Medicine case study Term Paper Assignment

Medicine case study

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there are 3 case studies. I prefer to do case study 1. please find attached information. you need to follow marking criteria(assessment task 2) on page number 15-16 of unit outline. for my university database, just google, acu leo page and login with details as follows :I normally use CINAHL database, or MEDLINE. REference style APA. font size 12, double spaced line.
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Medicine case study

Q.1. Congestive cardiac failure due to digoxin toxicity

 Causes:  Congestive cardiac failure (CCF) is caused by conditions that damage the cardiac muscle. This includes cardiac complications such as coronary artery disease (CAD) which causes the arteries to be blocked or narrowed severely; affecting the circulation of blood. Other disorders associated with overworking of the heart such as hypertension, cardiomyopathy, diabetes and kidney diseases are leading causes for congestive heart failure. In this context, Sharon McKenzie causes of congestive cardiac failure are attributable to digoxin toxicity. This could have deteriorated his renal function due to the electrolyte disturbances and hypertension. Additionally, digoxin toxicity also caused the alterations in heart rate and rhythm, irregular respiratory rate that had crackles in both lungs (Hosenpud & Greenberg, 2013).

Incidence: CCF is a lethal disease that affects about 3.5 million people by 2007-08. Despite the technological advancement, CCF is still the leading cause of death in Australia; and the most expensive accounting close to $5.2 billion. One of the key causes for CCF is digoxin toxicity which accounts for 10-20% of patients who are on long term use of digoxin therapy- more common among the elderly (National Heart foundation of Australia, 2011).

Risk factors: Digoxin toxicity risk factors vary with individuals attributes.  To start with, individuals use of diuretics –the stronger the diuresis effect of furosemide the greater the risk for digoxin toxicity. This is also influenced by individual’s ability to regulate electrolyte disturbances. Other risk factors include age due to age related kidney and thyroid complications. CCF due to digoxin toxicity is also influenced by the concomitant medications such as herbal remedies taken by the patient which increases the concentration of the serum digoxin (Hosenpud & Greenberg, 2013).

Impact on the family and the patient: Other than the physical impact, the patient may become psychologically affected   and could feel like their dignity is reduced- particularly when they have to become dependent on other people.  The major impact of CCF to the family is financial burden. Although there is no precise data existing on the economic burden of the disease at family level, a rough estimate indicated that approximately $411 million is spent annually to cater for hospitalization costs and nursing home costs. The family members are psychologically affected to see their loved ones suffer.  In most cases, the family members may undergo grief period because they fear that their loved ones could die- especially if the person is aged. The CCF patient needs care all the time, which could be a challenge, especially if the family members are working ((National Heart foundation of Australia, 2011).

2. 2. CCF pathophysiology

1. 3 Common classes of CCF drugs

Cardiac glycosides have been used to treat CCF for over 3000 years. This group comprises of Digitoxin (crystodigin), Deslanoside (Cedilanid-D) and Digoxin (Lanoxin).  The natural extracts main mechanism of action is by increasing the pressure for cardiac contraction.  Cardiac glycosides increase the concentration of intracellular electrolytes- mainly sodium- using Na+ K+ ATPase; an enzyme that cleaves ATP to ADP. The energy releases from this metabolic hydrolysis drives the Na+ K+, thereby increasing the force and the the velocity of the muscle contraction. The second mechanism is through the rise in intracellular calcium. The rise in calcium ions also increases the contraction velocity and force.  Consequently, the heart rate is slowed, increased filling volumes because contraction is stronger/ greater, the velocity of the AV node conduction is reduced and the AV nodal refractory duration is increased.   However, these drugs side effects include EKG changes, anorexia, vision disturbances and headaches (Katz & Konstam, 2012).

Angiotensin Converting Enzyme Inhibitors (ACE inhibitors) drug group members include Captropril (Capoten), Lisinopril (Prinivil) and Enalapril (Vasotec).  The ACE inhibitors main mechanism is through regulation of the blood pressure using Renin Angiotensin Axis. Renin is produced by kidney and released to the blood when Bp is low. Once released in blood, it is converted to angiotensin I, then to angiotensin II- which is potent vasoconstrictor. Angiotensin II causes vasoconstriction and causes disturbances in the homeostasis balance causing water retention. High blood pressure resulting due to vasoconstriction results to the overload of the left ventricle, and if untreated the ventricle will fail. ACE inhibitors work by blocking the conversion of Angiotensin I to II, by inhibiting the enzymatic activity  of the enzyme responsible for the conversion, this way; it reduces he systemic blood pressure and consequently improves the  the cardiac function. The reduced blood pressure lowers the oxygen demand by the myocardial, reduces the preload and afterload. Other studies indicate that ACE inhibitors also work by widening the blood vessels, thus improves the blood flow reducing the work load of the heart and thereby reducing the blood pressure. However, there are side-effects include distress in the gastro intestines, dizziness and skin rashes (Katz & Konstam, 2009).

4. 4. Nursing care interventions for CCF digitalis toxicity

Despite the advancement in CCF management, digoxin toxicity is reported. In this case study, it is most likely that the patient was prespribed a dose that is high than the renal function. The main post admission nurse intervention is to a) stop digoxin toxicity, b) control disease symptoms, and c) monitor the patient’s levels of digoxin. In this context, the nurse must assess the severity of the toxicity. The nurse should also assess the etiology of the toxicity  i.e. is it accidental ingestion of more than recommended dosage, was the overdose deliberate or is is due to  reduced metabolism of the  digoxin  due to  drug interaction or due to other prevailing  medical  complications such as  diminished renal function. Other factor that must be put into consideration is the patient age, ECG changes, the chronicity of the intoxication and patient’s medical history. The findings from this assessment will guide the nurse when making clinical decision on the treatment (Wang Et al., 2010).

To stop the toxicity, the patient will have to be discontinued from taking the digoxin therapy. Instead, the patient will be given digoxin fab fragments to reduce the toxicity. In some cases, activated charcoal can be used for an acute overdose.  The patient results indicate the possibility of renal failure; the best approach is to administer binding resin, which has been found. Other supportive care includes   hydration of the patient using IV fluids, support of the ventilator function using oxygenation.  Potassium supplements can be used to raise the potassium supplements. The nurse should continue monitoring the digoxin levels until the ideal levels for digoxin (0.5-0.8ng/ML is reached. Simultaneously, other function such as renal function and potassium levels should be done. Calcium and magnesium supplements should be used to correct the electrolyte imbalance.  If the patient is acidotic, sodium bicarbonate can be administered to reduce hypertension, the patient should be treated using other groups of medicines including ACE inhibitors. This remedy reduces vasoconstriction and fluid retention (Yang Et al., 2012).

The patient should indicate relief of symptoms. The nurse will ensure that toxicity symptoms such as shortness of breath, irregular heartbeat and peripheral oedema are reduced. The nurse will monitor the apical-radial pulse after every medication administration in order to monitor changes in cardiac rhythm. Additionally, patient serum level will be monitored regularly to determine the therapeutic activity on toxicity. This will include monitoring the levels of magnesium, calcium, potassium and creatinine. From the report findings, the nurse can evaluate the effectiveness of the medical intervention. The patient should be discharged only when the expected outcome (relief of the symptoms and reduction of digitalis toxicity) is achieved (Wang Et al., 2010).

To prevent toxicity in the future, there is need to regularly monitor the levels of digoxin in the blood. Additionally, the patient and their family should be empowered to ensure that they are aware of indicators of digitalis toxicity. The patient should be encouraged to reduce stress, have adequate sleep, regular exercise and eat balanced meal, particularly the Mediterranean diets.  The patient should be instructed to report any changes in their body such as depression, weakness, vomiting or general body weakness (Wang Et al., 2010).

References

National Heart foundation of Australia. (2011). 2011 addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand guidelines for the management of acute coronary syndromes (ACS) 2006. Heart, Lung And Circulation, 20(8), 487-502. doi:10.1016/j.hlc.2011.03.008

Hosenpud, J., & Greenberg, B. (2000). Congestive heart failure; pathology, diagnosis and comprehensive  approach to management. Philadelphia: Lippincott Williams & Wilkins.

Katz, A., & Konstam, M. (2009). Heart Failure: epidemiology, molecular biology and clinical management. Philadelphia: Lippincott Williams & Wilkins.

Patel, C., & Deoghare, S. (2015). Heart failure: Novel therapeutic approaches. Journal Of Postgraduate Medicine, 61(2), 101. doi:10.4103/0022-3859.153104

Wang, M., Su, C., Chan, A., Lian, P., Leu, H., & Hsu, Y. (2010). Risk of digoxin intoxication in heart failure patients exposed to digoxin-diuretic interactions: a population-based study. British Journal Of Clinical Pharmacology, 70(2), 258-267. doi:10.1111/j.1365-2125.2010.03687.x

Yang, E., Shah, S., & Criley, J. (2012). Digitalis Toxicity: A Fading but Crucial Complication to Recognize. The American Journal Of Medicine, 125(4), 337-343. doi:10.1016/j.amjmed.2011.09.019

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