On 29 July, 2014, ONE News published a report of a nurse who was ordered to make a written apology to a patient who was injected with a syringe previously used on another patient (ONE News, 2014). After realizing her mistake, the nurse then delayed informing the patient until the fifth day post injection.
The injury sustained by the patient in the report is termed a Needle Stick Injury. This is defined as an incident that induces a blood wound that introduces “blood or other hazardous material through a hollow bore needle or sharp instrument” (Malik, Shaukat, & Qureshi, 2012, p. 114). Though there was a low risk of acquiring of blood-borne viruses (BBV) through occupational sources, both the initial mistake (of re-using a syringe) and the …show more content…
The first level of defense is non-specific and includes the physical barrier to entry of any foreign invader(McKinley, O 'Loughlin, & Bidle, 2013). This line of defense includes the skin and mucous membranes (McKinley et al., 2013; Pallasch, 2011). When these barriers are breached, elements of the second and third line of defense work to try protect and aid the host combat disease (Pallasch, 2011). Although not all microbial agents cause harm to the human body, for example, the bacteria that live in the intestines that produce Vitamin K (Guarner & Malagelada, 2003), those that do damage to the host are termed pathogenic (Lee & Bishop, 2002; McKinley et al., …show more content…
This is the second line of defense which is still non-specific (Lee & Bishop, 2002). This means that this response occurs whatever causes the injury—even a sterile instrument like a sterile scalpel blade. Chemical mediators are released from mast cells, basophils, the damages cells and the invading microbes themselves to induce vascular changes in the area of injury (McKinley et al., 2013). For example, vasodilation is facilitated by histamine release from platelets, mast cells and basophils. This result in an increase in blood flow into the area of injury. Histamine also makes endothelial cells shrink and draw away from adjoining cells. This creates spaces between cells making the capillaries permeable. Another form of vascular change include the display of cell adhesion molecules which induce leukocytes to line up against the cell walls in a process called margination (McKinley et al., 2013).The inflammatory cells then squeeze through the now permeable capillaries in a process called diapedisis. This migration of cellular products and vascular fluid, collectively know as exudate, to the site of injury (chemotaxis) brings the leukocytes and lymphocytes that will help combat the foreign invader and aid in repair. The influx of red blood cells in the area leads to redness and
The injury sustained by the patient in the report is termed a Needle Stick Injury. This is defined as an incident that induces a blood wound that introduces “blood or other hazardous material through a hollow bore needle or sharp instrument” (Malik, Shaukat, & Qureshi, 2012, p. 114). Though there was a low risk of acquiring of blood-borne viruses (BBV) through occupational sources, both the initial mistake (of re-using a syringe) and the …show more content…
The first level of defense is non-specific and includes the physical barrier to entry of any foreign invader(McKinley, O 'Loughlin, & Bidle, 2013). This line of defense includes the skin and mucous membranes (McKinley et al., 2013; Pallasch, 2011). When these barriers are breached, elements of the second and third line of defense work to try protect and aid the host combat disease (Pallasch, 2011). Although not all microbial agents cause harm to the human body, for example, the bacteria that live in the intestines that produce Vitamin K (Guarner & Malagelada, 2003), those that do damage to the host are termed pathogenic (Lee & Bishop, 2002; McKinley et al., …show more content…
This is the second line of defense which is still non-specific (Lee & Bishop, 2002). This means that this response occurs whatever causes the injury—even a sterile instrument like a sterile scalpel blade. Chemical mediators are released from mast cells, basophils, the damages cells and the invading microbes themselves to induce vascular changes in the area of injury (McKinley et al., 2013). For example, vasodilation is facilitated by histamine release from platelets, mast cells and basophils. This result in an increase in blood flow into the area of injury. Histamine also makes endothelial cells shrink and draw away from adjoining cells. This creates spaces between cells making the capillaries permeable. Another form of vascular change include the display of cell adhesion molecules which induce leukocytes to line up against the cell walls in a process called margination (McKinley et al., 2013).The inflammatory cells then squeeze through the now permeable capillaries in a process called diapedisis. This migration of cellular products and vascular fluid, collectively know as exudate, to the site of injury (chemotaxis) brings the leukocytes and lymphocytes that will help combat the foreign invader and aid in repair. The influx of red blood cells in the area leads to redness and