1) PadiatricMrs.King 2,5 year-old Billy to the pediatricians officer because he has been irritable and faversh since last night. Further history reveals that Billy also had a runny nose snd cough for two day, and that has appatide and fluid intake have decreased since the fever started .Billy is otherwise healthy,this is the first episodic illness. His physical examination reveals slight, irritable , 2,5 year old girl ,pulling eat ears, temperature of 120 F , nasal congestion with clear discharge ,tympanic membranes red and bulging bilaterally ,pharynx slightly red without exudates. Chest clear ,abdomen soft without hepatosplenomegaly (HSM) and no meningeal signsThe pediatrician diagnoses an upper respiratory infection (URL) an bilateral otitis (BOM) and order amoxicillin 250 mg t.d.s for 10 day. You as the officer nurse, are to perform the parentss teaching for Billys home care. During your discussion with Mrs. King ,she tells you that she is concerned that Billy is jealous of his new baby sister when she holds the baby. She is concerned about Billys development because he recently started to refuse using the potty, a skill that is newly acquired Mrs. King is very attentive to both new baby and Billy throught the interview, and she asks you for suggestions in how to help Billy cope to the arrival. While doing so, she point out that her husband has been extra attentive to Billy since his sister was born.

Subjective and objective Data1. Billy 2,5 years-old2. Runny nose and cough for two days3. Got fever, so that appetite and fluid intake have dicrease4. Temperature of 102 0F5. Tympanic membranes red and bulging bilaterally6. Upper respiratory infection (URI)7. Bilateral otitis media (BOM)8. Amoxicillin 250 mg

EtiologyEtiology of Upper respiratory infectionUpper respiratory infection is generally caused by the direct invasion of the inner lining (mucosa or mucus membrane) of the upper airway by the culprit virus or bacteria. In order for the pathogens (viruses and bacteria) to invade the mucus membrane of the upper airways, they have to fight through several physical and immunologic barriers. Etiology of bilateral otitis mediaOtitismediaismiddle earinfectioncausedby bacteria,fungi,andvirusesthat causeinflammation of themucosallining. Viral pathogensRSV is a large RNA paramyxovirus that is most commonly associated with bronchiolitis and pneumonia in very young persons, though it may cause acute respiratory disease in persons of any age group.[ In northern climates, RSV is normally identified during annual epidemics in the winter and early spring, but it should be considered in any neonate with lethargy, irritability, or apnea, with or without otitis media. In older infants and children, respiratory symptoms are usually more prominent, making diagnosis easier.RSV was identified early as a pathogen that appeared to create long-term pulmonary complications, primarily asthma, in as many as half of infants with bronchiolitis. RSV may be particularly lethal for children with congenital heart disease, cystic fibrosis, immunodeficiency, bronchopulmonary dysplasia, or prematurity of less than 37 weeks gestational age.RSV-specific intravenous (IV) immunoglobulin prophylaxis is recommended only for high-risk children. When treating a child with concomitant pneumonia or other systemic disease and otitis media, the practitioner must ensure appropriate diagnosis and management of all aspects of the childs illness. Drainage of the ear by tympanocentesis or myringotomy for culture and therapy may be necessary in some cases. Drainage is mandatory in neonates who are suspected to be in a septic state or in children who are immunosuppressed.

Bacterial pathogensPathogenic bacteria are recovered from the middle ear effusion in at least half the children with AOM, and bacterial DNA or cell wall debris is found in another quarter to a third of specimens previously classified as sterile. Four bacterianamely,S pneumoniae, H influenzae, Moraxella catarrhalis,andStreptococcus pyogenesare responsible for the majority of episodes of AOM in persons older than 6 weeks. Other bacteria recovered and implicated in AOM includeStaphylococcus aureus,viridans streptococci, andPseudomonas aeruginosa.The emergence of resistance to antimicrobial agents is of increasing importance in the management of AOM and other bacterial illnesses.[6]The various mechanisms used by bacteria to confer this resistance will be delineated as the common pathologic agents linked to AOM are described. Streptococcus pneumoniaeS pneumoniaeis the most common etiologic agent responsible for AOM and for invasive bacterial infections in children of all age groups.[7]It is a gram-positive diplococcus with 90 identified serotypes (classified on the basis of the polysaccharide antigen), the frequency of which varies between age groups and geography. On direct culture, various studies have shown these bacteria to be responsible for 29-40% of isolates, but additionally pneumococcal antigens are recovered from approximately a third of those cultures classified as sterile.Pneumococcal infections are probably responsible for at least 50% of AOM episodes. Serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F are responsible for most invasive pneumococcal disease in America; in ear aspirates from patients with AOM, serotypes 19 (23%), 23 (12.5%), 6 (12%), 14 (10%), 3 (8.5%), and 18 (6%) are isolated most commonly. The polyvalent pneumococcal vaccine confers immunity to approximately 85% of those serotypes responsible for AOM.S pneumoniaewas once susceptible to almost all common antibiotics, including penicillin G, erythromycin, and most sulfonamides. Alteration of the cell walls penicillin-binding protein (the antimicrobial target) has led to the appearance of multidrug-resistantS pneumoniae(MDRSP), which is resistant to beta-lactam compounds, macrolides, and sulfonamides. Resistance rates as high as 40% have been reported for these 3 antimicrobial groups. Serotypes 6B, 9V, 14, 19A, 19F, and 23F have the highest frequency of penicillin resistance.Ceftriaxone, cefotaxime, rifampin, and vancomycin still appear to have therapeutic efficacy, as does immunization with polyvalent pneumococcal vaccine for prevention. Unfortunately, polysaccharide antigens are not immunogenic early in life. To overcome this problem, conjugated antigens, in which the polysaccharide antigen is attached to a protein carrier, may be administered to induce production of antibodies to these polysaccharides. Some conjugated antigens (eg, vaccinations forH influenzaetype b [Hib]) are in widespread use.A heptavalent vaccine forS pneumoniaeis now in widespread use and appears to have made an impact on the number of cases of invasive pneumococcal disease. This vaccine confers long-term immunity to 7 of the most common and invasive strains. Emerging evidence suggests that other serotypes are beginning to be recovered more frequently in ear and sinus infections. This might render the vaccine less useful in future years. In North America, this vaccine has now been replaced by an updated 13-valent vaccine that contains conjugated antigenic material for 6 of those additional serotypes of the pneumococcus. Haemophilus influenzaeIn middle ear aspirates from patients with AOM,H influenzaeis the second most frequently isolated bacterium and is responsible for approximately 20% of episodes in preschool children. The frequency may be higher in otitis-prone children, older children, and adults who have received the pneumococcal vaccine.The bacterium is a small, pleomorphic, gram-negative coccobacillus. Those bacteria encapsulated with a polysaccharide coating are classified into 6 distinct types (a-f); nonencapsulated types are referred to as nontypeable and are responsible for the great majority of AOM episodes. (The nonencapsulated strains have been subtyped biochemically and antigenically, but, to date, this classification has limited clinical application.)Traditionally, Hib has been found responsible for most invasive illnesses attributed to these bacteria and for meningitis, epiglottitis, and septicemia. Hib accounts for only 10% of all episodes of AOM in whichH influenzaeis recovered. In areas of the world where the aforementioned Hib-conjugated vaccine is administered early in life, risks from this potentially lethal strain have greatly diminished.Antimicrobial resistance in Hib is conferred almost exclusively (95%) by the formation of a single enzyme, triethylenemelamine 1 lactamase, which, in some series, is secreted by as many as 40% of all nontypeable strains. This resistance is overcome relatively easily by using blocking agents, extended-coverage cephalosporins, broad-spectrum macrolides, or sulfonamides.H influenzaemay participate more widely in head and neck infections than was once believed. One of the principal mechanisms is related to the ability of the bacterium to hide and recover from antibiotic action by forming a mucous complex known as a biofilm. Research has focused on enhancing penetration of or dissolving the protective biofilm. Moraxella catarrhalisIn the mid-1970s,M catarrhaliswas classified as nonpathogenic in middle ear infections, even though under its previous name,Neisseria catarrhalis,it constituted approximately 10% of all isolates from middle ear aspirates. At that time,M catarrhaliswas almost universally susceptible to ampicillin-type penicillins. After 20 years and 2 name changes (fromN catarrhalistoBranhamella catarrhalistoM catarrhalis), it is isolated in up to a quarter of children with AOM, and resistance to the ampicillin-type beta-lactams is almost universal.M catarrhalisis a gram-negative diplococcus and is considered part of the normal flora of the human upper respiratory tract. Resistance is conferred by the secretion of multiple isoenzymes of lactamase, which may be plasmid or chromosomal in origin and which may be inducible (ie, present only in low levels until a substrate is provided). More than 1 isoenzyme may be secreted by a single bacterium.At present, almost all forms are blocked by clavulanic acid, and most are still susceptible to sulfonamides, lactamase-stable cephalosporins, or broad-spectrum macrolides.M catarrhalisis often found to coexist with other airway pathogens. The lactamases (cephalosporinases) thatM catarrhalissecretes may protect those other bacteria from antimicrobial agents to which the second target pathogen might ordinarily be susceptible. Streptococcus pyogenesAlthoughS pyogenes(a gram-positive coccus that constitutes the group A streptococci [GAS] in the Lancefield classification), is still the fourth most commonly isolated bacterial pathogen from ears with AOM, it has shown a steady decline in frequency of recovery from the ear and in virulence over the past half-century. Similarly, a substantial decline in the major complications of streptococcal infection, rheumatic fever, glomerulonephritis, and scarlet fever has occurred.Spyogenesmay be associated with streptococcal toxic shock syndrome, which may include coagulopathy, soft tissue necrosis or fasciitis, desquamating rash, and liver or renal involvement.It is primarily a pathogen of the pharynx, with more than 80 distinct M-protein strains identified. Currently, with the improvement in primary care and the availability of rapid identification tests, early aggressive treatment is normally instituted against this bacterium, which has shown minimal ability to develop resistance to antimicrobial agents.Acute necrotic otitis media was associated with scarlet fever in the early 1900s; however, the condition was also associated with measles, pneumonia, and influenza. Generally, the patient was extremely ill with the systemic component of the disease and presented with a spontaneous perforation shortly after the onset of otalgia.Early inspection of the ear would show the perforation to be moderate to large; within days, significant evidence of tissue necrosis would be observed, perhaps including the entire tympanic membrane, ossicles, the tympanic mucoperiosteum, or the bone of the mastoid air cells. The patient would demonstrate a marked conductive hearing loss, although sensorineural loss was not uncommon.Pathologically, the ear showed a marked paucity of the normal vascular proliferation associated with an inflammatory reaction. Instead, a complete loss of the vascularity normally associated with vasculitis or toxin exposure occurred. Healing was never normal; tissue was replaced by epithelial invasion or scar tissue formation.In industrialized societies, acute necrotic otitis media is now primarily of historic interest. The disease is still reported in aboriginal populations living in areas where modern medicine has not yet penetrated.In the preantibiotic era,S pyogenesalso appeared to be the organism most commonly recovered from patients with acute coalescent mastoiditis. In the 1990s,S pyogenesrelinquished this distinction toS pneumoniae,but it remains a prominent pathogen when this disease is encountered in very young persons. Other aerobesExcept in neonates and children with chronic disease, few other pathogens have been demonstrated in aspirates from the middle ears of immunologically intact individuals.S aureusis rarely recovered, except in Japan, where studies indicate a somewhat higher incidence (up to 10%).Mycobacterium tuberculosisis most often associated with chronic otitis media but should be considered when a patient presents with painless otorrhea as an initial complaint and/or has multiple tympanic perforations. Any patient with a compromised immune system may be at risk for this opportunistic infection.Chlamydia pneumoniais an uncommon but significant pathogen in persons with AOM and responds only to macrolide therapy. AnaerobesAnaerobic bacteria have been recovered from the middle ears of children with AOM, but the data do not support a prominent role for these microorganisms in persons with otitis media, at least in the acute form. They may, however, play a greater role in chronic inflammation of the adenoid bed and biofilm formation. When recovered from ears of children with AOM, the anaerobic pathogen most often is not the sole pathogen cultured. Common bacterial pathogens in neonatal periodIn the perinatal period, theEscherichia coli, Enterococcusspecies, and group B streptococci are the etiologic agents most commonly responsible for sepsis and meningitis. These agents are often recovered from the middle ear, though the total percentage is probably less than 10% of neonates with AOM.Spneumoniaeremains the most common pathogen responsible for AOM in all age groups, including neonates. The nonencapsulatedH influenzaeand nontypeable varieties may be invasive in these infants and constitute the second most common pathogens recovered from the ear.Because bacteremia is common in all neonates with AOM, tympanocentesis should be performed for both diagnosis and therapy in any infant with signs of AOM or generalized sepsis and any middle ear effusion. This should be part of any septic workup in neonates.

ProblemsRecurrentotitis mediamaycausedamage to thebone,the facial nerveand thecochlea,causinghearing lossispermanent.Otitis media can beacuteorchronic.The acuteformusually associatedwith infections of theupper respiratorytractwhereas persistentformknownaschronicsuppurativeotitismedia.

2. Medical SurgicalA. Diabetes MellitusMrs. Jody, 78 years old, has history of insulin-dependent diabetes (IDDM). When you wigh her during your weekly home visit, you note that she weigh 98 pounds. Which is 12 pounds less then she weighed at your last visit. You try to weigh her at the same time of day each week-09.30. She usually has breakfast at 06.30 and takes her morning NPH insulin, 40 units at 07.30. Today she tells you that she has been urinating a lot and that she has had flu for about three days, with nausea and just a little vomiting. She says she has not been eating well but ads, Im keeping my blood sugar up by drinking orange juice.On assessment, you note that she has soft, sunken eyeball and her tongue is dry and furrowed. Her blood pressure is 140/86 (usual is 150/88), her pulse is 92, and respiration are 22. The temperature is 99.4F. Her finger stick blood glucose (FSBG) is 468 mg/dl (usual is 250-300). Mrs. Jody refuses to check finger stick blood glucose herself. When asked what she did not call the nurse or the doctor when she became ill, she stated, I didnt think it was that serious, I didnt have a high temperature. Key word: blood pressure is 140/86 (usual is 150/88), her pulse is 92, and respiration are 22. The temperature is 99.4F. Her finger stick blood glucose (FSBG) is 468 mg/dl (usual is 250-300). Problem: she has been urinating a lot and that she has had flu for about three days, with nausea and just a little vomiting. She says she has not been eating well but ads. Diabetes mellitus type 2Diabetes mellitus type 2 formerly non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. Diabetes is often initially managed by increasing exercise and dietary modification. If the condition progresses, medications may be needed. Often affecting the obese, diabetes requires patients to routinely check their blood sugar.Unlike type 1 diabetes, there is very little tendency toward ketoacidosis although it is not unheard of. One effect that can occur is nonketonic hyperglycemia. Long-term complications from high blood sugar can include increased risk of heart attacks, strokes, diabetic retinopathy where eye sight is affected, and kidney failure. For extreme cases, circulation of limbs is affected, potentially requiring amputation. Loss of hearing, eyesight, and cognitive ability has also been linked to this condition.1. Signs and symptomsThe classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), fatigue and weight loss. Type 2 diabetes has been associated with an increased risk of cognitive dysfunction and dementia through disease processes such as Alzheimer's disease and vascular dementia. Researchers have shown that reduced glucose tolerance has deleterious effects on memory in the elderly, and concomitant hippocampal atrophy.2. CauseType 2 diabetes is due to a combination of lifestyle and genetic factors. Recently, intrauterine growth restriction (IUGR) or prenatal undernutrition (macro- and micronutrient) was identified as another probable factor A clue for this concept was the Dutch Hunger Winter (19441945) during World War II, and the pioneering work of Professor Barker3. LifestyleA number of lifestyle factors are known to be important to the development of type 2 diabetes. In one study, those who had high levels of physical activity, a healthy diet, did not smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was included, the rate was 89% lower. In this study, a healthy diet was defined as one high in fiber, with a high polyunsaturated to saturated fat ratio, and a lower mean glycemic index. Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes, and decreasing consumption of saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the risk. The increased rate of childhood obesity between the 1960s and 2000s is believed to have led to the increase in type 2 diabetes in children and adolescents. Dietary fat intake is linked to diabetes risk.A 2010 meta-analysis of eleven studies involving 310,819 participants and 15,043 cases of type 2 diabetes found that "SSBs [sugar-sweetened beverages] may increase the risk of metabolic syndrome and type 2 diabetes not only through obesity but also by increasing dietary glycemic load, leading to insulin resistance, -cell dysfunction, and inflammation."Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A weak positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 diabetes.4. Medical conditionsThere are many factors which can potentially give rise to, or exacerbate, type 2 diabetes. These include obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and with the condition often termed metabolic syndrome (it is also known as Syndrome X, Reavan's syndrome, or CHAOS). Other causes include acromegaly, Cushing's syndrome, thyrotoxicosis, pheochromocytoma, chronic pancreatitis, cancer, and drugs. Additional factors found to increase the risk of type 2 diabetes include aging, high-fat diets and a less active lifestyle.Subclinical Cushing's syndrome (cortisol excess) may be associated with type 1 diabetes. The percentage of subclinical Cushing's syndrome in the diabetic population is about 9%. Diabetic patients with a pituitary microadenoma can improve insulin sensitivity by removal of these microadenomas.Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with type 2 diabetes, even if the exact mechanism by which testosterone improves insulin sensitivity is still not known.

5. GeneticsThere is also a strong inheritable genetic connection in type 2 diabetes: having relatives (especially first degree) with type 2 increases risks of developing type 2 diabetes substantially. Genetic risk for type 2 diabetes decreased as humans first began migrating around the world, implying a strong environmental component has affected the genetic-basis of type 2 diabetes. In addition, there is also a mutation to the Islet Amyloid Polypeptide gene that results in an earlier onset, more severe, form of diabetes.There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 diabetes have a much higher risk of developing type 2 diabetes, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[31][32] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1.[33] Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.[34]Monogenic forms, e.g., MODY, constitute 15 % of all cases.[35]Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.Gene expression promoted by a diet of fat and glucose, as well as high levels of inflammation related cytokines found in the obese, results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.6. PathophysiologyInsulin resistance means that body cells do not respond appropriately when insulin is present.This is a more complex problem than type 1, but is sometimes easier to treat, especially in the early years when insulin is often still being produced internally. Severe complications can result from improperly managed type 2 diabetes, including renal failure, erectile dysfunction, blindness, slow healing wounds (including surgical incisions), and arterial disease, including coronary artery disease. The onset of type 2 diabetes has been most common in middle age and later life, although it is being more frequently seen in adolescents and young adults due to an increase in child obesity and inactivity. A type of diabetes called MODY is increasingly seen in adolescents, but this is classified as a diabetes due to a specific cause and not as type 2 diabetes.In the 2008 Banting Lecture of the American Diabetes Association, DeFronzo enumerates eight main pathophysiological factors in the type 2 diabetic organism Diabetes mellitus with a known etiology, such as secondary to other diseases, known gene defects, trauma or surgery, or the effects of drugs, is more appropriately called secondary diabetes mellitus or diabetes due to a specific cause. Examples include diabetes mellitus such as MODY or those caused by hemochromatosis, pancreatic insufficiencies, or certain types of medications (e.g., long-term steroid use).Recent studies of pancreatic beta cells have indicated a molecular connection between diet, obesity that involves the role of fat in activating a pathway to type 2 diabetes. In this mechanism, loss of beta cell glucose sensing contributes substantially to the early manifestation of diabetes, and beta cell dysfunction is responsible for the onset and severity of multiple systemic disease signs including impaired glucose tolerance, hyperglycemia, hepatic steatosis and insulin resistance in muscle and adipose cells. Previous work published in past decades by the laboratories of Roger Unger, Jerrold Olefsky, and Bernard Thorens alluded to the possibility of the importance of beta cell function and glucose sensing in these disease signs. This mechanism of beta cell dysfunction may be contributing substantially to the current epidemic of type 2 diabetes.

7. Diagnosis2006 WHO Diabetes criteria edit Conditionmmol/l(mg/dl)2 hour glucose Fasting glucose:mmol/l(mg/dl)

1. Normal2. Impaired fasting glycaemia3. Impaired glucose tolerance4. Diabetes mellitus 1.