a rapidly growing aggressive form of breast cancer. Surgical Margins The surgeon examines the rim of the tissue removed (surgical margin). If there are no cancerous cells on the outer rim of the removed tissue it is described as clear, it there is cancerous cells present it is called positive and if there is cancerous cells close to the edge it is called close. Vascular or Lymphatic Invasion Describes whether the cancerous cells have infiltrated the vascular/lymphatic system supplying the breast. Ploidy Diploid cancers cells have the same amount of chromosomes as normal cells and tend to be slower growing, less aggressive cells. Aneuploid cancer cells have too many/too little amount of chromosomes and tend to be rapid growing aggressive cells. Hormone Receptor Status Hormone receptor status determines if hormone therapy would be appropriate. Tumour is < 5 cms across, and has spread to underarm lymph nodes that T0 N2 M0 are attached to each other or nearby tissue. Or may have spread to lymph nodes behind the breastbone but T3 N2 M0 not spread to underarm lymph nodes. Tumour can be any size and has grown into the chest wall or the skin of T4 N0 M0 the breast. T = Status of primary tumour, N = Regional lymph nodes, M = Distant metastases (Singletory and Connelly, 2006) 23 Psychological impact of a breast cancer diagnosis The obtaining of a cancer diagnosis is a very emotional time for a woman, the following are common reactions: Shock and blame Sadness Fear, anxiety and panic Uncertainty and loneliness Anger and resentment Fatigue Depression and denial Vulnerability Expressive coping and actively processing emotions is of benefit to patients at the time of diagnosis. It leads to lower medical appointments due to cancer related morbidities plus a higher quality of life (Stanton et al, 2002). However the expression of fear and anxiety is associated with lower quality of life and higher depression (Lieberman and Goldstein 2006). The New Zealand cancer foundation provides a variety of methods for dealing with such a stressful time in a person’s life: http://www. Due to the rarity of this condition, it is often over looked and when found, is at an advanced stage. Signs and symptoms, diagnosis and treatment options are all the same as those previously described. After lumpectomy, all the tissue removed from the breast is examined carefully to see if cancer cells are present in the margins. If cancer cells are found in the margins, additional surgery (re-excision) will be performed to remove the remaining cancer. Sometimes both breasts are removed (a double mastectomy), often as preventive surgery in women at very high risk for breast cancer. Modified Radical Mastectomy Involves the removal breast tissue and axillary lymph nodes (B and C in illustration). Less extensive surgery (such as modified radical mastectomy) has been found to be just as effective and so radial mastectomies are now rarely performed. However, this operation may still be done for large tumours that are growing into the pectoral muscles under the breast. Subcutaneous (“Nipple Sparing”) Mastectomy All of the breast tissue is removed, but the nipple is left alone. Skin Sparing Mastectomy Technique that preserves as much of the breast skin as possible during simple, total, or modified radical mastectomy to provide the skin needed for immediate reconstruction. Only the skin of the nipple, areola, and the original biopsy scar are removed to create a small opening for removal of the breast tissue. Usually done at the same time as the mastectomy or lumpectomy, but can also be performed after through a separate incision. This procedure is a way of learning if cancer has spread to lymph nodes without removing as many of them. In this procedure the first lymph node to which a tumour is likely to drain is removed (known as the sentinel node). Infection of the mastectomy wound may progress to late postoperative lymphoedema of the arm (Morrow et al, 2009). Risk factors include; open biopsy before mastectomy, obesity, diabetes, increase in age and prolonged suction catheter drainage (Vitug and Newman, 2007). After mastectomy, seromas occurs in the dead space beneath the elevated skin flap in approximately 30% of cases (Hashemi et al, 2004).