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By W. Reto. North Carolina School of the Arts.

Individuals may spread influenza virus from up to two days before to approximately 5 days after onset of symptoms kamagra gold 100mg without a prescription. Avian influenza viruses bind to cell-surface glycoproteins containing sialyl-galactosyl residues linked by a 2-3-linkage buy cheap kamagra gold 100 mg line, whereas human viruses bind to receptors that contain terminal 2-6-linked sialyl-galactosyl moieties quality kamagra gold 100 mg. For an avian virus to be easily transmitted between humans discount kamagra gold 100 mg with visa, it is fundamental that it acquires the ability to bind cells that display the 2-6 receptors so that it can enter the cell and replicate in them. While single amino acid substitutions can significantly alter re- ceptor specificity of avian H5N1 viruses (Gambaryan 2006), it is presently un- known which specific mutations are needed to make the H5N1 virus easily and sustainably transmissible among humans, but potential routes whereby H5N1 might mutate and acquire human specificity do exist (Stevens 2006). Apart from H5N1, human infection generally resulted in mild symptoms and rarely in severe illness (Du Ry van Beest Holle 2003, Koopmans 2004). H5N1: Making Progress At the moment, H5N1 infection in humans is relatively rare, although there must have been widespread exposure to the virus through infected poultry. This in an indicator that the species barrier to the acquisition of this avian virus is still quite high for H5N1 – despite having been in circulation for nearly 10 years. However, over the past years, H5N1 strains seem to have become more pathogenic and to have expanded their range of action: Individual Management 29 • The H5N1 influenza strain continues to evolve (Li 2004), and some clones have broader binding properties which may reflect a certain degree of adapta- tion in human hosts (Le 2005). H5N1 has expanded its host range not only in avian species (Perkins 2002), but also in mammals, naturally infecting humans, tigers, leopards, domestic cats and a stone marten (Keawcharoen 2004, Thanawongnuwech 2005, Amonsin 2006). However, when fed with H5N1 virus-infected chickens, cats developed severe disease and trans- mitted the virus to other cats (Kuiken 2004). Cats may excrete virus not only via the respiratory tract but also via the digestive tract (Rimmelzwaan 2006), suggesting that spread by potentially novel routes within and between mam- malian hosts might be possible. In influenza manage- ment, this one-line medical wisdom theoretically translates as: 1) three prophylaxis defence lines (exposure prophylaxis, vaccination, prophylactic use of antiviral drugs); and 2) one treatment defence line (antiviral drugs). Due to the very nature of influenza infection – infected individuals may be infectious for as long as 24– 48 hours before the onset of symptoms – exposure prophylaxis is virtually impossible during an ongoing epidemic or pandemic, especially in our highly 30 Influenza 2006 during an ongoing epidemic or pandemic, especially in our highly mobile and densely populated world. Epidemic Prophylaxis Exposure Prophylaxis Basic personal hygiene measures, invented more than a century ago, are still the cornerstones of prophylaxis. Vaccination Vaccination against influenza viruses is the second cornerstone in preventing influ- enza. Recommendations regarding the composition of the vaccine are issued yearly on the basis of detailed investigations of circulating strains. The rate of influenza vaccination depends on a number of variables, including explicit physician recommendation and media coverage (Ma 2006). In healthy primed adults, the efficacy after one dose may be as high as 80-100 %, while in unprimed adults (those receiving their first influenza immunisation), effi- cacy is in this range after two doses. The evidence of efficacy and effectiveness of influenza vaccines in individuals aged 65 years or older has recently been reviewed. Well matched vaccines prevented hospital admission, pneumonia, respiratory diseases, cardiac disease, and death. The effectiveness is better in people living in homes for the elderly than in elderly indi- viduals living in the community (Jefferson 2005). Inactivated vaccine reduces exac- erbations in patients with chronic obstructive pulmonary disease (Poole 2006). In- fluenza vaccines are efficacious in children older than two years but little evidence is available for children under two (Smith 2006). Nasal spray of live vaccines seemed to be better at preventing influenza illness than inactivated vaccines. Antiviral Drugs In selected populations, antiviral drugs may be a useful option in those not covered or inadequately protected by vaccination. It should be emphasised, though, that the prophylactic use of available antiviral drugs is by no means a substitute for the yearly vaccination recommended by national health services. Individual Management 31 Candidates for short-term prophylactic use of antiviral drugs are high-risk patients who are vaccinated only after an epidemic has already begun, as well as unvacci- nated high-risk contacts of an individual with influenza. In some cases, prophylaxis could be indicated when a current epidemic is caused by a strain which is not repre- sented in the vaccine. Of the two available drug classes, the adamantanes (amantadine, rimantadine) re- cently came under pressure when the global prevalence of adamantane-resistant influenza viruses was found to have significantly increased from 0. During this period, oseltamivir or zanamivir should be selected if an antiviral medication is used for the treatment and prophylaxis of influenza. Epidemic Treatment In uncomplicated cases, bed rest with adequate hydration is the treatment of choice for most adolescents and young adult patients (Hoffmann 2006b). If rimantadine and amantadine are used, it is important to reduce the emergence of antiviral drug-resistant viruses. The newer neuraminidase inhibitors are licensed for treatment of patients aged 1 year and older (oseltamivir) or 7 years and older (zanamivir). They are indicated in patients with uncomplicated acute illness who have been symptomatic for no more than 2 days. Pandemic Prophylaxis The problem with a new pandemic influenza strain is that there is no hiding place on earth. Virtually any single human being will eventually become infected with the new virus, be it the beggar from Paris or the President of a wealthy western country. If you don’t get the virus during the first wave of the pandemic, you’ll probably get it during the second. If a novel pandemic influenza strain takes over as the driver of influenza disease in humans, everyone needs to mount a protective antibody response against the virus – simply because the virus is bound to stay with us for many years. Antibodies will provide some protection against the new influ- enza strain, but to develop antibodies you have to either be infected or vaccinated. Once a new virus has been shown to be effectively transmitted among humans, it will take approximately 6 months to start the production of the corresponding vac- cine. Thereafter, vaccine supplies will be exquisitely inadequate, and years will be needed to produce enough vaccine for 6. In addition, production capacities are concentrated in Australia, Canada, France, Germany, Italy, Japan, the Netherlands, the United Kingdom, and the United States, and vaccine distribution can be expected to be controlled by the producing nations (Fedson 2005). It is therefore reasonable to assume that the vast majority of people living today will have no access to either vaccine or antiviral drugs for many, many months. With no vaccine available or vaccine arriving too late, individuals might wish to work out strategies to deal with a pandemic situation. Indeed, there is conflicting evidence about the most adequate moment for getting infected: • In the 1918 epidemic, the first wave which occurred during the spring months, was less deadly than the second, autumn wave (Barry 2004). It is reasonable to believe that people infected during the first wave had some protection during the second wave. Cities struck later generally suffered less, and individuals in a given city struck later also tended to suffer less. Thus, the West Coast American cities, hit later, had lower death rates than the East Coast cities; and Australia, which was not hit by the second wave until 1919, had the lowest death rate of any developed country (Barry 2004). A commonly observed phenomenon in infectious diseases is that pathogens become less virulent as they evolve in a human population. An additional advantage of this choice is that several months after the start of the pandemic, the initial chaos the health systems will inevitably face during a major outbreak, will have at least partially resolved. The most extreme option of avoiding influenza would be to flee to remote areas of the globe – a mountain village in Corsica, the Libyan Desert, or American Samoa (Barry 2004). If the direct and unprotected con- frontation with the new virus becomes inevitable, some protection is still possible: face masks (but: will masks be available everywhere? Global Management 33 Pandemic Treatment We don’t know whether the next pandemic influenza strain will be susceptible to the currently available antiviral drugs. If it is caused by a H5N1 virus, the neura- minidase inhibitors oseltamivir and zanamivir may be critical in the planning for a pandemic (Moscona 2005). Even in countries which have stockpiled oseltamivir, distribution of a drug that is in short supply will pose considerable ethical problems for treatment. Global Management The management of an influenza outbreak is well-defined for epidemics, and less well-defined for pandemics. Vaccine production is a well-established procedure: throughout the year, influenza surveillance centres in 82 countries around the world watch circulating strains of influenza and observe the trends. Pre- dicting the evolutionary changes of the viral haemaglutinin is not easy and not al- ways successful. In years when the anticipated strain does not match the real world strain, protection from influenza vaccine may be as low as 30 %. Managing uned- ited situations requires some appreciation of the magnitude of the problems that lie ahead. The impact on human health may be highly variable and is expressed in the number of • infected individuals • clinically ill individuals • hospitalised patients • deaths. It is generally assumed that during the first year of the next pandemic 2 billion peo- ple will become infected with the new virus and that half of them will have symp- toms. Less accurate are the estimates of the number of people that will require hos- pitalisation and the death toll. During the 1957 and 1968 pandemics, the excess mortality has been estimated at around one million deaths each. Excess mortality during the last influenza pandemics varied from 26 to 2,777 per 100,000 population (Table 2). A devastating pandemic might therefore, in the course of only a few months, cause three times as many deaths as would normally occur in an entire year. In a world of extensive mass media coverage of catastrophic events, the resulting atmosphere would probably come close to war-time scenarios. In contrast, a mild pandemic similar to the 1968 epi- sode would go nearly unnoticed and without considerable impact on national healthcare systems and on the global economy. The concern that the world might be in for a revival of the 1918 scenario is based on the observation that the currently spreading H5N1 virus shares disturbing char- acteristics with the virus of the 1918 pandemic (Taubenberger 2005). However, if Global Management 35 H5N1 is to be the candidate virus for the next devastating influenza pandemic, why has it not yet acquired the ability to spread easily between humans? It is true that of the 16 influenza H subtypes, only three (H1, H2 and H3) are known to have caused human pandemics (1918, 1957, 1968, and probably 1889 [Dowdle 2006]), and it has even been hypothesised that H5 viruses are inherently incapable of transmitting efficiently from human to human. Shall we one day dis- cover that H5 viruses are not good for human pandemics, because not all possible subtypes can reassort to form functional human pandemic strains? Apart from stepwise mutations that transform an avian influenza virus into a human influenza virus, reassortment is the second way in which new pandemic viruses are generated. There is some preliminary experimental evidence that reassor- tants of the 1918 virus might be less virulent than the co-ordinated expression of all eight 1918 virus genes (Tumpey 2005). Does that mean that pandemics resulting from reassortment events of a human and an avian virus are milder than pandemics caused by a virus which slowly accumulates mutations in order to “migrate” from water fowl hosts to human hosts? As it is impossible to predict whether the next pandemic will result in ~20 or ~2,000 deaths per 100,000 people, the international community should prepare for the 2,000 figure. Containment Containment and elimination of an emergent pandemic influenza strain at the point of origin has been estimated to be possible by a combination of antiviral prophy- laxis and social distance measures (Ferguson 2005, Longini 2005). If the pandemic cannot be contained early on during an outbreak, rapid intervention might at least delay international spread and gain precious time.

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Clinical Practice Guideline: management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation cheap 100mg kamagra gold with mastercard. New Standard of Practice New standards for phototherapy require all babies to receive intensive phototherapy discount 100 mg kamagra gold free shipping. Intensive phototherapy is defined as ‘the use of high levels of irradiance purchase kamagra gold 100 mg otc, usually 30 μW/cm2/nm or higher quality 100 mg kamagra gold, delivered to as much of the infant’s skin surface area as possible. If the infant does not require immediate treatment, the results should be plotted on the predictive (screening) nomogram to determine the risk of progression to severe hyperbilirubinemia. Joseph’s has a reliable Transcutaneous Bilirubin meter which accurately and consistently measures serum bilirubin levels. Guidelines for detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants (35 or more weeks’ gestation). ClinicalPracticeG uideline:m anagem entof hyperbilirubinem iainthenewborninfant35orm oreweeksof gestation. G uidelinesfordetection,m anagem entandpreventionof hyperbilirubinem iainterm andlatepreterm newborninfants(35orm oreweeks’gestation). Joseph ’s h as areliable Transcutaneous B ilirubinm eterwh ich accurately and consistently m easures serum bilirubinlevels. Donottreatanear-term (35to38wk)infantasaterm infant;anear-term infantisatm uchhigherriskof hyperbilirubinem ia. Perform apre-dischargesystem atic assessm entonallinfantsfortheriskof severehyperbilirubinem ia. Some rules intended to reduce the potential for medication errors: • Write orders clearly and concisely. R x Interactions:Ç levels of m idaz olam ,carbam az epine,theophylline,cyclosporine,phenytoin C larith rom ycin R x Interactions:theophylline,carbam az epine,cisapride,digox in,cyclosporine,tacrolim us. O totox icityandnephrotox icity m ayoccur,considerm onitoring trough levels (target<2m g/L )inpatients atriskfor nephrotox icity;septic shock,concurrentnephrotox ins,fluctuating renalfunctionorex tended treatm entcourses. F eeds,form ula,calcium ,m agnesium ,iron,antacids andsulcralfate reduce absorption,holdfeeds for1hourbefore and2hours afterdose. Aspergillus species andCandida kruseiare intrinsicallyresistant,Candida glabrata m ayrespondto higherdoses. A single dose greater than 150 mg/kg is generally considered to be toxic, but toxicity has been reported at lower doses (90-120 mg/kg/day). Morphine is the preferred oral opiate for the treatment of acute pain Morphine has important effectiveness and safety advantages and is preferred over codeine (which historically had been the most commonly used oral opiate at McMaster Children’s Hospital). Codeine is a weak opiate analgesic with minimal intrinsic analgesic activity; it must first be metabolized to morphine which provides most of the analgesic effect. Up to 10% of the population does not effectively metabolize codeine to morphine, resulting in poor pain control. To avoid the unpredictably variable analgesia and potential for toxicity, a simpler approach is to use morphine. Consider supplemental steroids at times of stress if patient has received long-term or frequent bursts of steroid therapy. Prolonged weakness may occur when corticosteroids are used concurrently with non-depolarizing neuromuscular blocking agents. Fast onset and short duration of action with single doses, duration of action prolonged with continued use. Epinephrine (Racemic) Post-extubation stridor/croup: Use 1:1000 epinephrine(racemic 2. Higher doses may be required if administered through a ventilator due to loss of drug in the circuit. Consider supplemental steroids at times of stress if patient has received long-term or frequent bursts of steroid therapy. Prolonged weakness may occur when corticosteroids are used concurrently with non-depolarizing neuromuscular blocking agents. With continuous infusions measure blood glucose q1h initially, adjust dose as required based on blood glucose measurements. Higher doses may be required if administered through a ventilator due to loss of drug in the circuit. Give in water or juice, do mix with fruit juices with high potassium content such as orange juice. Consider supplemental steroids at times of stress if patient has received long-term or frequent bursts of steroid therapy. Prolonged weakness may occur when corticosteroids are used concurrently with non-depolarizing neuromuscular blocking agents. Extrapyramidal reactions occur more commonly in children and may be treated with diphenhydramine. Use with caution in non-ventilated patients due to potential for respiratory depression. To prevent withdrawal, avoid abrupt cessation following high doses or long duration of therapy (> 5 days). Improving the treatment of pain at McMaster Children’s Hospital Morphine is the preferred oral opiate for the treatment of acute pain Morphine has important effectiveness and safety advantages and is preferred over codeine (which historically had been the most commonly used oral opiate at McMaster Children’s Hospital). Codeine is a weak opiate analgesic with minimal intrinsic analgesic activity; it must first be metabolized to morphine which provides most of the analgesic effect. Up to 10% of the population does not effectively metabolize codeine to morphine, resulting in poor pain control. To avoid the unpredictably variable analgesia and potential for toxicity, a simpler approach is to use morphine. Hydromorphone or oxycodone are alternatives for patients who cannot tolerate morphine because of adverse effects. An oral solution is available for doses other than 10 and 20 mg but is very unpalatable and should be given via feeding tube. Hold feeds before and after enteral administration as continuous feeds and formula may decrease bioavailability of oral products. Significantly increased free fraction in patients with hypoalbuminemia may result in underestimation of effective drug concentration and difficulty in interpretation of drug levels and toxicity may occur at “therapeutic” serum levels. Consider supplemental steroids at times of stress if patient has received long-term or frequent bursts of steroid therapy. Prolonged weakness may occur when corticosteroids are used concurrently with non- depolarizing neuromuscular blocking agents. Higher doses may be required if administered through a ventilator due to loss of drug in the circuit. Titrate dose to effect and/or adverse effects (tachycardia, tremor and hypokalemia). For most patients metered dose inhalers with a spacer device are the preferred method of drug delivery. Some patients, particularly those receiving opiates may require higher doses and/or more frequent administration. Use lower doses if there is no significant bleeding and patient will require warfarin in the future. They were developed taking into consideration services provided at different levels within the health system and resources available. These guidelines are intended to standardize care at both tertiary and secondary levels of service delivery across different socio- economic stratifcations of our society. The clinical conditions included in this manual were selected based on facility reports of high volume and high risk conditions treated in each specialty area. The guidelines were developed through extensive consultative work sessions, which included health experts and clinicians from different specialties. The work group brought together current evidence-based knowledge in an effort to provide the highest quality of healthcare to the public. It is my strong hope that the use of these guidelines will greatly contribute to improved diagnosis, management and treatment of patients. And, it is my sincere expectation that service providers will adhere to these guidelines/protocols. The Ministry of Health is grateful for the efforts of all those who contributed in various ways to the development, review and validation of the National Clinical Treatment Guidelines. We would like to thank our colleagues from district, referral and university teaching hospitals, and specialized departments within the Ministry of Health, our partners and private health practitioners. We also thank the Rwanda Professional Societies in their relevant areas of specialty for their contribution and technical review, which enriched the content of this document. Finally, we wish to express thanks to all those who contribute to improving the quality of health care of the Rwanda population. Weak / absent breathing Circulation Cold Hands with any of: Immediate transfer to emergency area: 1. Classifcation of pain severity - Self-reporting: use of number or faces scale - Observational: based on behaviors (crying, shaking, etc. Acute Gastroenteritis Defnition: Gastroenteritis is an infammation of the stomach and intestines that causes diarrhea, vomiting, nausea and other symptoms of digestive upset. Causes - Viral gastroenteritis: Rotaviruses are the most likely cause of infec- tious diarrhea in children under the age of 5 - Bacterial gastroenteritis : Campylobacter, Salmonella or E. Persistent Diarrhea Defnition: Persistent diarrhea is a diarrhea, with or without blood, which begins acutely and lasts for 14 days or longer. Bloody Diarrhea Defnition: Frequent (>3/day) passage of blood and/or mucus in the stool Causes - Amoebic dysentery is the most common serious cause in children - Bacterial infections (e. Peptic Ulcer Disease Defnition: Tis refers to ulceration of gastric or duodenal mucosa that tends to be chronic and/or recurrent Causes - Helicobacter pylori (H. Te symptoms associated with peptic ulcers are not sensitive or specifc and the diferential diagnosis is broad. Causes - Foods : Some mushrooms, polluted drinking water, certain im- properly prepared or handled food - Drugs : Sometimes drugs may be toxic and even deadly when taken in excess e. B It is ofen not possible to distinguish viral pneumonia from disease caused by bacterial pathogens. Wheezing child Defnition: A wheeze is a musical and continuous sound that originates from oscillations in narrowed airways. Wheezing is heard mostly in expira- tion as a result of critical airway obstruction. Causes/ diferential diagnosis - Bronchiolitis - Asthma - Oesophageal foreign bodies - Aspiration Syndrome (gastro-oesophageal refux diseases) 3. Acute Bronchiolitis Defnition: Bronchiolitis is an infammation of the bronchiole tubes due to viral organism resulting in wheezing. If bronchodilators to be used, closely monitor efect as it might worsen respiratory distress. Asthma Defnition: Asthma is a chronic infammatory condition of the lung air- ways resulting in episodic airfow obstruction. Note: Kilopascals are also used internationally; conversion would be appropriate in this regard. Asthma attack requires prompt treatment • Bronchodilators Ș Salbutamol: begin with 2-4 pufs/20 min frst hour then depending on severity: ■ Mild: 2-4 pufs/3 hours ■ Moderate: up to 10 pufs / hour ■ Alternatively (especially in severe cases), use nebuli- zation of Salbutamol 2.

Rapid bacterial growth discount kamagra gold 100 mg visa, most commonly Streptococcus pneumoniae generic 100 mg kamagra gold with amex, Staphy- lococcus aureus generic 100 mg kamagra gold free shipping, and Haemophilus influenzae purchase kamagra gold 100 mg without prescription, may begin in the very early phase of viral replication (for more details, see the chapter on Pathogenesis). The influenza A and B virus genomes consist of 8 separate segments covered by the nucleocapsid protein. Matrix protein (M): M1 constructs the matrix; and in influenza A viruses only, M2 acts as an ion channel pump to lower or maintain the pH of the endosome 8. It spans the lipid membrane so that the major part, which contains at least 5 antigenic domains, is presented at the outer surface. Haemagglutinin is the main influenza virus antigen; the antigenic sites being A, B (carrying the receptor binding site), C, D, and E. The antigenic sites are presented at the head of the molecule, while the feet are embedded in the lipid layer. Prominent mutations in the antigenic sites reduce or inhibit the binding of neutral- ising antibodies, thereby allowing a new subtype to spread within a non-immune Structure 89 population. The mutations that cause the antigenic drift are the molecular explanation for the seasonal influenza epidemics during winter time in temperate climatic zones. This may happen when a cell is infected by 2 dif- ferent influenza viruses and their genome segments are exchanged during replica- tion. Although the birds are seldomly symptomatic after infection, the virus is shed in their faeces for several months. It also serves as an important antigenic site, and in addition, seems to be necessary for the pene- tration of the virus through the mucin layer of the respiratory epithelium. Mutations that have been observed include: • R292K • H274Y, R152K, E119V The letters represent amino acids (R, arginine; K, lysine; H, histidine; Y, tyrosine; E, glutamic acid; V, valine): the former letter is the original amino acid, and the latter the amino acid after mutation occurred. When the amino acid arginine (R) is replaced by lysine (K) at position 292 of the neuraminidase glycoprotein, complete resistance may result. Position 292 is so significant because mutation may induce resistance not only against the substance oseltamivir, but also against zanamavir and two other new prodrugs. M2 protein When the virus particle is taken up in the endosome, the activity of the M2 ion channel is increased so that ions flood into the particle, inducing a low pH. The sialic acid linkage to the penultimate galactose, either alpha 2,3 (in birds) or alpha 2,6 (in humans), deter- mines host specificity. Entry of the virus After attachment, the virus is taken up by the cell via a clathrin-coated receptor- mediated endocytosis process. When internalised, the clathrin molecules are liber- ated and the vesicle harbouring the whole virus fuses with endosomes. The contents of the vesicle are usually digested through a stepwise lowering of the pH within the phagosome. Other newly synthesised viral proteins are processed in the endoplasmic reticulum and the Golgi apparatus where glyco- sylation occurs. Finally, the particle is extruded from the membrane and will be liberated by the neuraminidase activity. Shedding of the virus and infectivity Immunohistological pictures show that foci of virus-producing cells are clustered in the mucous layer of the respiratory tract, in the gut and even in endothelial layers, myocardium and brain. At least during the early course of influenza infection, the virus can be found also in the blood and in other body fluids. Due to the conformation of the lipid bilayer, survival under normal environmental conditions should be shorter. Infectivity of the influenza virus particle is easily inactivated by all alcoholic disin- fectants, chlorine and aldehydes. Evaluation of neuraminidase enzyme assays using different substrates to measure susceptibility of influenza virus clinical isolates to neuraminidase inhibitors: report of the neu- raminidase inhibitor susceptibility network. First, is the ability to emerge and circulate in avian or porcine reservoirs by either genetic reassortment or direct transmission and subsequently spread to humans at irregular intervals. Second, is the fast and unpredictable antigenic change of important immune targets once the virus has be- come established in a human. A highly contagious virus causing extensive morbidity and major case fatality rates is an archetypal anxiety. The influenza virus, as a pathogenic agent for humans, has been circulating in the hu- man population since at least the sixteenth century (Cox & Kawaoka 1998) leading to recurrent epidemics of febrile respiratory disease every 1 to 3 years. In addition, each century has seen some pandemics rapidly progressing to involve all parts of the world due to emergence of a novel virus to which the overall population holds no immunity. The characteristics of pandemics include occurrence outside the usual season, extremely rapid transmission with concurrent outbreaks throughout the globe, and high attack rates in all age groups with high mortality rates even in healthy young adults. Given the growing world population and international travel and tourism, impending pandemic influenza outbreaks gain the potential to spread even more rapidly. In order to understand the background of this global epidemic threat more thoroughly, this chapter aims to describe both the pathogenesis of the disease and the contest between the virus and the immune system. Pathogenesis The pathogenicity and virulence of the influenza virus is determined by several in- teracting factors: a) Host factors: • Presence of target receptors on host cells • Availability of enzymes in host cells which are essential for viral entry and replication • State of immunocompetence of the individual host • Specific immunity against certain viral epitopes in the individual host and target population • Ability of the immune system to control the viral replication ef- fectively without causing serious collateral damage for the host by its inflammatory response Pathogenesis 93 b) Viral factors: • Ability to bind to host cells • Ability of virus shedding • Restriction of cytopathogenic effects to allow for an appropriate balance between viral replication and control by the host • Escape from immunosurveillance by evolution of antigenic varia- tion driven by selective pressure of the immune response • Escape from immunosurveillance by recombination with different virus strains from zoonotic disease • Modulation of the immune response to attenuate effective host defense mechanisms Viral entry: How does the virion enter the host? The predominant way in which influenza is transmitted is from person to person by aerosols and droplets. In a human lung there are about 300 million terminal sacs, called alveoli, that function in gaseous exchange between inspired air and the blood. The resting ventilation rate in humans is about 6 liters of air per minute, which introduces large numbers of foreign parti- cles and aerosolized droplets potentially containing virus into the lungs. Deposition of foreign particles depends on their size: inhalation of very small particles does not result in absorption through the alveoli or bronchial system. Much larger particles are either not able to enter the respiratory system or are deposited in the upper respiratory tract (Figure 1A). The respiratory tract is covered with a mucociliary layer con- sisting of ciliated cells, mucus-secreting cells and glands (Figure 1 B). Foreign par- ticles in the nasal cavity or upper respiratory tract are trapped in mucus, carried back to the throat, and swallowed. From the lower respiratory tract foreign particles are brought up by the ciliary action of epithelial cells. In the alveoli that lack cilia or mucus, macrophages are responsible for destroying particles (Figure 1). Binding to the host cells The main targets of the influenza virus are the columnar epithelial cells of the respi- ratory tract. However, this simplified model is often insufficient to explain viral tropism since the receptor distribution in the host is generally more widespread than the observed virus tro- pism. Hosts may prevent the attachment by several mechanisms: (1) specific immune response and secretion of specific IgA antibodies, (2) unspecific mechanisms, such as mucociliary clearance or production of mucoproteins that able to bind to viral hemagglutinin, and (3) genetic diversifi- cation of the host receptor (sialic acid), which is highly conserved in the same spe- cies, but differs between avian and human receptors (Matrosovich 2000). As a re- sult, the avian virus needs to undergo mutations at the receptor binding site of he- magglutinin to cross the interspecies barrier between birds and humans. In pigs, polymorphisms of sialic acid species and linkage to galactose of both humans and birds are co-expressed in the tissue. Therefore, co-infection with avian and human influenza can occur in pigs and allow genetic reassortment of antigenic properties of both species in the co-infected cells. Recently, it has been shown that certain avian influenza viruses in human and birds are able to bind to different target cells (Matrosovich 2004). This could explain the observation of several cases since the end of the 1990s with transmission of avian influenza directly from poultry to hu- mans. H5N1 and some other subtypes of influenza A virus are able to bind to re- ceptors in the human eye (Olofson 2005). Pathogenesis 95 As essential as the binding of the influenza virus is its cleavage from the binding site at the host cell. The virulence of the influenza virus depends on the compatibility of neura- minidase with hemagglutinin. A virulent virus which has undergone mutations in the hemagglutinin needs compensatory mutations in the neuraminidase to maintain its virulence (Baigent & McCauley 2003, Hulse 2004). As a consequence, viral fitness and virulence were found to be reduced in influenza viruses resistant to neu- raminidase inhibitors (Yen 2005). Once the cell membrane and the virus have been closely juxtaposed by virus- + receptor interaction, the complex is endocytosed. Cellular proteases are often required to cleave viral proteins to form the mature in- fectious virus particle. In humans, the replication of the influenza virus is generally restricted to the epithelial cells of the upper and lower respiratory tract. This is be- cause of the limited expression of serine protease, tryptase Clara, secreted by non- ciliated Clara cells of the bronchial epithelia. This may cause altered tropism and additional sites of rep- lication in animals and humans (Gamblin 2004). Thus, H5N1 viral replication in humans may be restricted to the respiratory and intestinal tract in contrast to disseminated infections documented in other mammals and birds. Once influenza has efficiently infected respiratory epithelial cells, replication oc- curs within hours and numerous virions are produced. Infectious particles are pref- erentially released from the apical plasma membrane of epithelial cells into the air- ways by a process called budding. This favors the swift spread of the virus within the lungs due to the rapid infection of neighboring cells. This would explain why many of the individuals infected with avian influenza (H5N1) in Hong Kong had gastrointestinal, hepatic, and renal, as well as respiratory symptoms and why viruses from these patients were neurovirulent in mice (Park 2002). Whether these symptoms result from hematogenic spread or reflect non-pulmonal means of viral entry into the host re- mains unclear. These findings suggest a means by which influenza A viruses, and perhaps other viruses as well, could become highly pathogenic in humans. Finally, animal studies have revealed that the site of inoculation can determine the pathway of spread of the influenza virus in the host. Although a frequent disease, the specific inflammatory patterns or regulation of immune response and the pathogenesis of cytopathic effects in human influenza is incompletely understood. Cytokines and fever A central question is how an infection essentially localized to the respiratory tract can produce such severe constitutional symptoms. As in many other infectious dis- eases, it is the unspecific and adaptive immune response that contributes substan- tially to the clinical signs and symptoms in influenza and finally to the control of infection. Cytokines, rapidly produced after infection by epithelial and immune cells of the respiratory mucosa, are local hormones that activate cells, especially within the immune system. For example, influenza infection induces in human plasmacytoid and myeloid dendritic cells a chemokine secretion program which allows for a coordinated attraction of the different immune effectors (Piqueras 2005, Schmitz 2005). Most of these cytokines have been detected in nasopharyngeal washes of humans who have been experimentally or naturally infected with influenza (Brydon 2005). It is proposed that these cytokines, produced locally or systemically following in- teraction of exogenous pyrogens (e. There is a small area in the hypothalamus, called the Organum vasculosum laminae terminalis, which has a reduced blood-brain-barrier and allows the passage of pyrogens. At this site, in a dose-dependent manner, they induce the production of prostaglandins and especially prostaglandin E2. These mediators in- crease the thermostatic set point and trigger complex thermoregulatory mechanisms to increase body temperature.

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Systemic treatment: - for impetigo contagiosa purchase kamagra gold 100 mg overnight delivery, a single dose of benzathin penicillin coupled with local care discount kamagra gold 100mg mastercard. The underlining skin conditions such as eczemas trusted 100mg kamagra gold, scabies kamagra gold 100mg low cost, fungal infection, or pediculosis should be treated. When impetigo is neglected it becomes ecthyma, a superficial infection which involves the upper dermis which may heal forming a scar. A furuncle is an acute, deep-seated, red, hot, tender nodule or abscess that evolves around the hair follicle and is caused by staphylococcus aureus. A carbuncle is a deeper infection comprised of interconnecting abscesses usually arising in several adjacent hair follicles. Cellulitis and Erysipelas Cellulitis is bacterial infection and inflammation of loose connective tissue (dermis subcutaneous tissue) Erysipelas is a bacterial infection of the dermis and upper subcutaneous tissue; characterized by a well-defined, raised edge reflecting the more superficial (dermal) involvement Etiology The most common etiologic agent is group A β hemolytic streptococcus. In young children, Hemophilus influenza type B should be considered as a possible etiology for cellulites especially of the face (facial cellulitis). Classical erysipelas starts abruptly and systemic symptoms may be acute and severe, but the response to treatment is more rapid. In erysipelas, blisters are common and severe cellulitis may also show bullae or necrosis of epidermis and can rarely progress to fasciitis or myositis. A skin break, usually a wound even if superficial, an ulcer, or an inflammatory lesion including interdigital fungal or bacterial infection, may be identified as a portal of entry. Complications Without effective treatment, complications are common - fasciitis, myositis, subcutaneous abscesses, and septicemia. Crystalline penicillin or procaine penicillin is the first line therapy and oral Ampicillin or Amoxicillin may be used for mild infection and after the acute phase resolves. It is caused by over growth of Corynebacterium minutissimum, which usually is present as a normal flora of the skin. It occurs most commonly in the groins, axillae and the intergluteal and submammary flexures, or between the toes. The duration of therapy varies, but 2 weeks is usually sufficient for topical fucidin and erythromycin. In these cases, the usual approach adopted is to give long-term antiseptic soaps, such as povidone-iodine and to use drying agents, such as powders, in the affected areas. Superficial fungal infection of the skin Superficial fungal infections of the skin are one of the most common dermatologic conditions seen in clinical practice. However, making the correct diagnosis can be difficult, because these infections can have an atypical presentation or be confused with similar-appearing conditions. Superficial fungal infections can be divided into three broad categories: dermatophytic infections, Pityriasis versicolor and cutaneous candidasis 3. Dermatophytes Specifically Trichophyton, Epidermophyton and Microsporum species, are responsible for most superficial fungal infections. Dividing infections into the body region most often affected can help in identification of the problem. Tinea Capitis Tinea capitis is a dermatophytic infection of the head and scalp, usually found in infants, children, and young adolescents. Around puberty, sebum production by sebaceous glands becomes active, and as a result, it tends to disappear. Commonest presentation is scaly patches on the scalp with variable degree of hair loss and generalized scaling that resembles seborrhic dermatitis may occur on the scalp. An unusual scaling reaction known as favus may give the scalp a waxy or doughy appearance with thick crusted areas. Griseofulvin in a dose of 10-20 mg per kg for six weeks to 8weeks is the first-line treatment of Tinea capitis. Lesions are round, scaly patches that have a well defined, enlarging border and a relatively clear central portion. Itching is variable and not diagnostic Tinea corporis can assume a giant size (Tinea incognito) when steroids are applied for cosmetic reasons or as a result of miss diagnosis. Tinea pedis Tinea pedis is fungal infection of the feet and is usually related to sweating and warmth, and use of occlusive footwear. It may also present with a classic pattern on the dorsal surface of the foot or as chronic dry, scaly hyperkeratosis of the soles and heels. Tinea versicolor (Pityriasis versicolor) Versicolor versicolor is a common, benign, superficial cutaneous (stratum corneum) fungal infection at the level of stratum corneum characterized by hypo pigmented or hyperpigmented macules and patches with faint scale on the chest and the back. Etiology: Malassezia furfur (Pityrosporon ovale,) M furfur is a member of normal flora of the skin found in 18% of infants and 90-100% of adults. Predisposing factors include - genetic predisposition, warm, humid environments, excessive sweating, immunosuppression, malnutrition, and Cushing disease. Treatment Patients should be informed that it is caused by a normal flora of the skin hence it is not transmitted and any skin color alterations resolve within 1-2 months after treatment. Effective topical agents include: Sodium thiosulphate solution, selenium sulfide and azole, ciclopiroxolamine, and allylamine antifungals. Weekly applications of any of the topical agents for the following few months may help prevent recurrence. Ketoconazole 200-mg daily for 10-days and as a single-dose 400-mg treatment, have comparative results. Oral therapy does not prevent the high rate of recurrence, unless repeated on an intermittent basis throughout the year. Candidiasis Candida infections caused by yeast-like fungi Candida albicans commonly occur in moist, flexural sites. Under certain conditions, they can become so numerous that they cause infections, particularly in warm and moist areas. Pruritic rash that begins with vesiculopustules, which enlarge and rupture, causing maceration and fissuring. Paronychia and onychomycosis Frequently, paronychia and onychomycosis are associated with immersion of the hands in water. Patients present with a painful and erythematous area around and underneath the nail and nail bed, warm, glistening, tense, and tender. There is secondary nail thickening, ridging, discoloration, and occasional nail loss in chronic cases. Physical examination reveals a diffuse erythema and white patches that appear on the surfaces of the buccal mucosa, throat, tongue, and gums. The presence of retrosternal pain, epigastric pain, nausea, and vomiting may suggest esophageal candidiasis Vulvovaginal candidiasis: This is the second most common cause of vaginitis. A patch resembling thrush appears on the glans and may spread to the thighs, gluteal folds, buttocks, and scrotum. Treatment Candida intertrigo - Topical azoles and polyenes, including clotrimazole, miconazole, and nystatin, are effective. Paronychia - the most important intervention is drainage followed by oral antifungal therapy with either ketoconazole, fluconazole or itraconazole. Single daily dose of itraconazole taken for 3-6 months or a pulsed-dose regimen that requires a slightly higher dose daily for 7 days, followed by 3 weeks off therapy. Vulvovaginal candidiasis – Azole suppository or pessaries , in resistant case systemic therapy for 10 days. Warts Warts or verrucae are benign growths on the skin or mucous membranes that cause cosmetic problems as well as pain and discomfort. The incubation period of a wart is 2 to 9 months during which time an excessive proliferation of skin growth slowly develops. Common warts, especially in children, do not necessarily need to be treated, because they exhibit a high rate of spontaneous remission. Treatment ™ Salicylic acid 25% ointment twice daily followed by cutting or scraping ™ Preparation of salicylic acid 5-20% and lactic acid 5-20 in collodion are easier to use ™ Electrodessication and curettage ™ Freezing with liquid nitrogen if available. Protect the skin around the wart with Vaseline apply the podophyllin with a match stick carefully on the top of the war and wash after 6 hours. Molluscum contagiosum Molluscum contagiosum is a viral infection of the skin that causes discrete papules that may be mistaken for warts. The rash of molluscum contagiosum is characterized by discrete, 2 to 5 mm papules that are flesh- colored (skin color) and dome-shaped with a central umbilication (depressed centre). Cryosurgery - Using liquid nitrogen to freeze the lesion Salicylic Acid (Compound W) - A solution applied to the lesion with or without tape occlusion 3. Pathogenesis of herpes simplex virus 30 Primary infection Latency Transmission can occur in all stages; more at the primary Reactivation stage What causes latency? Herpetic Whithlow Infection of pulp of fingertips, it could appear after touching a primary lesion of ones owns lesion or that of others. Lesions are bilateral and symmetrical, inguinal lymph nodes may be enlarged, fever and flu like symptom may be there. Manifestations: Skin vesicles, Encephalitis, Hepatitis, Pneumonia, Coagulopathy Mortality rate (M/R) >50% in ideal setting. Scabies Definition: - scabies is one of the commonest intensely pruritic, highly contagious infectious conditions of the skin caused by a mite Sarcoptis scabei and transmitted by close personal and sexual contacts 34 Historically It has been recognized as a disease for over 2500 years. In 1687 Francesco Redi identified Sarcoptes scabei Scabies is one of the first diseases with a known cause. Romans used the term to describe any pruritic skin disease; so, it has been known as the great imitator Etiologic agent Sarcoptes scabei var. Epidemiology 9 Commoner in children and adolescents 9 It is a disease of disadvantaged community 9 Epidemic occurs during wars and social upheavals 9 Endemic in many developing countries Transmission Pathogenesis Female and male make mating on the surface of the skin. The male mite dies and the gravid female mite burrows into the epidermis lays up to 3 eggs per day for the duration of her 30-60 day lifetime. It starts on the wrist, finger webs and on the medial sides of fingers, the flexor aspect of 35 the wrist, the elbows and the anterior axillary folds, the genitalia and inner thighs and the gluteal folds More disseminated presentation in infants and toddlers. Scabies in infants and young children 9 Distribution and morphology:- generalized 9 The face the scalp, palms an soles are affected 9 Papules, vesicle and pustules 9 Secondary eczematization and impetiginazation are common Crusted (Norwegian) scabies In 1848, Danielssen and Boeck described a highly contagious variant of scabies occurring in immunocompromised patients, elderly or mentally incompetent patients. In Norwegian scabies, pruritus may not be there (in about 50% of the cases do not itch) It is psoriasiform and generalized with nail changes and scalp involvement Skin becomes thickened and involves all part of skin including face, palms and sales. Diagnosis of scabies o Itching, worse at night o Presence of similar condition in the family or intimate contacts o Characteristic distribution of lesions o Demonstration of the mite, eggs or feces o Therapeutic test Management o Treat with a scabicide agent o All family members and close contacts should receive treatment at the same time o Provide antihistamines to alleviate pruritus. Complications of scabies Bacterial super infection Eczematization Nodule formation Urticaria Treatment of complications: - Use antibiotic and anti histamine. Causes of therapeutic failure Improper counseling Poor compliance of patient 37 Inadequate application Improper application Not treating family members who have close contacts 3. Eczemas Eczemas are groups inflammatory skin conditions manifesting either as acute eczematous lesions, which are characterized by active papules; erythema, excoriations and oozing (weeping), sub acute eczemas, also have excoriation, erythema with papules and scales or as a chronic eczematous lesion, characterized by thickening of the skin, and accentuation of the creases (lichenification) and hyperpigmentations 3. The hereditary tendency to develop allergies to food and inhalant substances as manifested by eczema, asthma and hay (allergic conjunctivitis and allergic rhinitis) fever is called atopy. More than ¼ of the offsprings of atopic mother develop atopic dermatitis in the first 3 months of life. If one parent is atopic, more than 50% of the children would develop allergic symptoms by the age of two years and if both parents are affected, the chance of the child to have allergic symptoms would be about 79%. Diagnostic Criteria for Atopic Dermatitis The diagnosis of atopic eczema is made by constellation of criteria. Evidence of pruritus ™ Three minor features are: Xerosis/ ichthiosis / hyperlinearity of palms and soles Perifollicular accentuation Post auricular fissure Chronic scalp scaling The hall mark of atopic eczema is pruritus and dryness of the skin. Long standing pruritus results in lichenified dry skin which would call for further scratching and in this way the itch -scratch cycle establishes which assumes a vicious form. Based on that atopic eczemas are classified in to: infantile eczema (from 2 39 months up to 2 years), childhood atopic eczema (from 2 years to 10 years) and atopic eczema of adolescents and adults.

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Induction of Anesthesia Induction of anesthesia is to make the patient unconscious discount kamagra gold 100mg with amex. Before giving the drugs to make the patient sleep you should let him/her breathe 100% oxygen order kamagra gold 100 mg with amex, which will be used as a reserve during the time of intubation kamagra gold 100mg without prescription. Induction can be performed: • With intravenous anesthetic agents: Ketamine + Atropine or Thiopentone • With inhalation agent (e order 100mg kamagra gold visa. Halothane) After the patient is induced, the anesthesia can be continued with intubation or with out (mask ventilation or spontaneous breathing). Endo tracheal intubation: It is a technique of passing an endotracheal tube into the trachea of the patient for securing the airway, and to make easier ventilation. For Intubation the patient should be adequately relaxed with inhalation agent or muscle relaxant. The relaxant used for intubation is Suxamethonium, which has fast onset of action and short effect. Monitoring: During anesthesia it is important to do strict monitoring of heart beat, blood pressure, respiration, temperature, fluid balance and urine output. The carrier gas for volatile anesthetic agent can be atmospheric air or oxygen from compressed source depending on the type of Anesthesia machine in use. Recovery and Extubation: During recovery phase the patient recovers from: • Inhalation agents by exhalation and/or metabolism • Ketamine by excretion and metabolism • Muscle relaxants by excretion and/or metabolism and/or reversal with neostigmine Before extubation • Be sure that the patient is breathing adequately (reversed from relaxant) • Suck oropharyngeal secretion • Deflate the cuff (which is used for adults) and remove the endotracheal tube Transportation and immediate postoperative care: • Transport in the recovery position • Check and observe closely the pulse rate, blood pressure, respiratory rate, urine output hourly, any abnormal and continuing blood loss and presence of pain. Because of these reasons it can be used alone for short procedures and surgery, which does not require relaxation and intubation. Dose and route of administration: ƒ Intramuscular: 5-10 mg/kg ƒ Intravenous: 1-2 mg/kg The effect of one single dose lasts for about 15 min. Treatment of systemic toxicity • The best treatment of systemic toxicity is prevention by meticulous attention to technique and recognition of intravascular injection. Commonly used local anesthetic drugs 118 Lidocaine (Xylocaine) 1%, 2% or 5% with or without Adrenaline in dose of: With Adrenaline: 7 mg/kg Without Adrenaline: 3 mg/kg • Bupivacaine (Carbosthesin, Marcain) 0. The level of lumbar puncture is at the rd th interspaces between the 3 and 4 lumbar vertebrae. Turn the patient to a supine position with pillow under the head in the case of heavy (hyperbaric) local anesthetic drug. Complications of spinal anesthesia and measures to take • Drop in blood pressure-due to high spinal block - Give Oxygen - Make faster the drip if that does not help. Commonly performed nerve blocks: o Digital nerve block o Axillary block of the brachial plexus o Wrist-block 122 C) Field block Field block is injection of local analgesic so as to create a zone of analgesia around the operative field. It can be used for: o Repair of an inguinal hernia o Caesarean section o Circumcision D) Infiltration Infiltration is direct injection of drugs into the area to be incised and between bone ends in fractures. E) Topical anesthesia This can be performed simply by applying 4% lidocaine to the mucus membrane, for minor surgery and instrumentation of: o Nose o Mouth o Eye o Pharynx and larynx o Urethral procedures 123 Review Questions 1. After evaluation by the surgeon, it is decided to take him to the operating theater. A 17 year old girl is brought to the Emergency department with polytrauma after a car accident. L Bartholomeusz: Safe Anesthesia: A Training manual, where facilities are limited. Outline management options for thyroid carcinomas Thyroid Enlargement: Goiter Goiter refers to a generalized enlargement of the thyroid gland which is normally impalpable. Inflammatory • Autoimmune (chronic lymphocyte thyroiditis, Hashimoto’s disease) • Infectious • Acute (bacterial thyroiditis, viral,) • Chronic (tuberculous, syphilitic) 126 Simple Goiter Patho-physiology: Simple Goiter is enlargement of the thyroid gland as a result of stimulation of the thyroid gland by high levels of circulating thyroid stimulating hormone. Defective hormone synthesis also cause goiter and it accounts for many sporadic goiters. In endemic goiter, it usually occurs at puberty when metabolic demands are high, this is reversible if stimulations cease. As a result of fluctuating stimulation of the thyroid gland, areas of active lobule and inactive lobules will develop. Active lobules become more vascular and hyperplasic until hemorrhage occurs causing necrosis. These necrotic lobules coalesce to form nodules filled with either iodine free colloid or inactive follicles. Secondary changes like cystic degeneration, hemorrhage and calcification occur at late stages. Diagnosis Clinical presentation: Discrete swelling in one lobe with no palpable abnormality else where is called solitary (isolated) nodule. The Goiter is painless and freely moves with swallowing and usually patients are euthyroid. Complications • Tracheal obstruction can occur due to gross lateral displacement or compression. Prevention and treatment Prevention In endemic areas the incidence of goiter can be significantly reduced by the introduction of iodized salt. In early stages, a hyper-plastic goiter may regress if thyroxin is given in a dose of 0. Operation might be indicated • On cosmetic grounds • Tracheal compression and • When malignancy cannot be excluded The options of surgical treatment are • Near total thyroidectomy • Subtotal thyroidectomy Toxic goiters Thyrotoxicosis - is a condition in which there is increased metabolic rate due to high level of circulating thyroid hormone. Clinical features The most significant symptoms are • Loss of weight in spite of good appetite, • A recent preference of cold • Palpitation. The most important clinical signs of thyrotoxicosis commonly seen are • excitability of the patient, • the presence of goiter, • hot and moist palms, • exophthalmus in primary type • tachycardia with cardiac arrhythmia 128 • Weakness of the proximal limb muscles • The goiter in primary thyrotoxicosis (Grave’s disease) is diffuse and vascular, it may be large or small, firm or soft and bruit may be present. Diffuse toxic goiter: Primary toxic goiter or Grave’s disease is a diffuse vascular goiter appearing at the same time as symptoms of hyperthyroidism. The hypertrophy and hyperplasia are due to abnormal thyroid stimulating antibodies Toxic nodular goiter: A simple nodular goiter is present for a long time before the hyperthyroidism, and hence termed secondary thyrotoxicosis. It is usually seen in middle aged or elderly people and less frequently associated with eye signs. In many cases of toxic nodular goiter, the nodules are inactive and it is the intermediate thyroid tissue that is involved in hyper secretion. Toxic nodule: This is a solitary hyperactive nodule which may be part of a generalized nodularity or a true toxic adenoma. It is autonomous and its hypertrophy and hyperplasia are not due to thyroid stimulating antibodies. Diagnosis of thyrotoxicosis • Most cases are easily diagnosed by the clinical picture. This helps to determine the functional activity relative to the surrounding gland according to isotope uptake. Treatment of thyrotoxicosis Treatment of thyrotoxicosis includes specific and non-specific measures. The specific measures are • the use of antithyroid drugs • surgery • radioiodine The nonspecific measures which include rest and sedation are not commonly recommended. But it should be clear that antithyroid drugs cannot cure a toxic nodule since the overactive thyroid tissue is autonomous and recurrence of the hyperthyroidism is certain when the drug is discontinued. Surgery: Surgery cures thyrotoxicosis by reducing the mass of overactive tissue below critical mass. Preoperatively, the patient must be prepared with antithyroid drugs so that the patient becomes euthyroid. Post-operative complications • Hemorrhage - a tension hematoma may develop deep to the cervical fascia – which is potentially life threatening • Respiratory obstruction - can occur due to laryngeal edema or secondary to tension hematoma. It occurs if a thyrotoxic patient has been inadequately prepared for thyroidectomy. Neoplasms of the thyroid Classification of thyroid neoplasm Benign: follicular adenoma Malignant: Primary - Follicular epithelial: follicular, papillary, anaplastic - Para follicular epithelium: medullary - Lymphoid cells: lymphoma Secondary -M etastatic - Local infiltrations 130 Benign tumors Follicular adenomas present as clinically solitary nodules and the distinction between a follicular carcinoma and an adenoma can only be made by histological examination. Malignant Tumors Clinical feature: The commonest presenting symptom is • thyroid swelling • Enlarged cervical lymph node may be the presentation of papillary carcinomas. Prognosis: Prognosis is influenced by histological type, age, extra thyroid spread, and size of tumor. With regard to age, males of more than 40 years of age and females over 50 years have worse prognosis. Local infiltration is an early feature of these tumors with spread by lymphatics and blood stream. They are extremely lethal tumors with death occurring in most cases within months. Many lesions present in advanced stages with tracheal obstruction and require urgent tracheal decompression. Radiotherapy should be given in all cases and may provide a worth while period of palliation. Compare and contrast papillary and follicular thyroid carcinoma with respect to root of metastasis, overall mortality and location of recurrence? This is due to lack of screening facilities, low index of suspicion among health professionals, poverty and lack of knowledge. Benign conditions of the breast are important because of the discomfort they produce and frequent confusion with neoplastic disease. Anatomy nd • The protuberant part of the human breast is generally described as overlying the 2 th to 6 ribs, • It extends from the lateral border of the sternum to the anterior axillary line, between th th clavicle and to the 7 and 8 ribs below. The nipple contains smooth muscle fibers arranged concentrically and longitudinally. These could be secondary to either benign disease conditions, or fatal carcinomas. Students should be familiar with some of differentiating mechanisms between malignant and benign breast lumps. Breast cysts This is a rare condition which may occur in the last decade of reproductive life due to a non- integrated involution of stroma and epithelium. If there is residual lump after aspiration, if fluid is blood stained, or if cyst recurs, local excision for histological diagnosis is advisable. Fibroadenoma Usually occurs during 15-25 years of age and arises from hyperplasia of a single lobule. Most fibroadenomas can be excised through periareolar incision with good cosmetic result. Phyllodes Tumor • Are benign tumors • Usually occur in women over 40 years but can appear in younger woman. Ductectasia/ periductal mastitis Definition: This is dilatation of the breast ducts associated with periductal inflammation. Pathogenesis: Dilatation of lactiferous ducts that will be subsequently filled with a stagnant brown or green secretion. The fluid sets up an irritant reaction in surrounding tissue leading to periductal mastitis, even abscess or fistula formation. When the diagnosis of carcinoma is in doubt There are cases where one cannot be sure whether the particular lump in the breast is area of mammary dysplasia, benign tumor or an early carcinoma. If there is doubt on clinical, cytological or radiological examination, it is essential to obtain a tissue diagnosis. Bacterial mastitis is the commonest variety of mastitis and nearly always commences acutely.

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