Physical Health Status & Analyse Health
Discuss the Case study for Physical Health Status & Analyse Health.
Answer:
a. Request/consent form should be there with information containing Mr Marconi name, date of birth, age, full address, clinical history and medications. Mr Marconi should wear name band.
List vital signs recorded at 06:30
List the vital sign | |
Respiratory Rate |
21-30 |
O2 Saturation |
≥ 93 % |
O2 Flow Rate |
> 5 (L / min) |
Systolic BP |
120 |
Heart Rate |
90 |
Temperature |
≥ 38.6°C |
4 Hour Urine Output |
450 mL |
Consciousness |
Alert |
List the vital sign | ||
O2 Saturation |
≥ 93 |
Slightly hypoxemia |
Systolic BP |
120 |
Prehypertension (it is clearly mentioned prehypertnesion not hypertension) x 120 is not hypertensive |
Temperature |
≥ 38.6°C |
Hyperthermia |
Respiratory Rate |
21-30 |
Tachycardia |
ADDS Score :
ADDS Score | |
Respiratory Rate |
1 |
O2 Saturation |
0 |
O2 Flow Rate |
2 |
Systolic BP |
0 |
Heart Rate |
0 |
Temperature |
2 |
4 Hour Urine Output |
0 |
Consciousness |
0 |
Total ADDS |
5 |
Nurse should accompany Mr Marconi when he leaves the ward to go to the X-ray department.
Polypharmacy is the major cause of fall in the elderly patients. Mr Marconi is on the medicines like atenolol, ramipril, lantus and Lipitor. Most of these medications are for cardiovascular disorders and it is well established that cardiovascular drugs are the cause of fall in elderly patient.
Dibetes mellitus is responsible for fall in Mr Marconi because it is evident in literature that fall in elderly patients with diabetes is due to the reduced walking and poorer cognitive performance.
Increased vital signs like tachycardia and tachypanea are responsible for fall in Mr Marconi, as these vital signs leads to anxiety and disorientation in Mr Marconi.
As Mr Marconi was going to bathroom, when fall occurs and fall of the elderly patient in the bathroom was identified as one of major factor may be sleepy surface in the bathroom. These were the reasons for fall of Mr Marconi (Chester and Rudolph, 2011; Fialova et al., 2005; de Mettelinge et al., 2015).
External respiration mainly occurs in the lungs. In external respiration O2 diffuse into the blood and CO2 diffuses into the alveoli. Small amount of oxygen is transported into the lungs in the dissolved form and large amount of oxygen is transported into the blood in haemoglobin bound form in red blood cells. Small amount of carbon dioxide is carried in dissolved form and bound to haemoglobin and large amount is carried in the form of bicarbonate ions.Due to the accumulation of fluid in the alveoli there is the edema formation in the alveoli. This edema formation in the alveoli leads to blocking of air flow in the alveoli and decreases external respiration. This decreased respiration leads to the impaired gas exchange. Thus it results in the alteration on the patient’s O2:CO2 ratio due to decrease in absorbed oxygen. This results in the increased carbon dioxide level in the blood. Chemical control of breathing is specifically relying on the carbon dioxide in the blood. Increased carbon dioxide level produces increased respiratory rate. This respiratory rate can be measured using spirometer (Lahiri et al., 1978; Brunner, et al., 1982).
a. Gases detected in the blood are O2 and CO2.
These gases are detected at peripheral chemoreceptors through innervation of glossopharyngeal (IX) nerve b in the carotid arteries and vagus (X) nerve in the aortic arch. These gases are also detected at baroreceptors in the walls of blood vessel.
Its control centre respiratory rhythmicity centre is located in the medulla oblongata which includes a dorsal respiratory group (DRG) and a ventral respiratory group (VRG). In Mr d. Marconi SaPO2 is 91% (2L/min). This results in the altered O2:CO2 ratio. In this case it produces decreased level of O2 and increased level of CO2 in the blood. Also fever produces more CO2 in the body. To compensate for the excess production of CO2 , body needs to breathe at faster rate. CO2 is exchanged in the form of bicarnonate ion between alveoli and blood. Increased level of CO2 leads to anaerobic respiration which leads to increased rate of respiration (Lahiri and Forster, 2003; Brendan, et al., 2000).
First step in the analysis of sputum sample is to identify type of gram stain. This is called culture method in which sputum sample is incubated on the culture media and this culture media allowed the growth of bacteria. These bacteria can be pathogenic or non-pathogenic. If pathogenic bacteria are identified, antimicrobial susceptibility testing should be performed. Antimicrobial susceptibility testing should be performed to identify the antibiotic resistance to identified bacteria. This helps in the prescription of the bacteria so that prescribed antibiotic is susceptible to the identified bacteria. Susceptibility testing can be performed using broth micro dilution or rapid automated instrument method (Jorgensen and Ferraro., 2009).a. Sympathetic nerve stimulation β1-adrenoceptors on the juxtaglomerular (JG) cells, decreased level of tubular NaCl and decrease in the afferent arteriole pressure leads to renin release.Renin targets angiotensinogen in the liver by converting angiotensinogen into angiotensin I.
Angiotensin-converting enzyme is responsible for the conversion of angiotensin I to angiotensin II and this enzyme mainly found in the lung and also found in the endothelial and kidney epithelial cells.
Angiotensin II acts on the adrenal gland to secret aldosterone which leads to the tubular Na+ Cl- reabsorption and K+ excretion, which leads to the increase in the blood pressure. Angiotensin II acts on the AT1 receptor which releases Ca++, this results in the decreased level of cAMP and increased blood pressure.
Ramipril inhibits angiotensin-converting enzyme (ACE) and it useful in the treatment of hypertension and congestive heart failure. (Paul et al., 2006; Kumar et al., 2008; Frampton and Peters, 1995)
Insulin binds to the extracellular portion of cell membrane-bound insulin receptors. In the presence of insulin molecule, insulin and its receptor gets converted into tyrosine kinase. Tyrosine kinase phosphorylates insulin receptor substrate 1 (IRS-1) and IRS-1 bound to the activated insulin receptor. This leads to the incorporation of glucose transporter type 4 (GLUT4) into the cell membranes of adipose tissue and skeletal muscle. GLUT4 promotes uptake of glucose in the tissues from the blood. Insulin also promotes storage of glucose in liver and skeletal muscle in the form of glycogen. It produces this action by activating glycogen synthase enzyme. Insulin leads to the dephosphorylation of phosphofructokinase which leads to the glycolysis i.e. breakdown of glucose (Sonksen and Sonksen 2000; Berg et al., 1995).
Abnormal signs | |
O2 Saturation |
85-89 % |
O2 Flow Rate |
> 5 (L / min) |
Systolic BP |
190 |
Heart Rate |
120 |
Blood glucose level |
3.1 mmol/L |
Urine |
Leucocytes and ketones |
Consciousness |
To Voice |
Decreased level of consciousness in Mr. Marconi can be concluded form his decreased sleep and his refusal for eating. As a result there is reduced alert, voice, pain, unresponsive (AVPU) scale in Marconi. As, Mr. Marconi is diagnosed with pneumonia, there is increased breathing rate in Mr Marconi. Increased breathing rate is related to the decreased AVPU scale. Impaired glycaemic control is associated with reduced consciousness level. Mr. ,arconi is hypoglycaemic and this hypoglycaemic condition is responsible for the reduced AVPU scale in Mr. Marconi. Mr Marconi consuming four drugs and as a result there is the possibility of drug-drug interaction within these drugs. These drugs can negatively affect treatment of other drugs and can amplify adverse effects of other drugs. Hence consumption of atenolol, ramipril, lantus and lipitor together is responsible for deterioration of the condition of Mr Marconi (Sprague and Arbeláez, 2011; Golden et al., 1997). Particularly, Ramipril is unable to completely recover hypertension in older patients. If patient stand up from sleeping and seating position, there is the possibility of fall in the patient.
References:
Berg, JM., Tymoczko, J.L., & Stryer, L. (1995). Biochemistry. (Fourth ed.). New York: W.H. Freeman and Company.
Brendan, C., Kevin, G., & Cliffoed, W.Z. (2000). The control of breathing in clinical practice. Chest.
Brunner, M.J., Sussman, M.S., Greene, A.S, Kallman, C.H., & Shoukas, A.A (1982). Carotid sinus baroreceptor reflex control respiration. Circulation Research.
Chester, J.G., & Rudolph, J.L. (2011). Vital signs in older patients: Age-related changes. Journal of the American Medical Directors Association.
de Mettelinge, T.R., Cambier, D., Calders, P., Noortgate, N. V. D., & Delbaere, K. (2015). Understanding the Relationship between Type 2 Diabetes Mellitus and Falls in Older Adults: A Prospective Cohort Study. PLoS One, 8(6), e67055. doi: 10.1371/journal.pone.0067055.
Fialova, D., Topinkova, E., Gambassi, G., Finne-Soveri, H., Jonsson, P., Carpenter, I., et al. (2005). Potentially inappropriate medication use among elderly home care patients in Europe. Journal of the American Medical Association.
Frampton, J.E, & Peters, D.H. (1995). Ramipril. An updated review of its therapeutic use in essential hypertension and heart failure. Drugs.
Golden, F.S.C., Tipton, M.J. & Scott, R.C. (1997). Immersion, near-drowning and drowning. British Journal of Anaesthesia, 79, 214-225.
Hao, W., & Friedman, A. (2014). The LDL-HDL profile determines the risk of atherosclerosis: a mathematical model. PLoS One, 9(3), e90497. doi: 10.1371/journal.pone.0090497.
Jorgensen, J.H., and Ferraro, M.J. (2009). Antimicrobial susceptibility testing: A review of general principles and contemporary practices. Clinical Infectious Diseases.
Lahiri, S., & Forster, R.E. (2003). CO2/H(+) sensing: Peripheral and central chemoreception. International Journal of Biochemistry and Cell Biology.
Lahiri, S., Mokashi, A., Delaney, R.G., & Fishman, A.P. (1978). Arterial PO2 and PCO2 stimulus threshold for carotid chemoreceptors and breathing. Respiration Physiology.
Libby, P. (2002). Inflammation in atherosclerosis. Nature.
Kumar, R., Singh, V.P., & Baker, K.M. (2008). The intracellular renin-angiotensin system: implications in cardiovascular remodeling. Current opinion in nephrology and hypertension.
Nuber, G.W., Assenmacher, J., & Bowen, M.K. (1998). Neurovascular problems in the forearm, wrist, and hand. Clinics in Sports Medicine.
Paul, M., Poyan Mehr, A., & Kreutz, R. (2006). Physiology of local renin-angiotensin systems. Physiological Reviews.
Sonksen, P., & Sonksen, J. (2000). Insulin: understanding its action in health and disease. British Journal of Anaesthesia.
Sprague, J.E. & Arbeláez, A. M. (2011). Glucose Counterregulatory Responses to Hypoglycemia. Pediatric Endocrinology Reviews, 9(1), 463–475.
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