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Differential Diagnosis
Primary Adrenocortical Insufficiency (Addison’s Disease) (e27.1)
Addison’s disease (AD) is an autoimmune disorder that is a type of autoimmune adrenalitis which causes adrenocortical insufficiency (Napier & Pearce, 2012). Pathophysiologically, adrenal glands produce insufficient amounts of cortisol, aldosterone, and adrenal androgen; in fact, this often occurs due to the destruction of a large part of the adrenal cortex by autoimmune attacks. The symptoms include fatigue, feeling nauseous, dizziness, anorexia/weight loss, as well as cramps in muscles. One of the signs is hyperpigmentation (Napier & Pearce, 2012). Laura, in fact, has most of these signs and symptoms, which is why AD is a possible condition.
Seropositive Rheumatoid Arthritis (M05)
Rheumatoid arthritis is a highly prevalent inflammatory disease of the autoimmune nature in which joints are the primal target of the autoantibodies (Smolen, Aletaha, & McInnes, 2016, in press). Pathophysiologically, “autoantibodies against citrullinated peptides (ACPAs) and autoantibodies against IgG (rheumatoid factor [RF])” are formed (Smolen et al., 2016, in the press, p. 1). ACPAs are capable of binding with citrullinated residues of numerous proteins such as fibronectin, vimentin, type II collagen, etc. Leucocytes invade the synovial compartments, cause inflammation, and destroy the tissues (Smolen et al., 2016, in press).
The symptoms of rheumatoid arthritis are usually unspecific (Smolen et al., 2016, in press), but often develop slowly and may include “general systemic manifestations of inflammation, weakness, weight loss, malaise, fatigue, anorexia, aching, and stiffness” (Buttaro, Trybulski, Bailey, & Sandburg-Cook, 2013, p. 1197). The signs may include alopecia, Raynaud’s phenomenon, Sicca syndrome, etc. However, the signs and symptoms may vary significantly, and are often very unspecific, which makes diagnosing difficult (Smolen et al., 2016, in press). In Laura, most of the named symptoms are present, which justifies checking for this disease.
Acute Hepatitis B (B16), or Acute Hepatitis C (B17.1)
Viral hepatitis is caused by a viral infection and is characterized by liver inflammation. Five types of viral hepatitis (A, B, C, D, E) exist, but their pathophysiology is similar. Liver cells become inflamed and damaged, which may lead to scarring, fibrosis, and focal necrosis. The degeneration of liver cells is followed by their shrinkage; the space is then filled by monocytes. Progressing fibrosis and inflammation may cause cirrhosis if unaddressed (Buttaro et al., 2013).
General symptoms of acute viral hepatitis include malaise, nausea, vomiting, abdominal discomfort, anorexia, alterations in the senses of smell and taste, and fatigue (Goroll & Mulley, 2014). In addition, jaundice may occur among patients with hepatitis B (33%) and C (25%), fever is uncommon for hepatitis B and C, and these two types of hepatitis can be transmitted sexually (Buttaro et al., 2013). Signs may include pseudomononucleosis syndrome, bone marrow suppression, and systemic vasculitis. Hepatitis A can also be transmitted sexually and often causes jaundice, but it also commonly causes fever; and it is unknown whether hepatitis D and E can be transmitted sexually (Buttaro et al., 2013).
Because Laura shows the general symptoms of acute viral hepatitis, but does not have a fever, and engages in unprotected sex with different partners, hepatitis B or hepatitis C are more likely than other types of hepatitis.
Further Questions
Addison’s Disease
Have you experienced salt craving? Have you felt that your strength was reduced? Have you lost any pubic or axillary hair? Have you had any eating disorders or the desire to eat less (Napier & Pearce, 2012)?
Seropositive Rheumatoid Arthritis
Have you experienced dry mouth or eye dryness? Have your fingers or toes go numb and/or colorless? Have you lost any hair? Have you had swollen joints and/or morning stiffness (Smolen et al., 2016, in press)?
Acute Hepatitis
Have you felt any changes in the senses of taste and smell? Have you experienced a desire to reduce the amount you eat? Have you felt discomfort in your abdomen (Buttaro et al., 2013)?
Body Systems to Examine, and Diagnostic Tests
Addison’s Disease
Systems to examine. Endocrine system: adrenal glands (more than 90% of the adrenal cortex is usually destroyed before the emergence of symptoms (Napier & Pearce, 2012, p. e627)). Immune system: autoantibodies against the tissues of the adrenal cortex. Digestive system: anorexia. Nervous system: dizziness, fatigue, nausea. Circulatory system: hypoglycemia, hyponatremia, hyperkalemia, lymphocytosis, eosinophilia (these are mediated by the lack of glucocorticoids). Integumentary system: hyperpigmentation of the skin, especially in the areas which are often subjected to friction, such as elbows (Napier & Pearce, 2012).
Diagnostic tests. It is necessary to establish whether there is an adrenocortical failure; if yes, its etiology should be established. A blood test assessing levels of cortisol and ACTH should be carried out. Further, biochemistry may show hyponatremia or hyperkalemia (Napier & Pearce, 2012, p. e629).
Seropositive Rheumatoid Arthritis
Systems to examine. Skeletal system: joints swelling and inflammation, morning stiffness. Immune system: the presence of autoantibodies such as ACPAs and RFs. Cardiovascular system: Raynaud’s phenomenon. Digestive system: anorexia nervosa (Smolen et al., 2016, in press).
Diagnostic tests. Testing tender, swollen, or otherwise suspicious joints (once these are present) by using ultrasound or MRI; serological markers (ACPA- and/or RF-positivity), erythrocyte sedimentation rate, and other markers of systemic inflammation. Because the disease is difficult to detect and differentiate from a number of other illnesses, the procedure of diagnosing may take a long (Smolen et al., 2016, in press).
Acute Hepatitis
Systems to examine. Neurological system: fatigue, anorexia, changes in taste and smell. Integumentary system: skin (color). Digestive system: liver. Immune system: bone marrow suppression.
Diagnostic tests. Testing for hepatitis B includes tests for HBsAg, as well as anti-HBs, anti-HBe, HBeAg, and immunoglobulins IgM and IgG to hepatitis B (Trépo, C., Chan, H. L. Y., & Lok, 2014). Tests for hepatitis C include nucleic acid amplification test for RNA of the virus, as well as IgM and IgG for the virus (Webster, Klenerman, & Dusheiko, 2015).
References
Buttaro, T.M., Trybulski, J., Bailey, P., & Sandburg-Cook, J. (2013). Primary care: A collaborative practice (4th ed.). St. Louis, MO: Elsevier Mosby.
Goroll, A. H., & Mulley, A. G. (2014). Primary care medicine: Office evaluation and management of the adult patient (7th ed.). Beijing, China: Wolters Kluwer.
Napier, C., & Pearce, S. H. S. (2012). Autoimmune Addison’s disease. La Presse Médicale, 41(12), e626-e635. Web.
Smolen, J. S., Aletaha, D., & McInnes, I. B. (2016). Rheumatoid arthritis.The Lancet. Web.
Trépo, C., Chan, H. L. Y., & Lok, A. (2014). Hepatitis B virus infection. The Lancet, 384(9959):2053-2063.
Webster, D. P., Klenerman, P., & Dusheiko, G. M. (2015). Hepatitis C. The Lancet, 385(9973), 1124-1135.
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