Management And Treatment And Psychosocial Aspects Of Pneumonia Biology Essay

Management And Treatment And Psychosocial Aspects Of Pneumonia Biology EssayThis evidence will explore the pathophysiology, management and manipulation, and psychosocial aspects of pneumonia in an adult patient. In takeation has been obtained by the means of report taking, examination, and analysing the patients medical records to form a case subject argona in which the sections mentioned will be considered in relation to the case study. incision A Case HistoryVD is a 68 form old female who was admitted into the penetrative medical unit (AMU) on 29/1/11 following complaints of generally feeling un headspring and dressing table pain. She had a history of feeling unwell since 25/1/11 coupled with actors assistant pain. This pain was a sharp pain below her ripe(p) breast which was intermittent and radiated around her chest to her approve. The pain was worse on inspiration or when spit uping, and was relieved by over-the-counter analgesia. She in any case felt sweaty, pyre xic (39.7 C), had rigors and aches over her body, however she was non short of breath. She alike had symptoms of a non productive dry cough, poor appetite and vomiting at one time in AMU (watery and colourless). She introductoryly had no episodes of nausea and vomiting, no palpitations or headaches, no urinary symptoms and median(prenominal) bowel movements. She has not had any recent contact with anyone who had akin(predicate) symptoms.In her past medical history she was diagnosed with Sjgrens syndrome and systemic sclerosis sustain year both systemic autoimmune diseases. She was on two courses of antibiotics stretch out year for associated pleuritic chest pain.Her family history consisted of her father having ischaemic rawness disease (IHD) and her mother dying from lung send awaycer, although she was a heavy smoker. She currently lives with her husband at home and her occupation is as a shop assistant this indicates that the transmission system she has is near likely to be community acquired. She has been a alivenesslong non-smoker and she does not drink alcohol. She was on no regular medication prior to world admitted, plainly is directly on 1000mg of paracetamol four times a daylight (QDS) and 500mg of amoxicillin three times a day (TDS). She has no allergies.On examination in a respiratory ward, VD was apyrexial with a furrow pressure reading of 95/65, a heart rate of 95 beats per minute and a respiratory rate of 18 breaths per minute. type O saturations (SATS) were 96% in air and she was speaking in full sentences, whilst facial expression generally comfortable at rest. Her hands seemed dry and scaly on inspection simply in that respect were no ab regulationities on her face. On palpation of her chest, in that respect was equal chest expansion and no tracheal deviation. at that place were also no en mountainousment of cervical or supraclavicular nodes. On percussion, in that respect were dull sounds that could be heard on both r ight and remaining lung bases. On ausculatation, coarse crackles could also be heard in the right and left lung bases. There were no abnormal heart sounds heard and her capillary tube refill time (CRT) was less than 3 seconds. Her abdomen was soft and non tender, and normal bowel sounds were heard. There was normal tone, power and reflexes in all 4 limbs and her Glasgow Coma Scale (GCS) score was 15/15.Her arterial blood plash values were as follows pH 7.43, pCO2 5.49, pO2 10.1, HCO3- 26.8, basal excess of 2.8 and glucose of 5.6 these values indicated that she was not in respiratory failure. She was also found to pass a raised(a) C reactive protein (CRP) of 210, with a high neutophil count of 10.1. Her chest roentgen ray film revealed con unfalteringation in her right lung base and no pneumothorax. The moving picture from the roentgenogram was that it was right lour lobar pneumonia ( sign 1 is an example of what VDs x-ray would have looked like). 1 No blood cultures were rec orded in her notes as it was assumed that cod to the neutrophilia the likely source was bacterial.After macrocosm ab initio treated with intravenous (IV) antibiotics in hospital, her symptoms were relieved, no crackles could be heard and her chest was induceing up on 1/2/11. She was then dismissed in the afternoon on 2/2/11 habituated the instructions to continue with her course of oral amoxicillin.Section B Pathophysiology knowledgeabilityPneumonia tolerate be described as an hullabaloo to the lungs distal airways, specially the alveoli, usually with a bacterial infection being the origin. 2 3 It clinically presents as an acute illness which tooshie take febrility, cough and purulent sputum, although the latter was not present in VD. Pneumonias can be classified by the site of the desegregation (anatomically), or by the aetiology of the disease (see Table 1). 2 3 VD was suspected to have lobar pneumonia after looking at her chest x-ray. The majority of lobar pneumonia s be due to Streptococcus pneumonia and can affect a large part, or a whole lobe of the lung. 3Lobar PneumoniaThere argon four awards to the pathology of lobar pneumonia, which is a classic example of acute inflammation these are congestion, red hepatisation, grey hepatisation and resolution. 3 Congestion is the first stage and lasts for round 24 hours. This is represented by protein-rich exudates leaking into the alveolar spaces and also causation venous congestion consequently causing the lung to become oedematous, heavier and redder in colour. 3 The next stage is red hepatisation which has a duration of a a couple of(prenominal) days. Large numbers of polymorphs (neutrophils and basophils) accumulate in the alveolar spaces along with more than or lesswhat lymphocytes and macrophages. 3 Many erythrocytes are extravasated from the distended capillaries into the lung tissue, along with the overlying pleura being cover with fibrinous exudates. 3 The lung is now solid and a irless, resembling a fresh liver. Figure 1 supports the latter statement by showing a solid consolidation in the right lower lobe. When the lung becomes grey and solid, this is grey hepatisation. This also lasts a fewer days and represents further accumulation of fibrin coupled with the wipeout of leukocytes and erythrocytes. 3 The final stage is resolution, whereby the lung reverts to its normal condition. 4 This happens at approximately 8-10 days in cases which are untreated and is when the carrells and fibrin in the alveoli undergo adipose degeneration. 3 4 This causes the exudates to be converted into an emulsion, producing a yellow pus-like appearance. 4 The exudates are now in a condition where they can be re take up, whilst preserving the underlying alveolar smother structure. 3 4 The lungs would be softer but remain solid, and this would be confirmed on an x-ray by consolidation of the lungs.Co-morbiditiesVDs history also mentioned having a background history of Sjgrens syndrome and systemic sclerosis both systemic autoimmune diseases. Sjgrens syndrome is an inflammatory disease that predominantly affects the duct gland glands with an association to HLA-B8/DR3, which usually causes dryness in the eyes and mouth. 2 5 However it can also cause extra glandular problems such as Raynauds phenomenon, arthritis and lung inflammation, causing degradation of the lining of the bronchioles and alveoli consequently causing lung infections. 2 5 6Systemic sclerosis, also known as systemic scleroderma, is a multi-system autoimmune disease in which the cause is unknown. 2 It principally causes tightness and hardening of the scrape (such as VDs hands) but other systems can also be affected, such as the lungs. 2 There is well-nigh destruction to the lungs in patients with scleroderma which can lead to right heart failure due to pulmonary hypertension. 7 Other complications that involve the lungs include pulmonary haemorrhage, pneumothorax and pneumonia. 7Summa ryVD had come in with an acute infection and was diagnosed with pneumonia. Her right lower lobe was consolidated meaning that she has had it for a few days as protein exudates have leaked into the alveolar spaces and becoming fibrinous, showing up as solid on the chest x-ray, with her CRP (a marker of inflammation) also being raised. VDs medical history last year stated that she had suffered from two previous chest infections that required antibiotics for her to recover. This could possibly be due to the autoimmune diseases said(prenominal) that she had recently been diagnosed with, causing her to be more predisposed to contracting infections, in particular in her respiratory tract. She is currently not on immunosuppressant drugs, but if she were to be for her autoimmune conditions it would then be detrimental to her immune system. This would depart her equable being prone to acquiring infections, leaving her in instead a predicament.Section C Treatment and ManagementVD was on 1000mg of oral paracetamol QDS and 500mg of oral amoxicillin three TDS by the time she was locomote to the respiratory ward. The main actions of these drugs were to improve her feverish symptoms and pain whilst also attempting to clear up her infection.ParacetamolParacetamol (also known as acet aminophen in the USA) is one of the most widely used non-narcotic, analgesic and antipyretic over-the-counter drugs in the world. 8-11 It has properties resembling those of nonsteroid anti-inflammatory drugs (NSAIDs) such as its analgesic and antipyrexic actions, which can be traced back to the hinderion of the central nervous systems prostaglandin (PG) tax write-off. 8 9 It also shares some anti-inflammatory properties, however it does not produce the platelet or stomachic side make that the other NSAIDs do, thus causing argument as to whether it should even be classified as an NSAID at all. 8 It is commonly given orally and is metabolised in the liver, with a half life of approximate ly 2-4 hours, hence why VD was given it QDS to avoid cyanogenic doses.Mechanism of ActionIt is considered that the main mechanism of paracetamol is the inhibition of the enzyme cyclooxygenase (COX), cyclooxygenase-2 in particular as studies have shown that it is highly selective towards it. referable to its high selectivity towards COX-2, its inhibition towards pro-clotting thromboxanes is limited. 9 It is said that paracetamol deeds centrally and is a weak inhibitor of PG synthesis in intact cells, if the concentrations of arachidonic acid available are low enough, through the inhibition of COX-1 and COX-2. 12 This concept was establish on research that discovered that PG production in the brain was more sensitive to inhibition from paracetamol by tenfold compared to the spleen. 9 The COX enzymes are responsible for the metabolism of prostaglandin H2 from arachidonic acid. 9 This is an unstable molecule that can form many pro-inflammatory compounds COX is highly active when oxi dised. 9 12 The oxidised form of the COX enzyme is reduced by paracetamol, stopping it from creating pro-inflammatory compounds. This lowers the amount of PGE2 in the central nervous system, therefore decreasing the set-point of the thermoregulatory core in the hypothalamus. 9Exactly how the mechanism of the inhibition of the COX enzymes is still in discussion. Due to the differences of activity mingled with NSAIDs and paracetamol, it is thought that there may be another translation of the COX enzyme that paracetamol interacts with, COX-3 a splice variant of the COX-1 enzyme however this is just a hypothesis and has yet to be proven. 8 9 12Side set upWhen paracetamol is given at therapeutic doses adverse effectuate are uncommonly seen, although allergic skin reactions are sometimes observed. 8 Fatal hepatotoxicity can be potentially caused by toxic doses of paracetamol (10-15 grams). 8 Initial symptoms are nausea and vomiting, followed by liver damage after 24-48 hours. 8 13 This happens when the enzymes in the liver, cytochrome P450, catalysing the normal conjugation reactions become saturated, and consequently causes the drug to be metabolised instead by mixed function oxidases. 8 A toxic metabolite, N-acetyl-p-benzoquinoneimine, is formed and inactivated by conjugation with glutathione. 8 13 However when glutathione levels are depleted, the toxic metabolite accumulates and reacts with nucleophilic constituents in the cell, causing necrosis in the liver and kidney tubules. 8ContraindicationsParacetamol is generally well tolerated by the liver when polypharmacy is involved. However, evidence has shown that chronic alcoholics are more sensitive to paracetamol hepatotoxicity, even at therapeutic levels. 13 Chronic alcohol consumption induces hepatic microsomal enzymes (CYP2E1) by twofold and can increase paracetamol hepatotoxicity, due to increased amounts of the toxic metabolite. 13AmoxicillinAmoxicillin is a weaken to broad spectrum, -lactam antibio tic that is commonly used to treat infections that are caused by susceptible bacteria, pneumonia being one of them. 8 14 A first derivative of penicillin, this semi synthetic -lactam antibiotic is created by adding different side imprisonment to the penicillin heart, causing it to become broad-spectrum. 8 It is sometimes combined with clavulanic acid in treatment to form co-amoxiclav, which is more effective in treatment straight off due to the increase in antibiotic resistance microorganisms are now developing a resistance to penicillins by secreting -lactamases and the addition of clavulanic acid inhibits this enzyme. 8Pharmokinetic AspectsThe routes of politics are quite vast when given orally, amoxicillin is absorbed to a different degree compared to other penicillins as it depends on their stableness in acid and their adsorption to foodstuffs in the gut. 8 It can also be administered through intramuscular or intravenous injections however intrathecal administration is gene rally avoided as it can cause convulsions. 8 Elimination of amoxicillin is rapid and mainly due to the kindneys, with 90% being through tubular secretion. This however may be advantageous as the inhibition to cell beleaguer synthesis is intermittent rather than continuous, and exposure to the drug is reduced. 8Mechanism of Action-lactam antibiotics inhibit the synthesis of the bacterial cell wall peptidoglycan leading to lysis of the bacterium this peptidoglycan is crucial for the structural integrity of the cell wall in bacteria, particularly organisms that are Gram-positive. 8 In the synthesis of a peptidoglycan, the final stage is transpeptidation which involves transpeptidases known as penicillin binding proteins (PDPs). -lactam antibiotics attach to these PDPs on bacteria and inhibit the transpeptidases that cross-link the peptide chains attached to the backbone of the peptidoglycan. 8 15 16 The -lactam antibiotics are closely related to D-alanyl, the terminal amino acid of th e peptidoglycan layer. 15 16 The similarity between these two structures ceases for the antibiotic and the amino acid to promote their binding to the PDP. 15 The binding of the -lactam nucleus to the residue of the PDP is irreversible, and it is this irreversible binding of the PDP that disrupts the final transpeptidation of the peptidoglycan layer and consequently inhibits bacterial cell wall synthesis. 8 15 16 The inhibition of transpeptidation due to the -lactams causes an accumulation of peptidoglycan precursors, which initiates autolytic enzymes to lyse the excess peptidoglycan. 8 Under normal circumstances, the peptidoglycan precursors inhibit the autolytic enzymes however the -lactams inactivate this and halt the process. 8Unwanted EffectsPenicillins are mainly free from toxic effects. The main side effects are hypersensitivity reactions caused by by-products of the breakdown of penicillin, which combine with the host protein and become antigenic. 8 Skin rashes and fever are common but much more serious is acute anaphylactic shock which can be bleak in some cases. 8 When administered orally, penicillins, particularly broad-spectrum types such as amoxicillin, can disturb the bacterial flora in the gut this can be associated with gastrointestinal (GI) disturbances. 8SummaryVD had no complications and responded well to the treatment that she was given. It was suspected that she had community acquired pneumonia and that the treatment would be a broad-spectrum antibiotic to date the infection. Paracetamol was also positive to alleviate her symptoms. As paracetamol and amoxicillin work on different receptors, there were no contraindications to her treatment. She was given medication intravenously, but once she moves onto oral amoxicillin, she must be aware of GI side effects that may occur.Section D Psychosocial Aspects and Public HealthPsychosocial AspectsAlthough initially there may not be many psychosocial aspects to pneumonia, VD could be pathetic i ndirectly from it. A sufferer of Sjgrens syndrome, VD is susceptible to fatigue which can be physically and mentally exhausting. This can lead to depression, emotional deform and general lethargy. As VD is susceptible to getting infections such as pneumonia due to Sjgrens syndrome, it can also further impact on her psychologically whilst dealing with those infections as her quality of life may be significantly reduced. 17 It is important that a patient with Sjgrens syndrome can address these issues to a health professional if they are ever in distress as psychosocial factors may lead to non-compliance in their treatment.EpidemiologyThere have been many commonwealth studies that have been investigating the annual incidence rate of community acquired pneumonia (CAP). In adults, this can vary from, 2.6-13.4 per 1000 inhabitants, with somewhat higher figures in males and at the extreme ages of life. 18 19 Rates of hospitalization range between 22-51%, with annual mortality rates bet ween 0.1-0.7 per 1000 patients. 20 In approximately 50% of patients with CAP, a pathogen of cause was determined. Streptococcus pneumoniae is found in 20-75% of the cases followed by Mycoplasma pneumoniae at 1-18%, Chlamydia pneumoniae at 4-19% and other viruses from 2-15%.20 C. pneumoniae, however, has arisen as a noted pulmonary pathogen in adult pneumonia patients requiring hospitalization. 20Cost-effectiveness of Patient CareOn average there are roughly 4.5 million visits annually to outpatient clinics, collar departments and physicians offices due to CAP. 21 However, there has been very little in price of studies gathering national data on the costs of CAP treatment. ace study showed that there was, a total cost of $4.8 billion for treating patients ancient 65 years and $3.6 billion for treating patients aged ConclusionVD was an antique woman who was admitted into hospital complaining of acute chest pain and fever for the last few days. After taking a detailed history and examination from her, and with confirmation from a chest X-ray she was diagnosed with right lower lobe community acquired pneumonia. Due to the high neutrophil count in her alveolar spaces, the causative pathogen was most likely to be bacterial and so VD was promptly treated with intravenous amoxicillin, a broad spectrum -lactam antibiotic that works by inhibiting peptidoglycan synthesis in bacterial cell walls. Paracetamol was also prescribed to alleviate her feverish and chest pain symptoms by inhibiting COX enzymes and PG synthesis in the CNS. Having been diagnosed with chronic autoimmune diseases that can lead to increased susceptibility to chest infections, this can lead to psychological issues such as depression. repeated admissions will also be costly to the NHS if alternative treatments that can allow patients to be treated in an outpatient setting are possible, then there could be significant reductions in cost, particularly for patients over 65.