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Significant findings of the physical examination
From the physical examination of the patient, it is derived that; dyspnea (shortness of breath) especially when talking is due to airway obstruction. The blood pressure is higher than normal (normal blood pressure is 120/80) indicating type1 hypertension. The respiratory rate is also higher than normal (normal rate 12-20 breaths per min). Yellowing of teeth is due to prolonged smoking while the pursed-lip breathing (wheezing) could be a result of airway obstruction. Moreover, the jugular distension could be due to hypertension. The use of accessory breathing muscles and the increased anteroposterior diameter of the chest wall indicated labored breathing.
A hyper resonant percussion and a decreased breath sound, increased fremitus on both lower lobes could indicate accumulation of fluid in both these lobes (Weir, 2005). The normal S2 and S1, a regular rhythm indicated lack of a cardiac disease. The drying of extremities and lack of finger clubbing of fingers could be due to hypoxia (reduced oxygen supply.).The bilateral edema in the ankles could have indicated the retention of fluid and salt due to some cardiovascular disorders.
Possible diseases causing the distress
This kind of distress could result from; a pneumonia infection, chronic bronchitis, or even emphysema.
Variation of the lab results from the normal range in terms of the disease process
The variations of these results from the normal ranges are due to the increase in the severity of the infection with time. For instance, the white blood cell count is higher than normal due to an increase in the number of immune cells entering the circulation following the infection. There is also a slightly increased HC (hematocrit levels from 48% to 39%) and this may be attributed to the fact that there is an elevation in the rate of red blood cell fragility and consequently hemolysis. There is also an increased Paco2 due to an accumulation of CO2 (Weir, 2005). This is mainly attributed to the fact that the exhalation of the CO2 is not adequate.
Pathogenesis of the disease and its risk factors
The chronic bronchitis Mr. Burns is suffering from is due to a bacterial infection. This could also be due to prolonged cigarette smoking. This is because persistent exposure to smoke causes hypertrophy of the mucous glands lining the trachea hence leading to partial obstruction of the airway. This led to the breathing difficulties he is experiencing. Cigarette smoking could also lead to the damage of alveoli. His condition could also be due to an infection by pneumonia causing bacteria and most probably he might have acquired it from his friends who had been previously infected. However, the symptoms could have been worsened by smoking.
The dramatization of his feet could have been due to a cardiac disorder that led to the accumulation of fluid in his feet and this may have been triggered by the respiratory disorder. The risk factors would include continued smoking as this would increase the irritation hence worsen the condition. Moreover, working in a dusty or smoke environment would further worsen the condition.
Classifications of possible medications and their modes of action
The expected drugs of choice should be broad-spectrum antimicrobial drugs. The administration of antibiotics takes care of any bacteria or microbes which can cause bronchitis or pneumonia. Moreover, the administration of antihypertensive therapy will lower his blood pressure back to normal (Weir, 2005).
Mr. Green’s infection with hepatitis C
The palpation of the lower border of the liver below the rib cage, tenderness with palpation over the right upper quadrant, and a slightly distended stomach indicated an enlarged liver size. Hepatitis C can cause this enlargement. An increase in the levels of circulating alkaline phosphatase, aspartate, and alanine transaminases can also be a possible indication of a hepatitis C infection. Moreover, the presence of circulating Anti-hepatitis C antibodies also indicates a recent Hepatitis C infection. The presence of slight scleral icterus.
Treatment for Hepatitis C
Hepatitis C has no vaccine. Although Hepatitis C is quite difficult to treat, a variety of methods are applied to try curbing the disease (Harris, 2008). Acute hepatitis C is rarely symptomatic thus its therapy is not also commonly administered. However, when administered, may be interferon application. With the chronic form of the disease, prompt action should be taken before there is large-scale liver damage. Most treatment involves a combined dose of interferon and ribavirin for not less than 24-48 weeks. This period depends on the strain of the causative agent. The form of therapy is also dependent on the presence of other secondary infections such as HIV. The treatment of hepatitis c is mainly initiated before the administration of ARV.
Symptoms that differentiate liver failure from cirrhosis
Cirrhosis is a milder form of the disease as compared to the liver or hepatic failure which signifies an 80-90% loss of functioning liver cells. Cirrhosis typically presents with among others; hepatic encephalopathy (confusion and coma), spider angiomata, palmar erythema, hemorrhagic esophageal varies, and changes at the nail plate (clubbing and Terry’s nails).
However, coagulopathy (a condition in which loss of the functional liver cells leads to decreased synthesis of clotting factors among them prothrombin and vitamin K.) and jaundice (characterized by yellowing of the sclera and mucous membranes due to accumulation of plasma bilirubin) are the cardinal symptoms of hepatic failure occasionally accompanied by renal failure and metabolic derangements.
Complications associated with cirrhosis
Liver cirrhosis refers to damage of the liver tissue (cells) and this may cause a marked number of complications depending on the extent or severity of the damage. These complications may include jaundice; which refers to the yellowing of mucous membranes due to an increase in the circulating bilirubin levels. This may primarily be attributed to the consequent inability of the liver to conjugate bilirubin for excretion in bile. A more serious condition in neonates and fetuses is known as Kincterus where unconjugated bilirubin crosses the blood-brain barrier hence causing damage to the brain tissue and is highly fatal (Champe, 2005). Liver cirrhosis may also cause liver disease and consequent liver failure.
This means that most of the central liver functions are arrested hence decreasing metabolic, secretory, and detoxification functions. Liver function may be compromised to a level that is not compatible with life thus death.
References
Champe, P. C., Harvey R. A. & Ferrier D.R. (2005). Biochemistry Lippincott’s illustrated reviews. Philadephia: Lippincott Williams & Wilkins.
Harris, E. (2008). American medical times. Michigan: University of Michigan.
Weir, M. R. (2005). Hypertension. Auckland: ACP Press.
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