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SELF-EFFICACY ENHANCEMENT DEVELOPMENT MODEL
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society and family through social mobilization, effective health education to treat tuberculosis in community and enhance independency of patient with tuberculosis during caring activity (WHO, 2006).
Stress change due to fear and anxiety will stimulate hypothalamus to secrete corticotropin releasing factor (CRF) which causes hypophysis gland secreting adrenocorticotropin releasing hormon (ACTH). ACTH stimulate adrenal cortex to secrete cortisol (McArdle, 2007). Increase of cortisol secretion in patient with pulmonary tuberculosis will leads adverse complication (Aditama, 2001). According to Sherwood (2001), cortisol canaffectsimmune system reduction and leads body metabolismexcess.The immune systemprotectshuman body from tuberculosis bacteria infection through the role of Cell Mediate Immunity (CMI) or cellular immunity. The cells consist T- lymphosite and macrophague which can protect body from two phases, pre-erythrocytic phase and parasite erythrocytic phase (Margono, 1980). T-lymphosite consist two types of cell: T-helper cell (Th Cell) or T Cell CD4 (Cluster of Differentiation) and T-suppressor Cell (Ts Cell) or T Cell CD8. T Cell CD4 has cell polarization based on cytocines profile, those are: Th1 and Th2 Cell group. Th1 Cell produces interleukin 2 (IL2) and interpheron gamma which has protective role to strengthen macrophague killing and digesting phagocytized microbas.
METHOD
This research conductedquasy experimental with non-randomized control group pretest posttest design. The number of sample were 42 respondents (21 respondents were treatment group and 21 respondentsswere control group). The treatment group and control group respondents lived in working region of Public Health Center of Surabaya City. Research sample were tuberculosis patients who did not have serious complication or did not treated in hospital and agreedto be respondent. Intervention variable (independent) on this research wasself-efficacy enhancement development model , while the outcome variable (dependent) was biologic response (cortisol levels) of patients with pulmonary tuberculosis. The self-efficacy enhancement development model hadbeen conducted in4 (four) meetings, every taking drugs in public health center (once in two weeks) or home visit during 8 (eight) weeks.
Self-efficacy enhancement development model has been applied through counseling and demonstration methods.Self-efficacy enhancement development model module contents included:
development of self-efficacy enhancement and basic concept of pulmonary tuberculosis disease, the magnitude of difficulties which were faced by the patients in relation with their attempts to overcome the disease and pulmonary tuberculosis medication tenets,general condition of the behavioral ability coverage and independent activities of pulmonary tuberculosis patients at home, andthe strength of individual beliefs associated withtheir ability and the treatment for patients with pulmonary tuberculosisat home. Data collection used questionaire and blood sampling to measure cortisol levels before and after the treatment. Bivariat analysis was conducted to prove differences before and after applications of the self-efficacy enhancement development model using Paired t Test which had significance level of 5% (α = 0,05). To find out the differences between treatment group and control group, this research used Independent t Test.Furthermore, to identify differences of independent variable or the development model variable to biologic response this research applied multivariate analysis (manova) and GLM analysis (mancova), used to analyze influence of confounding variable.
RESULT
Biologic response (cortisol levels) of patients with pulmonary tuberculosis in the public health center of Surabaya City region which was measured before and after interventions through
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the self-efficacy enhancement development model between treatment group and control group are resulting data as follows:
Table: The differences of cortisol levels of patients with pulmonary tuberculosis both treatment group and control group in public health center of Surabaya City region.
Group Count Pre test Post test
Intervention Max 27,25 25,02
Min 12,77 4,15
Mean 20,699 12,621
SD 4,470 6,1460
Mean difference -8,08
Paired t test 0,000
Control Max 26,24 95,80
Min 1,04 3,83
Mean 13,986 21,585
SD 7,1983 21,3998
Mean difference 7,6
Paired t test 0,124
Independen t test 0,003
The table above shows difference of pulmonary tuberculosis patient’s cortisol levels before and after the interventions, both treatment group (p=0,000) and control group (p=0,124). It finds reduction of cortisol levels deviation average value (-8,08) in treatment group and there is elevation of average value (7,6) in control group.
Considering the normal range of cortisol levels,measurement value for the morning sampling is 62-194 ng/ml and the afternoon sampling is 23-119 ng/ml. Samples from all respondents were taken in the morning.Thus,all of the results, regardless treatment group and control group,are changedup or down.
The result of independent t test showed that differences between posttest for intervention group and control group is significant. According to average range value between pretest and posttest, the intervention group result is decreased and the control group result is increased. So, it couldbe concluded that the differences between cortisol levels of patients with pulmonary tuberculosis is found. Logic and theory became author’s consideration to observe thosecortisol levels differences.It makes sense ifcortisol blood sampling is influenced by stress condition of patients with pulmonary tuberculosis before sampling action, sampling time difference though it was acted in one range, and the moment of sampling action.Cortisol levels reduction in treatment group becomefoundation that, in theory,self-efficacy enhancement development model could reduce biologic response (cortisol levels) of patients with pulmonary tuberculosis.
DISCUSSION
The results showed that there are differences in cortisol levels among patients with pulmonary tuberculosis before and after the intervention, both in the treatment group (p=0.124) and the control group (p=0.000). There is a reduction in the difference average levels of cortisol in the treatment group (-8,08) and an elevation in difference average level (7,6) in the control group who received the self-efficacy enhancement development model .
Cortisol is a steroid hormone from the group of glucocorticoids are generally produced in fasiculata zone in the adrenal gland as a response to ACTH stimulation and secreted by the pituitary gland, also as a reaction result of organic hidrogenation group of 11-keto molecule hormone cortisone which is catalyzed by 11β-hydroxysteroid dehydrogenation of type 1enzym and generally secreted by adipose tissue (fat) and liver (Ganong, 2008). Free cortisol in the blood have a negative feedback on the release of Corticotropin-Releasing Hormone (CRH) from the hypothalamus and the corticotrophin hypophysis. CRH flows through the veins of pituitary portal
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system to the anterior pituitary and triggers the secretion of ACTH (Adrenal Cortico Tropic Hormone). CRH response against any negative feedback is following the diural rhythm, so both ACTH and cortisol are in larger quantities in the morning and less at night, but in a stress condition, both physical and psychological, like pain, fear, surgery, infection, physical exercise, trauma, hypoglycemia or tumor and medicines like corticosteroid, hypnotic, may change the circadian rhytm.
The half-life of cortisol is 90 minutes. Due to circadian rhythm depend on cortisol secretion, so the normal value is vary according to time of day. The normal value at 09.00 am for a cortisol (11 hidroxycorticossteroid) is 170-720 nmol/1 (6-26 ᶬg/100ml), whereas in the midnight (12.00pm) the level is less than 220 nmol (<8 ᶬg/100ml) (Ganong, WF 2008). Cortisol levels is chosen in this research because it has characteristic that the patterns of cortisol secretion is increase and decrease slowly than other stress hormones (e.g. catecholamine) so measurement method is easier to be done.
The physiological responses of the human body which is very suceptible to distress are elevationof cortisol levels. Based on the psychoneuroimmunology concept, through hypotalamus hypophysis adrenal axis, that psychological stress will have an effect on the hypothalamus, then the hypothalamus affects the pituitary and it will express ACTH which ultimately can affect the adrenal glands, where the glands will produce cortisol. If the stress experienced by patients is very high, the adrenal glands will produce cortisol in large quantities so that it can suppress the immune system.
(Clancy, 1998).
In patients with pulmonary tuberculosis, the stressors, whether physical, psychological, social, and will be responded by the hypothalamus, so it secretes CRH. CRH response to the negative feedback following the diurnal rhythm, but in stress conditions, the circadian rhythm can be changed. A signal is sent to the pituitary that stimulates the secretion of ACTH. ACTH then captured by cells in the adrenal cortex to secrete cortisol (Guyton, 2012). In modern society, many physical and psychological stressors may increase the incidence of stress especially in patients with pulmonary tuberculosis. Ongoing stress can disrupt the whole immune system. Innate immunity, humoral immunity and cellular immunity (Celluler predator exposure) influence the hypothalamic- pituitary adrenal axis (HPA axis) so it produce the cortisol. The effects of cortisol are then distributed to various receptors that make a person more susceptible to infections.
Acceleration of adaptive responses in this disease affects coping mechanisms and reduce the activity of the HPA. Decrease in HPA activity affect the decrement, both on production and secretion of neuromodulators and neurotrasmiter (Ader, 2003). In a study group of patients who receiveself-efficacy enhancement development modelshowed a significant reduction in cortisol production.
CONCLUSION
In this research show that the self-efficacy enhancement development model againts biological response play a role through regulatory changes in the admission process of the disease, so it can decrease the psychological responses, through anxiety reduction regulation, and can reduce cortisol which induces the immune system to destroy tuberculosis.Self-efficacy enhancement development model againts biological response can regulate psychological response, resulting in decreased cortisol which induces an immune system and would damage or destroy the tuberculosis, so it can be concluded that accelerating the success of treatment process will be followed by a high cured rate in pulmonary tuberculosis. Further studies need to analyze another way of self-efficacy, which do not through the hypothalamus adrenal and stress is not related to self-efficacy but the test results of cortisol reduction, in effort to explore and develop beneficial
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nursing interventions to increase self-efficacy, treatment compliance, and quality of life of patients with pulmonary tuberculosis.
REFERENCES
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Clancy, J. (1998). Basic Concept in Immunology: Student’s survival guide. New York: The McGraw-Hill Companies.
Ganong. (2008). Buku ajar fisiologi kedokteran. 22nd ed. Jakarta: EGC.
Govier, I. (2000). Spiritual Care in nursing: a systematic approach. Nursing Standard, -.
Guyton A.C & Hall J.E. (2012). Textbook of Medical Physiology 11th ed. Philadelphia: WB Saunders Co.
Sherwood, L. (2001). Fisiologi Kedokteran: dari Sel ke Sistemi. Jakarta: EGC.
WHO. (2006). The Stop TB Strategy : Building on and enhancing DOTS to meet the TB-related Millennium Development Goals. Genewa: World Health Organization.
WHO. (2012). Global tuberculosis report 2012. Geneva, Switzerland: WHO Press.
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