NURSING ASSIGNMENT/ESSAY HELP/CASE STUDY HELP/NURSING TUTOR MELBOURNE SYDNEY BRISBANE

Part A

The clients with blood related cancer are prone to experience several kinds of pain. These pain syndromes may be a result of the disease, its complications, diagnostic testing or because of treatments with chemotherapy. Pain in cancer may be characterised as acute and chronic and is usually in virtue of the temporal pattern (Miladinia, 2015). The pain is more from a view point of neurobiology and is categorised as nociceptive which is inflammatory and neuropathic pain, which Sarita may be experiencing. In cancer patients like Sarita, the pain may be a result of unrecognizable noxious stimuli, which could be occurring due to central process in response to a somatosensory pathway lesion (Nijs, 2016). This is attributed to glia and neuronal cells activation and plasticity. If Sarita’s condition falls under malignant haematology, it is possible for her to experience breakthrough pain which is an intermittent intensification of pain occurring spontaneously or is perpetuated by movements, labelled as incident pain (Pinho-Ribeiro, 2017). The right lateral chest pain exacerbated on inspiration reported by Sarita is a clear sign of it to be a breakthrough pain. Breakthrough pain is a result of movement in cancer patients treated with opioid therapy (Mercadante, 2016).

Nociceptive pain include four specific processes: transduction, transmission, perception, and modulation. The process of transduction refers to the processes by which noxious stimuli activate primary afferent neurons called nociceptors, which are located throughout the body in skin, subcutaneous tissue and visceral and somatic structures (Hockley, 2017). These neurons have the ability to respond specifically to noxious stimuli generated as a result of tissue damage from mechanical causes like tumour growth and others like burns, chemotherapy, frostbite etc. noxious stimuli cause the release of number of excitatory compounds including serotonin, bradykinin, histamine, substance P, and prostaglandins, which move pain along the pain pathway (Tracey, 2017). At transduction site, the sodium channels are closed and inactive at rest but undergo changes in response to nerve membrane depolarisation. Transient channel opening leads to an influx of sodium that results in nerve conduction (Woller, 2017).

In the process of transmission, effective transduction generates an action potential that is transmitted along the A delta and C fibres. The endings of A delta fibres detect thermal and mechanical injury like tumour growth, allow relatively quick localisation of pain, and are responsible for a rapid reflux withdrawal from the painful stimulus. Unmyelinated C fibres are slow impulse conductors and produce poorly localized and often burning and aching pain such as in Sarita’s case (Zhang, 2015).

The noxious information passes through the dorsal root ganglia and synapses in the dorsal horn of the spinal cord. An action potential is generated, and the impulse ascends up to the spinal cord and transmits the information to the brain, where the pain is perceived (Yam, 2018). Extensive modulation occurs in the dorsal horn via complex neurochemical mechanism. The primary A delta fibres and C fibres release various neurotransmitters including glutamate, neurokinins, and substance P. Glutamate is a key neurotransmitter because it binds to the N-methyl-D –Aspartate receptor and promotes pain transmission (Yam, 2018).

Perception, the third process in nociception requires activation of higher brain structures for the occurrence of awareness, emotions, and drives associated with pain. In last stage modulation, the information generated in response to noxious stimuli occurs at every level from the periphery to the cortex and involves many different neurochemicals. The inhibitory neurotransmitters serotonin and norepinephrine are released in spinal cord and the brain stem by descending fibres of the modulatory system (Hua, 2015).

The positive significance of Panadeine forte in Sarita’s case is the relief of the nociceptive pain experienced in lieu of cancer. The negative effect of using Panadeine forte in this case, is that Sarita is experiencing breakthrough pain on account of use of opioid analgesic as evidenced by her verbalisation of the right lateral chest pain exacerbated on inspiration (Money, 2018). Besides that, Sarita can develop a spectrum of side effects in lieu of use of opioid for analgesia. These include constipation, dry mouth drowsiness, nausea, tiredness, poor appetite, confusion and physical dependence (Russo, 2019). Sarita is already reported to have anorexia and lethargy which may become significant on concomitant usage of Panadeine Forte. Besides this, the intake of Panadeine Forte may cause undue increase in non-specific bruising and nose bleed (Wiffen, 2017).

Sarita is currently having cough and upper respiratory tract infection. The intake of Panadeine Forte is bound to cause respiratory depression along with other side effects. The concomitant drowsiness produced by the drug along with cough and respiratory depression can cause severe and lethal breathing problems to Sarita even requiring mechanical support. The respiratory depression may significantly impair breathing, causing pulmonary complications (Wigmore, 2016).

Part B

Sarita is experiencing physical and psychological stress or the “alarm stage” of stress response. The effects of stress response on Sarita’s immune and cardiovascular systems in the ensuing resistance stage are discussed below.

Sarita is experiencing a stress response, the concept of which was explained through general adaptation syndrome. It has three phases; alarm, resistance and exhaustion. Sarita, in the resistance stage is adapting to the noxious stressor, and cortisol activity is increased. On account of tress, the sympathetic nervous system gets activated (Tan, 2018). Norepinephrine is released at nerve endings that are in direct contact with their receptive end organs to cause an increase in function of the vital organs and a state of general body arousal (Cunanan, 2018). In cardiovascular system, the heart rate increases and peripheral constriction occurs, raising the blood pressure. The purpose of shunting is to increase the blood flow to heart and other vital organs. The vasoconstriction occurring prevents undue blood loss (Cunanan, 2018).

The immune system is connected to the neuroendocrine and autonomic systems. Lymphoid tissue is richly supplied by autonomic nerves capable of releasing a number of different neuropeptides that can have a direct effect on leukocytes regulation and the inflammatory response. The stress experienced can alter the immune activity thus producing profound neurochemical and immunological changes (Dumbell, 2016). The fever, malaise, leucocytosis, anorexia experienced by Sarita are a part of an inflammatory response. The major immunosuppressive event is caused by the release of corticotrophin–releasing hormone which in turn causes further outflow of corticosteroids, some opiates and catecholamine by its action on sympatho-adrenergic system (Nezi, 2015). In the resistance stage, the release of growth hormone and prolactin is reduced causing injury to immune system. Further, the stress causes stimulated release of beta2–adrenoreceptor which causes the release of cAMP–protein kinase. This pathway is=n general is responsible for enhancement of humoral immunity and supresses’ cellular one (Michot, 2016). The stress in all is accountable for increased vulnerability to infection in lieu of disturbed homeostasis, labelled as allostatic load (McCreary, 2016). The altered endocrine function and maladaptive health care actions can also form a bridge to impaired immunity in stress, i.e. on stress, major system of endocrine are stimulated, with specific reference to sympathetic–adrenal medullary system, and HPA which are responsible for causing receptor activation of cortisol and catecholamine on the leucocytes. This produces significant effects on cellular trafficking, cellular proliferation, cellular differentiation and production of cytokines (McCreary, 2016).

The long term exposure to stressor eventually depletes the body reserves and the body enters the exhaustion stage of the stress. With this stage, there is increased susceptibility to infections and chronic illness. There are high chances of possible irreversible damage to the body. The result of which may be complete collapse and death (Gaillard, 2015). The irreversible damage is attributed to constant and persistent elevation of blood pressure and heart rate which can cause permanent organ damage. There are high chances of body experiencing shock and multiorgan failure due to persistent strenuous activity in response to stress (Bieliauskas, 2019).

The Systemic Inflammatory Response Syndrome offers a varied view of considering the stress in a critically ill patient. The systemic inflammatory response is common for both infectious and non-infectious stimulus. The constantly perturbed homeostasis in response to the external stressor causes friction in the forces that generate the pre-and anti-inflammatory response (Ding, 2018). This leads to high chances of developing multiorgan failure in adjunct to pre-existing morbidity like cancer in this case. The stress coping ability deteriorates significantly. The systemic inflammation poses a risk to cause multiorgan failure causing sepsis. The failed organ function coupled with sepsis causes poor prognosis (Ding, 2018).

Part C

Chronic lymphocytic leukaemia is typically derived from a malignant clone of B lymphocytes. It contrast to the acute form of leukaemia, most leukaemia cells in CLL are fully mature. One possible mechanism that can explain the oncogenesis is that these cells can escape apoptosis which is programmed cell death, which results in excessive accumulation of the cells in the marrow and circulation (Hallek, 2017). The disease is classified into 3-4 stages. In the early stage, an elevated lymphocyte count is seen, it can exceed 1, 00,000/mm3. Because the lymphocytes are small, they can easily travel through the small capillaries within the circulation, and the pulmonary and cerebral complications of leucocytosis are not found in CLL. It usually takes less than a month for the absolute number of lymphocytes to double in number making it chronic (Hallek, 2017).

CLL occurs in response to a point mutation in the DNA or in adjunct to chromosomal abnormalities. The combination of these genetic defects causes reduced tumour suppressor gene expression and increased oncogenic expression. In white blood cells and their precursors, there is lack of cell growth inhibition or apoptosis and overstimulation of cell growth (Saleem, 2016). The newly formed neoplastic blood cells are incapable of regulating cell division. The newly formed neoplastic cells uncontrollably divide in a monoclonal way, one neoplastic cell generates all successive cells. The genes regulating maturation remain intact, thus the affected neoplastic cells are capable of further differentiation. Some neoplastic cells take time to mature further, less rapid disease progression, thus causing cellular changes in CLL (de Souza, 2018).

The conjoint immunological changes are due to the proliferation of immature white blood cells. This impairs the immune system making it utterly less defensive. Certainly, there is less production of red blood cells, and platelets. This is why the clients with leukaemia report lethargy and anaemia is evident (Forconi, 2015). The decreased production of platelets causing poor coagulation thus leading to uncontrolled bleeding (in this case nose bleed, and non-specific bruising). There is hypertrophy of the bone marrow which is generally responsible for the bone pain manifested in clients with leukaemia. There are high chances of organ infiltration corresponding to splenomegaly, hepatomegaly and arthralgia (Curran, 2017).

Thrombocytopenia are essential for normal blood clotting and coagulation. Thrombocytopenia is a decrease in the circulating platelet count and is the most common cause of bleeding in patients with cancer and is usually defined as a count less than 100,000/mm3 (Di Paola, 2019). The risk for bleeding increases when the platelet count decreases to between 20,000 to 50,000mm3. A platelet count lower than 20,000mm3 is associated with an increased risk for spontaneous bleeding and thus require platelet transfusion (Di Paola, 2019).

The occurrence of bleeding and thrombosis are a major complication in clients with leukaemia and also contribute to increased mortality. The low platelet count (12 000 cells/μl [mm3] of blood) has severely increased risk of haemorrhage. Sarita, being diagnosed with leukaemia has a hypercoagulable state. There are increased chances of development of disseminated intravascular coagulation, even when there is no manifestation of thrombosis or bleeding (Shahrabi, 2018). The cells in leukaemia are procoagulant in nature which along with cytotoxic therapies and opportunistic infections cause clotting activation in clients with acute leukaemia. The clinical features range from localised venous bleeding to thrombus formation in artery which can cause life staking bleeding. Thus, Sarita, has predominantly increased risk of haemorrhage in response to ineffective coagulation (Just Vinholt, 2019).

Thrombocytopenia often results from bone marrow depression after certain types of chemotherapy and radiation therapy and with tumour infiltration of the bone marrow. In some cases, platelet destruction is associated with an enlarged spleen, like in Sarita’s case and abnormal antibody function, which occur which leukaemia and lymphoma (Just Vinholt, 2019).

The potential sites of bleeding in leukaemia begin from oral cavity, where bleeding from gums and oral mucosa are highly common. There is increase chance of suffering an intracranial haemorrhage. The bleeding inside the skull can be characterised by severe headache, stiff neck, and confusion and vomiting (Mantha, 2018). The other potential site for bleeding are lugs. Pulmonary haemorrhage can occur due to platelet deficiency which is evident as haemoptysis, breathing difficulties and central and peripheral cyanosis. The last and foremost potential site of bleeding in leukaemia is gastrointestinal bleeding. It is usually evident as hematemesis, and blood in stools. Thus, the patients with leukaemia may report dark coloured stools showing signs of passive bleeding (Mantha, 2018).

Sarita is currently having anaemia with blood pressure of 100/60mmHg. Hartmann solution is prescribed @ 82ml/hr. The patients with leukaemia as discussed above are at risk of developing septic shock and multiorgan failure. Also, the increased cardiac activity predisposes the client at the risk fluid volume deficit. Thus, clients with leukaemia require volume expanders to prevent the occurrence of shock (Blackburn, 2019). Volume expanders like Hartmann solution allow the body to maintain adequate fluid balance. The administration of these fluids boost the body fluid volume and maintain adequate circulation. The optimal body fluid volume ensures sufficient blood supply to body organs prevent multiorgan failure (Hahn, 2020). It will also help to stabilise the blood pressure and prevent tachycardia. Ringer lactate or Hartmann solution is also used to treat the metabolic acidosis state produces in clients with leukaemia. The composition of the fluid being a bicarbonate treats the metabolic acidosis and associated dehydration (Kraut, 2015).

Sarita on account of leukaemia is also administered packed red blood cells. The prime importance of administration of RBC is to treat anaemia (Hb 8.5mg/dl). The anaemia may produce symptoms of fatigue, weakness, shortness of breath ad tachycardia. The administration of RBC is also to provide mature cells for having transferred oxygenated blood to all the vital organs of the body (DeZern, 2016). The administration of only RBC will not induce any further leucocytes. The administration of packed RBC will also maintain certain immunity to protect from superficial infections. The administration of RBC will also stabilise the heart rate and prevent further anaemia (Leahy, 2017).

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