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Make sure to include intext citations :(Braun & Anderson, 2017)
Cystic Fibrosis (CF)
It is an autosomal recessive disorder of the electrolytes and water transport that affects the epithelial cells (Braun & Anderson, 2017). CF is caused by mutation of the CF gene located in the long arm of chromosome 7. To be expressed It must be homozygous and any career has one of the mutated gene. The mutation leads to impaired electrolyte transportation across the epithelial cells on the mucosal surfaces. CF is strongly associated with mucous plugging, inflammation, and infection in the lungs with respiratory failures as the most common cause of death (Braun & Anderson, 2017). There is an increase with infections because of lack of opsonization and phagocytosis. Permanent lung damage depends on the intense, chronic inflammatory response dominated by neutrophils. CF effects can go beyond perfusion and ventilation, reduced chloride secretion and restricted water into the intestinal tract can lead to obstructions of the intestines. Clinical manifestation varies depending on age of diagnosis and the rate of the disease progression. Clinical manifestations are associated tenuous secretion, recurrent respiratory inspection, chronic cough accompanied with mucoid or purulent sputum. Other manifestations include tachypnea, recurrent wheezing or crackles, hemoptysis, dyspnea on exertion, chest pain, barrel chest recurrent sinusitis, and development of nasal polyps. Newborns may experience intestinal obstruction at birth with a delayed or absent passage of the meconium stool. Children and infants demonstrate increased frequency of large, greasy, malodorous stool which indicates fats malabsorption (Braun & Anderson, 2017). The condition will be accompanied with abdominal pains, distention, and poor fat-soluble vitamins. Weight loss is common too. Males with CF are frequently sterile because they lack vas deferens, they may also have undescended testicle. Secondary sexual development is delayed in women and fertility is maintained or somewhat reduced. History of parents, and physical examinations noting the characteristics of clinical manifestation is usually used to diagnose the disease. It is the confirmed by sweat test which will show a chloride concentration of 60mEq/L or greater. Treatment involves maximizing ventilation, diffusion, and nutrition through clearing the air way, avoiding, and regulating respiratory infections, reducing inflammation, providing optimal nutrition and managing the disease complications (Braun & Anderson, 2017).
Disseminated Intravascular Coagulation (DIC) is a condition of uncontrolled activation of clotting factors that results in wide speared of thrombi formation, then depletion of coagulation factors and platelets leading to hemorrhage. it is initiated by tissue injury such as trauma, surgery, burns, malignant neoplasm, infections, and shock. Injury triggers imbalance between clotting and fibrinolysis. Thrombin and platelets accumulate throughout the cardiovascular hence cause widespread of tissue ischemia. This allows system hemorrhage which is a dangerous issue and must be recognized and treated immediately. Presence of excessive clotting and hemorrhage is seen. Blood may be in sputum, stool, emesis, and urine. Severe hemorrhage can lead to hypovolemic shock, this occurs as an acute DIC. Chronic DIC is characterized by excess thrombin formation (Braun & Anderson, 2017). It occurs commonly with malignancy, chronic renal disease, venous thrombosis, and certain connective tissue disorder. If thrombus is in the brain, it causes headache, weakness, seizures, or even comma. Within the kidney, poor urine output, which can progress to renal failure. In the hearts and lungs, manifestation include cough, shortness of breath, respiratory distress, or chest pain. physical and history examinations are done to identify the underlying cause. Laboratory tests include Prothrombin test (PT), activated partial thromboplastin time(aPTT), platelet count, and fibrinogen level (Braun & Anderson, 2017). The D- timer test measures the degradation of fibrin products (Braun & Anderson, 2017). This is the confirmatory test. Treatment should be focused on correcting the underlying cause. The goal is to replace the missing blood components. It is about careful balancing act focused on restoring the body’s ability to coagulate properly (Braun & Anderson, 2017).
