It is a chronic disorder of the airways, characterized by bronchoconstriction, airway edema and airway hyper-responsiveness and airway remodeling. During the acute exacerbation of asthma, the bronchial smooth muscles contract due to its exposure to a varieties of allergens or irritants. Inspissated mucus plugs can be formed including structural changes such as hyperplasia and hypertrophy in the airway of the smooth muscles (Hackett 2012). Furthermore sub epithelial fibrosis, thickening of the basement membrane can lead to narrowing of the airway causing respiratory distress. The mechanism involving the airway hyper-responsiveness includes the neuro-regulation and airway inflammation (Doeing and Solway, 2013).
Inflammation plays the central role in the clinical progression of asthma. The inflammation of the airway involves the interaction of several types of inflammatory cells like the lymphocytes, mast cells, Eosinophil, dendritic cells, neutrophils and the epithelial cells. There are several inflammatory mediators like cytokines, Chemokines, Cysteinyl-leukotrienes, Nitric oxide (NO). The inhaled allergen stimulates the T helper type 2 (Th2) cell proliferation, leading to the release of the Th2 cytokines, interleukin (IL)-4, IL-5 and IL-13 by the activation of the mast cells, eosinophil and the neutrophils (Kudo et al. 2013).IgE is the antibody that is accountable for the hypersensitivity reactions. The antibody attaches to the surface of the cell via high affinity receptors that release the chemical inflammatory mediators. The allergens can be taken up by the dendritic cells that process the antigenic molecules and present them to the naïve T –cells. Finally the allergen specific Th2 cells are activated.
Mode of action- It is normally used as an anti-inflammatory and immunomodulating agent. After the attachment of the cell surface receptor, the drug enters the nucleus of the cells where specific nuclear receptors are being bound that modifies the gene expression and inhibits the cytokine production.
Class-Ipratropium
Mode of action-It is used as a bronchodilator. It works as an anticholinergic agent. It blocks the muscarinic cholinergic receptors. It decreases the formation of cyclic guanosine monophosphate (cGMP). The effect of cGMP on the intracellular calcium ions, the contractility of the smooth muscle is decreased (LIU et al. 2013).
Pharmacokinetics- the drug is absorbed through the nasal mucosa having minimal systemic absorption. The drug is absorbed rapidly from the GI tract and the lungs.
Distribution- about 15 -10 % of the inhaled drug is deposited in the respiratory tract and the remaining drugs is deposited in the mouth and the oropharynx. 87 % of the drug bounds to the plasma proteins.
Metabolism- Metabolism of the drug takes place inside the liver. The portion hat is inhaled in to the respiratory tract is metabolized before its absorption in the systemic circulation.
Excretion- The metabolites are mainly excreted through the feces and some through the urine.
Pharmacodynamics
The drug stimulates the enzymes that are required to decrease the inflammatory action. It is used to prevent bronchiole asthma, avoid the recurrent of the nasal polyps after the surgery.
Pharmacokinetics-
Absorption- It is not readily absorbed in to the systemic circulation either from the GI tract or the lungs. The inhaled dose is normally swallowed.
Distribution- Not applicable
Metabolism- Hepatic metabolism and the half-life of elimination is 2 hours.
Excretion- The absorbed drug is normally excreted through bile and urine.
Pharmacodynamics-
Anticholinergic action- It antagonizes the action of acetyl choline, thus inhibiting the reflexes that is vagally mediated. The Anticholinergic inhibits the augmentation of the intracellular cyclic guanosine-monophosphate resulting in the interaction of the acetyl choline with the muscarinic receptor present on the bronchia smooth muscles.
Intervention |
Rationale |
Elevation of the head of the bed and changing the position frequently |
It promotes chest expansion, mobilization and expectoration of the mucus, aeration of the segments of lungs (Juthani-Mehta et al 2016). |
Teaching deep breathing exercises, splinting of chest and effective coughing remaining upright. |
It helps in the maximum expansion of the lungs. Splinting and effecting coughing decreases the chest discomfort. |
Warm fluids to should be given |
Warm fluids helps in mobilization and expectoration if the secretions. |
Mucolytics, bronchodilators, expectorants, analgesics can be given |
Medications would reduce the bronchospasms and mobilize the secretions. |
Continuous monitoring of the ABGs , pulse oximetry |
Helps to understand the progression of the disease facilitating modifications in the pulmonary therapy (Juthani-Mehta et al .2016). |
Administration of the oxygen therapy |
The PaO2level should be maintained above 60mm Hg. |
Administration of the analgesics, assisting the patient in the chest splinting, providing comfort such as position changes, backrubs, massage (Juthani-Mehta et al. 2016). |
Analgesic measures as well as non –analgesic measures can be useful in relieving pain. |
Diabetes management by medications and nutritional assessment |
Diabetic are at increased risk of compromised immunity and infections |
Assignment 2
HEPATITIS B
Mode of transmission –It is transmitted by fecal oral route, Ingestion of water or food that has been contaminated with the infected person’s feces. It can also be transmitted by unsafe sex practice, avoidance of undercooked raw shellfish.
Prevention- Maintenance of cleanliness and proper sanitation, use of protection during sex.
Modes of transmission- It is transmitted through exposure to infected blood, semen or other body fluids. It can also be transmitted from the mother to the child during birth or from the family members to the baby. It can also be transmitted during blood transfusion or being exposed to contaminated syringes and equipment (Bayliss et al. 2013). Health care workers can be accidently subjected to needle stick injury while taking care of the HAV patients.
Prevention- Safe handling of the contaminated equipment and body fluids, avoiding sharing of personal items like razors and tooth brushes and effective vaccination (Bhattarai et al. 2015).
Modes of transmission- It is mostly spread through the exposure to infected blood. It can occur during transfusion of the blood or blood products contaminated with the virus. Sexual transmission might be possible but is less likely (Jadoul and Barril, G. 2012).
Prevention- Maintaining Safety precautions while carrying out surgical procedures or while handling the blood products. There is no vaccine for this virus (Linas et al 2013).
Peter Mark has been diagnosed with hepatitis B and caring for hepatitis B patient without appropriate precaution might lead to transmission of the infection. Hepatitis B vaccine is recommended for those caring for the hepatitis B patient. Gloves, should be worn while taking care of the patient or dealing with used things of the infected patient. Gowns could be worn in case the clothing gets soiled. Proper hand hygiene should be maintained after touching the patient or any contaminated equipment. Used syringes and used articles by the patient should be discarded in labelled bags. If the hygiene of the patient is poor then he/she should be shifted to a separate room. Employee having a direct fecal –oral exposure should receive immune globulin as a preventive measure.
The period of incubation of the HBV ranges from 28 to 180 days. In most of the infections, the period of incubation is about 60- 100 days. The infection route has very less influence on the incubation period. A prodromal viral illness follows the incubation period which is again followed by afebrile jaundice. HBsAg can be detected in the serum 2±8 weeks before the raise of aminotransferases (Bayliss et al.2013). As the illness progresses, the level of the aminotransferases rise and the viral products can be easily detected including the viral DNA polymerase and HBeAg. Anti-HBc IgM can be detected at the outset of the disease.
Long term complications like hepatic encephalopathy, anorexia, decreased liver function and increased jaundice may occur. Further deterioration may lead to bacterial or fungal infection, pulmonary failure, renal failure and other electrolytic complications (Ngo-Metzger et al. 2013). In acute liver function failure, a liver transplant may be required. Very less percentage of the patients develop fulminant hepatitis.
Hand hygiene: The patient should be educated regarding the importance and the ways of proper hand washing, use of alcohol based hand rubs.
Patient should be recommended not to donate blood, body organs or other things or sharing of razors or tooth brushes.
Vaccination- 2 dose hepatitis B vaccine schedule ; Heplisav-B (Dynavax) should be given one month apart.
Practice safe sex- Protection should be used while having unsafe sex. Avoiding close contact with the infected individual.
References:
Bayliss, J., Nguyen, T., Lesmana, C.R.A., Bowden, S. and Revill, P., 2013, May. Advances in the molecular diagnosis of hepatitis B infection: providing insight into the next generation of disease. In Seminars in liver disease (Vol. 33, No. 02, pp. 113-121). Thieme Medical Publishers.
Bhattarai, S., Smriti, K.C., Pradhan, P.M., Lama, S. and Rijal, S., 2014. Hepatitis B vaccination status and Needle-stick and Sharps-related Injuries among medical school students in Nepal: a cross-sectional study. BMC research notes, 7(1), p.774.
Bourcier, J.E., Paquet, J., Seinger, M., Gallard, E., Redonnet, J.P., Cheddadi, F., Garnier, D., Bourgeois, J.M. and Geeraerts, T., 2014. Performance comparison of lung ultrasound and chest x-ray for the diagnosis of pneumonia in the ED. The American journal of emergency medicine, 32(2), pp.115-118.
De Paula, V.S., 2012. Laboratory diagnosis of hepatitis A. Future Virology, 7(5), pp.461-472.
Doeing, D.C. and Solway, J., 2013. Airway smooth muscle in the pathophysiology and treatment of asthma. Journal of applied physiology, 114(7), pp.834-843.
Franco, E., Bagnato, B., Marino, M.G., Meleleo, C., Serino, L. and Zaratti, L., 2012. Hepatitis B: Epidemiology and prevention in developing countries. World journal of hepatology, 4(3), p.74.
Hackett, T.L., 2012. Epithelial–mesenchymal transition in the pathophysiology of airway remodelling in asthma. Current opinion in allergy and clinical immunology, 12(1), pp.53-59.
Jadoul, M. and Barril, G., 2012. Hepatitis C in hemodialysis: epidemiology and prevention of hepatitis C virus transmission. In Hepatitis C in Renal Disease, Hemodialysis and Transplantation (Vol. 176, pp. 35-41). Karger Publishers.
Juthani-Mehta, M., Van Ness, P.H., McGloin, J., Argraves, S., Chen, S., Charpentier, P., Miller, L., Williams, K., Wall, D., Baker, D. and Tinetti, M., 2014. A cluster-randomized controlled trial of a multicomponent intervention protocol for pneumonia prevention among nursing home elders. Clinical Infectious Diseases, 60(6), pp.849-857.
Kudo, M., Ishigatsubo, Y., and Aoki, I. 2013. Pathology of asthma. Frontiers in Microbiology, 4, 263.
Linas, B.P., Barter, D.M., Leff, J.A., Assoumou, S.A., Salomon, J.A., Weinstein, M.C., Kim, A.Y. and Schackman, B.R., 2014. The hepatitis C cascade of care: identifying priorities to improve clinical outcomes. PloS one, 9(5), p.e97317.
LIU, C.D., DONG, P.P. and WANG, L.J., 2013. The Clinical Observation on the Efficacy of Oxygen Atomized Inhalation of 5% Hypertonic Saline and Atrovent in the Treatment of Bronchiolitis in Children. Chinese and Foreign Medical Research, 3, p.022.
Mukandala, G., Tynan, R., Lanigan, S., and O’Connor, J. J. 2016. The Effects of Hypoxia and Inflammation on Synaptic Signaling in the CNS. Brain Sciences, 6(1), pp.6.
Ngo-Metzger, Q., Ward, J.W. and Valdiserri, R.O., 2013. Expanded hepatitis B virus screening recommendations promote opportunities for care and cure. Annals of internal medicine, 159(5), pp.364-365.
Riedel, S., Bourbeau, P., Swartz, B., Brecher, S., Carroll, K. C., Stamper, P. D., …Doern, G. V. 2008. Timing of Specimen Collection for Blood Cultures from Febrile Patients with Bacteremia .Journal of Clinical Microbiology, 46(4), 1381–1385Trépo, C., Chan, H.L. and Lok, A., 2014. Hepatitis B virus infection. The Lancet, 384(9959), pp.2053-2063.
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