Discuss the Case study for Physical Health Status & Analyse Health.

 

Atheroma formation is triggered by the physical or chemical insults to the endothelial barrier of the arteries. Injury to the endothelium can exaggerate by trauma, free radicals due to smoking and pollution, high level of low density lipoproteins and high level of glucose. WBCs are not active in normal condition, however, in case of injury, WBCs get activated in the wall of arteries and produces inflammatory response. In response to inflammation, endothelium of the arteries gives rise to adhesion molecules such as vascular vell adhesion molecule 1 (VCAM-1) and secretes monocyte chemoattractant protein (MPC-1). VCAM-1 and MPC-1 attracts monocytes and T-lymphocytes to the site on injury by chemokines under the influence of LDL. These monocytes get diffentiated to the macrophases. Macrophases express scavenger receptors and these receptors bind to the modified lipoproteins and appearance of macrophases become foamy which is called macrophage foam cell. Macrophages get encapsulated in the collagen and smooth muscle and hardened plaque is formed. There is low level of HDL in atheroma formation. High level of HDL prevent atherosclerosis by eliminating cholesterol and inflammatory cells from foam cells (Hao and Friedman, 2014; Libby, 2002).     a. Neurovascular assessment of wrist injury includes pain, sensation (paresthesia), motor function (paralysis), temperature (pallor) and pulse.

 

Pain disproportionate to the injury indicates existence of neurovascular problem. Pain due to passive extension and flexion of wrist indicates neurovascular problem. In case of neurovascular problem, there is the decreased or loss of sensation (paresthesia), numbness, dysaesthesia and tingling. Reason behind these observations is nerve obstruction and injury to the peripheral nerve. Motor function (paralysis) also affected in case of neurovascular disease. There is the difficulty in movement in the wrist due to radial nerve and median Nerve. Temperature (pallor) in the affected region either cool due to inadequate arterial supply or hot due to inadequate venous return. Increased swelling is associated with the neurovascular problem. Neurovascular assessment of pulse can be performed by palpable peripheral pulses. In Mr. Marconi high pulse rate is there with weak pluses (Nuber, et al., 1998).
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 the vital sign
Respiratory Rate	21-30 Save Time On Research and Writing Hire a Pro to Write You a 100% Plagiarism-Free Paper. Get My Paper
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
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

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).

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.

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.