Case Study 3: Acute Rheumatic Fever - Pathophysiology, Nursing Care, and Family-Centered Approach

Running head: CASE STUDY 3: ACUTE RHEUMATIC FEVER 1
CASE STUDY 3: ACUTE RHEUMATIC FEVER
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CASE STUDY 3: ACUTE RHEUMATIC FEVER 2
CASE STUDY 3: ACUTE RHEUMATIC FEVER
Introduction
Acute Rheumatic Fever (ARF) describes a sequela of streptococcal infection-
characteristically after two to three weeks following group A streptococcal pharyngitis which
takes place most frequently among children and has cardiac, rheumatologic, and neurologic
manifestations. The ARF incident has dropped in advanced economies, and several physicians
have little or no practical experience with diagnosis alongside management of ARF. This paper
seeks to demonstrate the pathophysiology alongside main clinical presentations of ARF by
taking into account a particular case of Sue (case study 3), 14-year-old native girl, who was
diagnosed with ARF. Later, the paper would further focus on the nurse’ role in the provision of
suitable care to adolescents and members of their families taking into account the current nursing
practices.
Pathophysiology of Acute Rheumatic Fever
ARF is manifested by nonsuppurative inflammatory lessons of heart, joints, central
nervous system and subcutaneous tissue. The literature has demonstrated that, at least in
advanced economies, rheumatic fever proceeds pharyngeal infection with rheumatogenic group
A streptococci (Webb, Grant & Harnden, 2015). The rheumatic fever development risk
following a streptococci pharyngitis episode is estimated at 0.3 to 3 percent. Some studies have
also associated rheumatic fevers amongst the aboriginal population of Australia to streptococcal
skin infections (Burke & Chang, 2014).
The tissue injury occurring in rheumatic fever is accounted for by the molecular mimicry.
Both cellular and humoral host defense of a genetically vulnerable host remain engaged. The
immune responses of the patient, in this process for both T- and B-cell mediated cannot

CASE STUDY 3: ACUTE RHEUMATIC FEVER 3
distinguish between such microbes that invade and some host tissues. T helper1 alongside
cytokine Th17 seem to be central mediators of rheumatic heart disease. The resulting
inflammation might persist past acute infection and generates the rheumatic fever or protean
manifestation (Gewitz et al., 2015).
The initial step is a pharyngeal infection by Streptococcus pyogenes, proceeded by
antigens’ presentation to the immune B and T cell. The production of particular chronic and
acute stage antibodies (IgM and IgG) results from the CD4+ cells’ activation by lymphocytes.
Such antibodies alongside activated T cells react with structurally identical peptides or proteins
in tissues of the heart that is known as the cross-section.
Consequently, the heart will be inflamed. The joints will then develop swelling alongside
pain because of accumulation of immune complexes that antigen-antibody merger have formed.
The skin and chorea rashes or the nodules are the additional manifestations of such immune
activation, in basal ganglia alongside skin in that order. The M protein and N-acetyl-beta-D-
glucosamine antigens will mimic one another alongside the myosin in cardiac muscle.
Such molecules have an identical antigenic structure with myosin which is the human
muscle protein. Antibodies are formed hence reacting with human heart valve tissue. The CD4+
cells will stick to as well as burrow into endothelium of the valve due to VCAM-1 molecules
overexpression thereby activating the cellular immune response within the valve. The
inflammation of the valve tissue thus follows with new blood vessels’ growth.
The T cell’s availability thus ensues due to the surged supply of blood resulting from
such vessels. Several antigenic attraction spots will occur on the valve, on such proteins as
tropomyosin and vimentin thereby making T-cell attack stretch to further areas. The Aschoff
bodies or granulomas the form underneath endocardial heart layer. Calcification further takes