DQ Rewrite

Rewrites.docx

W1 DQ-2

Refer to "The Medical H and P" and "How to Create a Differential Diagnosis" videos in this topic. Discuss your observations. What questions did the videos raise for further exploration? Explain what else would you have added to the examination and patient interaction activities.

After watching the videos, I have learned the importance of using the patient history and physical as a basis for selecting relevant diagnostic testing, which leads to a timely and accurate diagnosis. This process protects the patients from the risks of unnecessary testing and is cost-effective. The videos are very helpful in breaking down step-by-step the process for bedside differential diagnosis. The videos also show that it is easy to get lost in certain diagnostics and diagnosis as well as the bias we may develop (Strong 2013). As the healthcare field continues to evolve, it is critical to include patients as active participants in their own healthcare, which begins by listening closely to their concerns through eliciting a comprehensive patient history. The data collected during the history will in turn lead to a focused and skilled physical exam, which will ultimately form the basis for selective testing and an improved diagnostic process (Bickley, Szilagyi, & Bates, 2017). A “differential diagnosis” is distinguishing a condition as the potential cause of a patient’s illness via process of elimination. Because the ultimate diagnosis is unknown at the time of assessment, it’s important for clinicians to consider multiple conditions that may cause similar observable symptoms and follow a process of elimination to rule them out. When a clinician considers differential diagnoses in determining a patient’s condition, they’re using what they know about pathophysiology and applying it with their assessment findings and the patient’s history. Although this process may not arrive at a concrete diagnostic certainty, it’s infinitely useful in narrowing the field of potential choices and zeroing in on needed treatments (Kaiser, 2016).

As Nurse practitioners, it is our role to refine and promote history and physical as a basis for the judicious selection of testing procedures, which will ultimately improve the diagnostic process. The end result will be to offer evidence-based and cost-effective care to patients within a reasonable time frame while also including patients as active participants in their own care.

Reference

Bickley, L., Szilagyi, P., & Bates, B. (2017). Bates guide to physical examination and history-taking (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Kaiser, C. (2016). Differential Diagnoses are Important for Patient Outcome. Retrieved from https://www.jems.com/2016/02/29/differential-diagnoses-are-important-for-patient-outcome/

Strong, E., (2013). How to Create a Differential Diagnosis. Retrieved from https://youtu.be/n48zY7GLqc0

W2DQ1

Select one head, eye, or ear condition or disorder. Summarize/Discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder. Explain why you selected these tests or tools as being appropriate to this process? Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials.

Cogan’s syndrome is a rare autoimmune systemic vasculitis characterized by intraocular inflammation and vestibulo-auditory dysfunction (usually neurosensory deafness, but also tinnitus and vertigo) (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015).

The typical form of Cogan’s syndrome is characterized by: 1. ocular involvement – non-syphilitic interstitial keratitis, sometimes associated with iritis, conjunctivitis or subconjunctival hemorrhage, 2. audiovestibular involvement similar to Meniere’s disease, progressive loss of hearing to the point of deafness within 1-2 months, 3. an interval between the onset of ocular and audiovestibular manifestations of less than 2 years (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015). Cogan’s syndrome is considered atypical if: 1. another type of ocular involvement is present (significant inflammatory eye lesion in addition to or instead of interstitial keratitis: scleritis, episcleritis, retinal artery occlusion, choroiditis, retinal hemorrhages, papilloedema, exophthalmos); cases of conjunctivitis, iritis or subconjunctival hemorrhage without interstitial keratitis are also classified as atypical CS, 2. typical ocular involvement is associated with audiovestibular symptoms that do not resemble Meniere’s disease or arise more than 2 years before or after ocular symptoms (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015).

Cogan syndrome is diagnosed when a doctor observes signs and symptoms consistent with the syndrome (Cogan’s Syndrome, n.d.). If Cogan syndrome is suspected, other diseases that may have similar signs and symptoms must be excluded. These diseases include syphilis, Lyme disease, Epstein-Barr virus, and Meniere disease. Laboratory tests to exclude other diseases may include blood tests, urinalysis, and studies to analyze liver function. In some cases, blood tests for a specific antibody related to Cogan syndrome may be completed. If a diagnosis of Cogan syndrome is suspected, it is suggested that the affected individual see an ophthalmologist and otolaryngologist to determine if there are other symptoms consistent with Cogan syndrome (Bickley, Szilagyi, & Hoffman, 2017).

References

Bickley, L., Szilagyi, P., & Hoffman, R. (2017). Bates guide to physical examination and history taking. Philadelphia: Wolters Kluwer.

Cogan's syndrome. (n.d.). Retrieved from https://rarediseases.info.nih.gov/diseases/1421/cogans-syndrome

Iliescu, D., Timaru, C., Batras, M., De Simone, A., & Stefan, C. (2015). COGAN'S SYNDROME. Romanian journal of ophthalmology, 59(1), 6–13.

W2DQ2

Review Chapters 1 and 2 of Bates' Guide to Physical Examination and History Taking and the condition or disorder you selected in DQ 1.

Imagine a patient comes into your office with your selected condition or disorder. What elements in the patient history and physical exam would indicate the patient has the selected condition or disorder?

The onset of the disease is preceded by an upper respiratory tract infection in approximately 27% of the cases, or, less common, by diarrhea, dental infection or immunization (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015). Usually, the first symptom affects either the eye (41%) or the ear (43%) alone. The interval between the involvement of the two organs varies from 1 month to 11 years (in atypical Cogan’s syndrome); rarely the two organs are affected at the same time (16%). The clinical spectrum of patients with Cogan's syndrome includes ocular manifestations, vestibulo-auditory symptoms and systemic features.

The physical exam should focus on the eye and ENT examinations. It should also search for adenopathies, heart or vessels murmurs, differences in pulse or blood pressure between the right and left sides (Bickley, Szilagyi, & Hoffman, 2017). Signs of systemic involvement should be searched for in a general medical history, as well as questions regarding weight loss, fever, cutaneous anomalies, hyperesthesia, motor weakness, pain or claudication. There is no specific marker to diagnose Cogan’s syndrome, but screening should include ESR, a complete blood count, infectious agents and antibodies. A chest X-ray may not show abnormalities, but an MRI could show high signals in the cochlear and vestibular structures and exclude the presence of an acoustic neurinoma. Ophthalmologic examination reveals ciliary injection with mild iritis and discrete opacities in the deep portion of the corneal stroma, an irregular, granular corneal infiltration, particularly in the posterior part of the cornea, near the limbus (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015). Audiovestibular physical examination can show a degree of ataxia and spontaneous nystagmus. Audiometry demonstrates sensorineural hearing loss affecting all frequencies; the hearing loss is more pronounced at the extreme frequencies, with relatively sparing of the mid-range.

The diagnosis is based on the audiovestibular symptoms, the ocular inflammation and nonreactive serological tests for syphilis, combined with laboratory findings, after eliminating the differential diagnosis (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015). The clinical diagnostic tests in patients with Cogan's syndrome should include audiogram, caloric test, echocardiography, Doppler test, and angiography when systemic vasculitis is suspected. The multisystemic aspect of the syndrome emphasizes the need for communication between ophthalmologist, otolaryngologist and internist.

Select two differential diagnoses that could be applied to this patient. How did you arrive at the two differential diagnoses? Include history and physical examination findings that would support each of the two alternative diagnoses.

There are several diseases that can be evoked as a differential diagnosis for Cogan’s syndrome because of the association of ocular and audiovestibular symptoms: congenital syphilis (an exclusion criterion for Cogan’s syndrome), Susac syndrome (retinocochleocerebral vasculopathy), Vogt-Koyanagi-Harada syndrome, the association of serous otitis and systemic vasculitis with episcleritis described as there is no inner ear involvement (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015) .

Vogt-Koyanagi-Harada syndrome associates audiovestibular involvement with uveitis, alopecia, poliosis and vitiligo (Iliescu, Timaru, Batras, De Simone, & Stefan, 2015). It is an uveoencephalitis with meningitis signs, decreased visual acuity with possible blindness, sensorineural hearing loss and discoloration of hairs (poliosis) or alopecia. Meningism is sometimes present in patients with Cogan’s syndrome, but poliosis and alopecia do not occur. Susac syndrome is caused by lesions of the retinal, cochlear and cerebral arterioles. It manifests as loss of visual acuity, deafness and central neurological disorders.

References

Bickley, L., Szilagyi, P., & Hoffman, R. (2017). Bates guide to physical examination and history taking. Philadelphia: Wolters Kluwer.

Iliescu, D., Timaru, C., Batras, M., De Simone, A., & Stefan, C. (2015). COGAN'S SYNDROME. Romanian journal of ophthalmology, 59(1), 6–13.

W3DQ1

Select one nose, mouth, or neck condition or disorder. Summarize/Discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder.

Explain why you selected these tests or tools as being appropriate to this process? Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials.

Sinusitis, also called rhinosinusitis because the symptoms involve both the nose and the sinuses, affects about one in eight adults annually (American Academy, 2019). For many, the inflammation starts when viruses or bacteria infect your sinuses (often during a cold) and begin to multiply. Part of the body’s reaction to the infection causes the sinus lining to swell, blocking the channels that drain the sinuses. This causes mucus and pus to fill up the nose and sinus cavities. If you have two or more of the symptoms listed below AND/OR thick green or yellow discharge you probably have acute sinusitis, which can last four or more weeks: facial pain/pressure, nasal congestion, cough (in adults), and diminished sense of smell. Symptoms for chronic sinusitis last twelve weeks or longer and can include: facial pain/pressure, facial congestion/fullness, stuffy nose, thick nasal discharge, and possible headache.

A physical exam is best performed after a topical decongestant. On exam, look for facial swelling, erythema, edema (most commonly periorbital), cervical adenopathy, postnasal drainage or pharyngitis (Bickley, Szilagyi, & Hoffman, 2017). Anterior rhinoscopy may reveal mucosal edema, mucous crusting, frank purulence, obstructive polyps or other anatomical defects. Percuss the forehead and cheeks for deep tenderness. Transillumination of the sinuses may be helpful. There are five independent predictors of sinusitis: maxillary dental pain, abnormal sinus transillumination, poor response to nasal decongestants or antihistamines, colored nasal discharge, and mucopurulent seen on examination. The presence of four or more is highly predictive of sinusitis. The overall impression of the examining physician may be more accurate than any single finding.

No laboratory tests are indicated in the emergency department for acute uncomplicated sinusitis because the diagnosis is usually clinical (Battisti & Pangia, 2018). A plain sinus x-ray is most accurate for the maxillary, frontal, or sphenoid disease but is not useful for evaluating the anterior ethmoid cells or the ostiomeatal complex from which most sinus disease originates. Positive findings on plain films are air-fluid levels, sinus opacity, or mucosal thickening of 6 mm or more. Coronal CT at a thickness of 3 mm to 4 mm is the modality of choice. The CT findings suggestive of sinusitis are sinus opacification, air-fluid levels, sinus wall displacement, and 4 mm or greater mucosal thickening. Culture and biopsy are indicated for chronic bacterial and fungal sinusitis.

Reference

American Academy of Otolaryngology–Head and Neck Surgery. (2019). Sinusitis. Retrieved from https://www.enthealth.org/conditions/sinusitis/

Battisti, A., & Pangia, J. (2018). Sinusitis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK470383/

Bickley, L., Szilagyi, P., & Hoffman, R. (2017). Bates guide to physical examination and history taking. Philadelphia: Wolters Kluwer.

W4DQ1

Select one pulmonary, cardiac, peripheral vascular, or lymphatic system condition or disorder. Summarize/Discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder. Explain why you selected these tests or tools as being appropriate to this process? Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials.

Acute pulmonary embolism (APE) is characterized by numerous clinical manifestations which are the result of a complex interplay between different organs; the symptoms are therefore various and part of a complex clinical picture. For this reason, it may not be easy to make an immediate diagnosis. This is a comprehensive review of the literature on all the various clinical pictures in order to help physicians to promptly recognize this clinical condition, remembering that our leading role as cardiologists depends on and is influenced by our knowledge and working methods. Clinical presentation of PE varies from an asymptomatic small pulmonary embolus with low mortality to a massive PE resulting in failure of the right ventricular (RV) with shock, and/or death. Pain can be related to local disturbances in pulmonary circulation, pleural involvement or impairment of coronary circulation. Central PE may produce typical angina also due to RV ischemia; while pleuritic chest pain can be the consequence of pleural irritation due to pulmonary infarction secondary to small distal pulmonary artery (PA) embolization. Dyspnea has a multi-factorial origin, resulting from bronchospasm or vasospasm, disturbances in pulmonary circulation, immobility or diminished respiratory excursion of the diaphragm, atelectasis and/or pulmonary infarction, anoxia, or impairment of cardiac function. In patients with pre-existing heart failure or pulmonary disease, deteriorating dyspnea may be the only symptom indicative of PE. Anoxia is manifested clinically by cyanosis. Hyperbilirubinemia may occur when hepatic congestion co-exists. Dyspnea, chest pain, and cough are the most frequent symptoms of PE, while fever, tachycardia, abnormal pulmonary signs, and peripheral vascular collapse are the most common physical findings. Cyanosis, hemoptysis, syncope, and the various manifestations of acute cor pulmonale are less commonly observed. Physical examination may reveal a calm, mildly symptomatic patient, and an anxious individual in extremis, or anything in between. Unexplained tachycardia suggests the possibility of acute PE. Younger patients may have relative increases in heart rate from baseline but may maintain rates below 100/min. Larger emboli that cause right ventricular dysfunction may cause hypotension. This symptom merits prompt evaluation, as massive PE (PE associated with hemodynamic compromise) may require aggressive measures, such as thrombolytic therapy or pulmonary embolectomy. Tachypnea is common in acute PE, but it may not be present. Chest wall tenderness can occur with acute PE because of pulmonary infarction.

References

Morrone, D., & Morrone, V. (2018). Acute Pulmonary Embolism: Focus on the Clinical Picture. Korean circulation journal, 48(5), 365–381. doi:10.4070/kcj.2017.0314

Tapson, V. (2019). Acute Pulmonary Embolism: Epidemiology, Clinical Manifestations, and Diagnosis. Retrieved from https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-medicine/acute-pulmonary-embolism-epidemiology-clinical-manifestations-and-diagnosis/

W5DQ1

Select one skin, hair, or nail condition or disorder. Summarize and discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder. Explain why you selected these tests or tools as being appropriate to this process. Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials.

Psoriasis is an immune-mediated disease that causes raised, red, scaly patches to appear on the skin.Psoriasis typically affects the outside of the elbows, knees or scalp, though it can appear on any location. Some people report that psoriasis is itchy, burns and stings. Psoriasis is associated with other serious health conditions, such as diabetes, heart disease and depression. While scientists do not know what exactly causes psoriasis, we do know that the immune system and genetics play major roles in its development. Usually, something triggers psoriasis to flare. The skin cells in people with psoriasis grow at an abnormally fast rate, which causes the buildup of psoriasis lesions. Men and women develop psoriasis at equal rates. Psoriasis also occurs in all racial groups, but at varying rates. About 1.9 percent of African-Americans have psoriasis, compared to 3.6 percent of Caucasians. According to current studies, more than 8 million Americans have psoriasis. Psoriasis often develops between the ages of 15 and 35, but it can develop at any age. About 10 to 15 percent of those with psoriasis get it before age 10. Some infants have psoriasis, although this is considered rare. Psoriasis is not contagious. It is not something you can "catch" or that others can catch from you. Psoriasis lesions are not infectious (National Psoriasis Foundation, 2020). Psoriasis is considered an incurable, long-term (chronic) inflammatory skin condition. It has a variable course, periodically improving and worsening. It is not unusual for psoriasis to spontaneously clear for years and stay in remission. Many people note a worsening of their symptoms in the colder winter months. Plaque psoriasis signs and symptoms appear as red or pink small scaly bumps that merge into plaques of raised skin. Plaque psoriasis classically affects skin over the elbows, knees, and scalp and is often itchy. Although any area may be involved, plaque psoriasis tends to be more common at sites of friction, scratching, or abrasion. Sometimes pulling off one of these small dry white flakes of skin causes a tiny blood spot on the skin. This is a special diagnostic sign in psoriasis called the Auspitz sign (Cole, 2019).

There are no special blood tests or tools to diagnose psoriasis. A dermatologist (doctor who specializes in skin diseases) or other health care provider usually examines the affected skin and determines if it is psoriasis. Health care providers may take a piece of the affected skin (a biopsy) and examine it under the microscope. When biopsied, psoriasis skin looks thicker and inflamed when compared to skin with eczema. Provider also will want to learn about your family history. About one-third of people with psoriasis have a family member with the disease (National Psoriasis Foundation, 2020).

Over the last decade, the management of psoriasis has witnessed a paradigm shift. Thanks to the increasing knowledge about the pathogenesis of psoriasis, targeted treatments with monoclonal antibodies have been developed. These antibodies, which target the pathogenic TNF/IL-23/IL-17-pathway, were shown to be safe and efficacious in the management of most patients with moderate to severe chronic plaque psoriasis. Recently, molecular and genetic studies in pustular and erythrodermic psoriasis have identified additional inflammatory pathways, providing evidence that psoriasis is a heterogeneous disease and highlighting the requirement for personalized disease characterization for treatment optimization (Conrad & Gilliet, 2018).

Reference

Cole, G. (2019). Psoriasis. Retrieved from https://www.medicinenet.com/psoriasis/article.htm

Condrad, C, Gilliet, M. (2018). Psoriasis: from Pathogenesis to Targeted Therapies. Retrieved from https://link.springer.com/article/10.1007/s12016-018-8668-1

National Psoriasis Foundation. (2020). About Psoriasis. Retrieved from https://www.psoriasis.org/about-psoriasis

W5DQ2

Review Chapters 1 and 2 of Bates' Guide to Physical Examination and History Taking and the condition or disorder you selected in DQ 1. Imagine a patient comes into your office with your selected condition or disorder. What elements in the patient history and physical exam would indicate the patient has the selected condition or disorder? Select two differential diagnoses that could be applied to this patient. How did you arrive at the two differential diagnoses? Include history and physical examination findings that would support each of the two alternative diagnoses.

Psoriasis usually appears as red or pink plaques of raised, thick, scaly skin. However it can also appear as small flat bumps, or large thick plaques. It most commonly affects the skin on the elbows, knees, and scalp, though it can appear anywhere on the body.

Symptoms of psoriasis may include the following:

· Worsening of a long-term erythematous scaly area

· Sudden onset of many small areas of scaly redness

· Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma

· Family history of similar skin condition

· Pain (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis)

· Pruritus (especially in eruptive, guttate psoriasis)

· Afebrile (except in pustular or erythrodermic psoriasis in which the patient may have high fever)

· Dystrophic nails

· Long-term rash with recent presentation of joint pain

· Joint pain without any visible skin findings

It is now apparent that patients with psoriasis are prone to a variety of other disease conditions, so-called comorbidities. Cardiovascular disease, diabetes, hypertension, inflammatory bowel disease, hyperlipidemia, liver problems, and arthritis are more common in patients with psoriasis. It is very important for all patients with psoriasis to be carefully monitored by their primary care providers for these associated illnesses. Findings on physical examination depend on the type of psoriasis present. The most common skin manifestations are scaling, salmon-colored/erythematous macules, papules, and plaques. Typically, the macules are seen first, and these progress to maculopapules and ultimately well-demarcated, noncoherent, silvery plaques overlying a glossy homogeneous erythema. The area of skin involvement varies with the form of psoriasis (Habashi, 2019).

Lichen planus characterized by violaceous, rectangular, shinypapules and sometimes scales on top of the papules and Wickhamnetwork. Plaque-type lichen resembles psoriasis and differential diagnosis should be done by biopsy and pathological examination. Histopathological signs of psoriasis are parakeratosis, acanthosis, and loss of granular layer, papillomatosis, microabscess, dermal vasculature proliferation and increased mitosis up to 50 fold. Signs of lichen planus are hyperkeratosis, hypergranulosis (wedge-shaped), irregular epidermal hyperplasia (saw tooth appearance), a band like alymphocyte infiltration, Civatte bodies, basal cell degeneration(vacuolar). Both of psoriasis and lichen planus shows Koebnerisation (Tuzun, 2016).

Allergic contact dermatitis generally occurs on the hands. Acute phase signs vesiculets and itching; chronic phase signs resemble psoriasis and dry, itchy erythema and squares. This square doesn’t show candle and Auspitz signs. Erythema is not infiltrating. Ifchronic hand eczema is a disease difficult to diagnose IL-36alpha maybe helpful. Dermoscopy of the hand lesions may be helpful. Whitescales were significant in palmar psoriasis whereas the presence of yellowish scales, brownish-orange dots/globules, and yellowish-orange crusts was significant in chronic hand eczema

Reference

Habashi, J. (2019). Psoriasis clinical presentaion. Retrieved from https://emedicine.medscape.com/article/1943419-clinical

Tuzun, B. (2016). The Differential Diagnosis of Psoriasis Vulgaris. Retrieved from https://www.hilarispublisher.com/open-access/the-differential-diagnosis-of-psoriasis-vulgaris-2376-0427-1000245.pdf

W6DQ1

Select one abdominal condition or disorder. Summarize and discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder. Explain why you selected these tests or tools as being appropriate to this process. Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials.

Celiac disease (CD) is a serious autoimmune disease that occurs in genetically predisposed people where the ingestion of gluten leads to damage in the small intestine. It is estimated to affect 1 in 100 people worldwide. Two and one-half million Americans are undiagnosed and are at risk for long-term health complications. When people with celiac disease eat gluten (a protein found in wheat, rye and barley), their body mounts an immune response that attacks the small intestine. These attacks lead to damage on the villi, small fingerlike projections that line the small intestine, that promote nutrient absorption. When the villi get damaged, nutrients cannot be absorbed properly into the body. Celiac disease is hereditary, meaning that it runs in families. People with a first-degree relative with celiac disease (parent, child, sibling) have a 1 in 10 risk of developing celiac disease. Celiac disease can develop at any age after people start eating foods or medicines that contain gluten. Left untreated, celiac disease can lead to additional serious health problems (Celiac.org, n.d.).

In recent years, there have been significant changes in the diagnosis, pathogenesis, and natural history of CD, with CD undergoing a true ‘metamorphosis’ due to the steady increase in the number of diagnoses identified, even in geriatric patients. This has been mainly attributed to the greater availability of sensitive and specific screening tests, which allow identification of the risk groups for CD and led to a significant raise in diagnoses worldwide. The real cause of the risk in CD diagnoses remains unknown. CD is diagnosed more frequently in women with a female-to-male ratio ranging from 2:1 to 3:1. However, based on serological screening, the actual female-to-male ratio is 1.5:1. The disease can occur at any age from early childhood to the elderly, with two peaks of onset – one shortly after weaning with gluten in the first 2 years of life, and the other in the second or third decades of life. The diagnosis of CD can be challenging since symptoms can vary significantly from patient to patient.

The gold standard for CD diagnosis is represented by the combination of mucosal changes detected by duodenal biopsy and by positivity of serological tests (anti-tTG antibodies, anti-endomysium antibodies (EmA), and deamidated gliadin peptide (DGP) antibodies). Despite the progress made in serology, no antibody test currently available provides a sensitivity and specificity of 100% (Table 3), thus requiring intestinal biopsy as a key adjunct for establishing a correct diagnosis. Current standard of care is based on the “four out of five rule”, which indicates that four out of five of the following criteria are enough to establish CD diagnosis: (1) typical signs and symptoms (diarrhea and malabsorption); (2) antibody positivity; (3) HLA-DQ2 and/or HLA-DQ8 positivity; (4) intestinal damage (i.e., villous atrophy and minor lesions); and (5) clinical response to gluten free diet (GFD). Additionally, this rule helps providers to identify the various subtypes of CD, i.e., seronegative CD (absence of point 2), potential CD (absence of point 4), non-classic CD (absence of point 1), and non-responsive CD (absence of point 5). Routine blood tests can lead to suspect CD. Low serum levels of hemoglobin, albumin, calcium, potassium, magnesium, and phosphorus are more commonly detected in CD with a classic rather than non-classic phenotype. Most patients develop an iron deficiency microcytic anemia with low ferritin values. Routine blood tests can lead to suspect CD. Low serum levels of hemoglobin, albumin, calcium, potassium, magnesium, and phosphorus are more commonly detected in CD with a classic rather than non-classic phenotype. Most patients develop an iron deficiency microcytic anemia with low ferritin values. Currently, the serological diagnosis of CD is based on tests that are highly predictive and widely validated, including EmA, anti-tTG, and DGP (Caio et al., 2019). Strict compliance with a GFD in most CD patients leads to the disappearance or significant decrease of antibodies within 12 months (18–24 months if the antibody titer is very high) together with regrowth of the intestinal villi. IgA anti-tTG antibodies are the most commonly used test to monitor CD patients during follow-up, although their disappearance does not reflect the regrowth of intestinal villi (Choung et al., 2015).

Reference

Caio, G., Volta, U., Sapone, A., Leffler, D., De Giorgio, R., Catassi C., Fasano, A. (2019). Celiac disease: a comprehensive current review. Retrieved from https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-019-1380-z?utm_campaign=BMCF_TrendMD_2019_BMCMedicine&utm_source=TrendMD&utm_medium=cpc

Celiac.org. (n.d.). What is Celiac disease. Retrieved from https://celiac.org/about-celiac-disease/what-is-celiac-disease/

Choung R., Ditah I., Nadeau A., Rubio-Tapia, A., Marietta, E., Brantner, T., Camilleri, M., Rajkumar, V., landgren, O., Everhart, J., Murray, J. (2015). Trends and racial/ethnic disparities in gluten-sensitive problems in the United States: findings from the National Health and nutrition examination surveys from 1988 to 2012. Am J Gastroenterol. 2015;110:455–61.

W6DQ2

A 40-year-old female presents with two years history of excessive hair fall and flatulence with recent worsening of her symptoms. Additional history revealed weight loss of 10kg in the last two years and occasional episodes of diarrhea without blood or mucous. The clinical examination revealed thin, pale and ill-looking patient with sunken eyes, scanty hair, angular stomatitis. . On laboratory investigation, she was found to be anemic. Upper GI endoscopy showed loss of kerckring folds in the descending duodenum and the histopathology revealed complete villous atrophy. The serology markers were positive for antigliadin, antireticuline and anti-endomysial antibodies. Based on the above findings, the diagnosis of celiac disease was strongly suspected and the patient was managed with gluten- free diet, vitamin and minerals. She responded nicely and all her symptoms and signs improved and she had 35kg gain. Repeated duodenal biopsy after one year of the treatment showed normal villous pattern. Classic symptoms of Celiac disease include chronic diarrhea, weight loss, and failure to thrive, which are quite rare. The more common, non-classical symptoms include iron deficiency, bloating, constipation, chronic fatigue, headache, abdominal pain, and osteoporosis (Lebwohl, Sanders & Green2018).

Two differential diagnoses include nonceliac gluten sensitivity and Crohn disease. Nonceliac gluten sensitivity may share similar symptoms with celiac disease, with improvement on a gluten-free diet. There should not be any villous atrophy. Tissue transglutaminase serology remains normal. CBC and iron levels also remain normal, because the condition does not induce malabsorption. Small intestinal histology is normal. There is improvement of symptoms after 6 weeks (or less) on the gluten-free diet and recurrence with reintroduction of gluten. Crohn disease can affect any part of the gastrointestinal tract, and symptoms may be extremely variable. The classic findings on histologic examination include granulomas, ulcerations, and acute and chronic inflammation often extending throughout all layers of bowel wall. Tissue transglutaminase serology is usually negative and there should be no response to gluten withdrawal (Epocrates, 2020).

Despite the increase in the prevalence of coeliac disease and improved recognition and rates of diagnosis, numerous avenues of investigation are necessary to better understand the pathogenesis and improve the treatment of patients with this condition. Advances in the pathophysiology of celiac disease could enable preventive strategies in individuals at high risk for disease development. The development of non-dietary therapies might alleviate symptoms among patients with celiac disease and inadvertent gluten exposure, and an effective replacement of the gluten-free diet could greatly enhance the quality of life of those many patients who find adhering to the diet challenging. Technologies for the detection of gluten in food and to monitor for recent gluten exposure (such as the detection of gluten peptides in stool or urine) could enhance the design of future clinical trials and might be of major value in patients' daily activities (Lebwohl, Sanders & Green, 2018).

References

Epocrates. (2020). Celiac disease. Retrieved From https://online.epocrates.com/diseases/63635/Celiac-disease/Differential-Diagnosis

Lebwohl, B., Sanders, D., Green, P. (2018). Coeliac disease. Retrieved from https://www.sciencedirect.com/science/article/pii/S0140673617317968

W7DQ1

You have reached the midpoint of the course. Provide a reflective analysis of the content and your learning thus far that addresses the following:

1. With which topic(s) do you find yourself struggling? Why do you think this is so? What element(s) are problematic to your comprehension?

2. What topic(s) come easiest to you? How can you apply your successful learning strategies in these areas to those content areas with which you are struggling?

I consider myself a very cautious person and nurse, and that is from charting to assessments, to medication administration to giving report. I really care about doing things the right way and not cutting corners, even if that means taking more time and getting behind. However, despite my passion for thoroughness, I still find myself missing things. Even with a checklist I made to prevent myself from forgetting something, it still seems like there is always something I miss when doing my respiratory and cardiac assessment in a nurse practitioner level. I'm having a hard time remembering every little detail to look for in each system. In my experience as a nurse, there's no substitute for real experience. Even practicing on family didn't help because it didn't even come close to mimicking the environment of a hospital. I know over time, I will get used to it. I just need to develop a pattern that works for me.

To be honest, nothing is easy in this class. But breaking every topic into categories makes it easier for us students to understand. I am a detailed oriented person and I find it easier to break my assessment down into categories and not individual tasks. At work, I use a brain sheet on every patient to help me organize my thoughts and to avoid missing tasks. By always using the same technique, it became much easier. As a student, it is important that I acquire a deep understanding of the relevance of a thorough assessment to recognize a potential problem.

W7DQ2

Using the information from the first discussion question in this topic, provide a proposed action plan for the remainder of the course that details the steps you will take to assist you in mastering the content you have identified as difficult by course end. Provide one to two references that support your proposed action plan rationale and methodology.

To assist me in mastering the content I am struggling with, I will utilize the Bates visual guides to physical examination more often. I have found that these videos are really helpful when I practice my assessment skills with my husband. Bates’ Guide to Physical Examination and History Taking provides authoritative, step-by-step guidance on performing the patient interview and physical examination, applying clinical reasoning, shared decision-making, and other core assessment skills all based on a firm understanding of clinical evidence. It helps us students perform an accurate, efficient, and effective physical examination with confidence (Wolters Kluwer Health, 2020). Abdominal and cardiac auscultation is an important clinical skill used by health care professionals during bedside patient evaluation and management. I have found online health assessment videos that help me develop foundational skills and knowledge. To help me with my abdominal and cardiac assessment, I will watch video vignettes employing narration, animation, heart sounds, and abdominal sounds which are being used in combination to introduce and compare the normal from abnormal sounds. I will utilize a cheat sheet to guide me when I do my physical assessment. I will also practice on every single patient I have to help build my confidence. Physical examination is a valuable diagnostic tool; there are many diagnoses that can only be made by physical examination. The information one gathers may not replace the need for testing, but having firm hypotheses in place allows the provider to order tests more judiciously and ask better questions of those tests. This, in turn, has the potential to reduce risk to the patient and save cost for the health care system. Furthermore, physical examination plays a critical role in the therapeutic patient-provider relationship (Talwalker, n.d.)

Reference

Talwalker, J. 9n.d.). general approach to physical exam. Retrieved from https://www.jove.com/science-education/10043/general-approach-to-the-physical-exam

Wolters Kluwer Health. (2020). Bates’ visual guide to physical examination. Retrieved from https://batesvisualguide.com/index.aspx

W8DQ1

Select one musculoskeletal system or extremity condition or disorder. Summarize and discuss the clinical characteristics and identify the appropriate laboratory, imaging, and other diagnostic and screening tools that apply to this condition or disorder. Why did you select these tests or tools as being appropriate to this scenario? Support your summary and recommended plan with a minimum of two peer-reviewed references in addition to the course materials. You may not select a condition or disorder that has already been profiled by another student; you must select a different one.

Bursitis is a swelling or inflammation of a bursa, which is a synovium-lined, sac-like structure found throughout the body near bony prominences and between bones, muscles, tendons, and ligaments. There are over 150 known bursae in the human body, and their function is to facilitate movement in the musculoskeletal system, creating a cushion between tissues that move against one another. When bursitis occurs, the bursa enlarges with fluid, and any movement against or direct pressure upon the bursa will precipitate pain for the patient. There are many causes of bursitis, including overuse injury, infectious disease, trauma, and inflammatory disorders. The name bursitis itself is often a misnomer, as not all forms of bursitis are due to a primary inflammatory process but are rather a swelling of the bursa due to a noxious stimulus (Williams & Sternard, 2019). Bursitis and tendinitis can affect people of any age, though the risk increases as people get older and tendons become less flexible. Some conditions, such as rheumatoid arthritis and diabetes, increase the risk of bursitis and tendinitis because they weaken soft tissue and make bursae and tendons more susceptible to irritation and inflammation (Todd, 2020).

Two forms of bursitis exist, chronic and acute, and the presentations of each will manifest differently from one another. A detailed medical history, as well as an understanding of the patient's daily routine, will help the clinician differentiate the 2 types of bursitis from each other and from other diagnoses. Acute bursitis typically arises from trauma, infection, or crystalline joint disease, while chronic bursitis is more likely the result of inflammatory arthropathies and repetitive pressure/overuse, or "microtraumas." In acute bursitis, patients generally present with pain on palpation of the bursa. The range of motion of the involved joint may be decreased secondary to pain. Contrary to the physical exam findings in acute bursitis, chronic bursitis is often painless. The bursa itself has had time to expand to accommodate the increased fluid, and the result is significant swelling and thickening of the bursa. An examination of the skin is very important in the evaluation of acute or chronic bursitis. The skin should be evaluated for trauma, erythema, and warmth. One study found that a temperature increase of just 2.2 degrees centigrade between the skin overlying the affected bursa compared to that overlying the unaffected, contralateral bursa was highly sensitive and specific for septic bursitis (William & Sternard, 2019).

MRI can be used to evaluate the deeper bursa, as can ultrasound which has the added benefit of showing real-time images within a joint or area surrounding the bursa and can be used to observe changes with active and passive movement.

Ultrasound is particularly helpful for visualizing cobblestoning of the fat overlying a bursa, which can help differentiate cellulitis from infectious bursitis. Color Doppler can likewise be used to show signs of infection, such as hyperemia of the bursa and the surrounding tissues.

Aspiration of the inflamed bursa can be helpful when there is a question of septic bursitis or bursitis secondary to crystalline disease. Aspirated fluid should be sent for cell count, Gram stain and culture, glucose, and analysis for crystals (William & Sternard, 2019).

Reference

Tood, D. (2020). Bursitis: An overview of clinical manifestations, diagnosis, and management. Retrieved from https://www.uptodate.com/contents/bursitis-an-overview-of-clinical-manifestations-diagnosis-and-management/print

Williams, C., Sternard, B. (2019). Bursitis. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513340/

W8DQ2

A 47 year old female patient presents to the clinic with a 12 week history of intermittent right sided hip pain. The episodes have become more frequent and her symptoms have increased in the two weeks prior to attending the clinic. Normally she jogs three times a week and also attends the gym twice a week, doing a mix of cardio and strengthening work. She complains of a deep aching or burning pain over the outer surface of her right hip radiating down the outer surface of the thigh above the knee. The pain gets worse by direct contact or increased activity. The pain was often more intense lying on the affected side (her preferred sleeping position). Her job required her to walk up and down several flights of stairs between classrooms and also stand for long periods at the front of the classroom. She was examined the symptoms were reproduced by palpating the right sided greater trochanter (the outer surface of the upper thigh). This is regarded as a classic physical finding. No swelling was evident in her case but the muscles immediate to the area had increased in tone. A number of orthopaedic tests were conducted to exclude other possible causes of hip pain. She was diagnosed with hip bursitis (specifically the trochanteric bursa).

Two differential diagnoses include: Osteoarthritis of the hip and and osteonecrosis of the hip. Osteoarthritis of the hip may be confused with subtrochanteric bursitis. Osteoarthritis of the hip presents with hip pain or stiffness in the groin and hip region on most days of the preceding month, often a loss of internal rotation initially. X-ray will show femoral or acetabular osteophytes and/or axial joint space narrowing. Osteonecrosis of the hip may also be confused with subtrochanteric bursitis. It also presents hip pain and/or stiffness in the groin and hip region. X-ray can demonstrate advanced stages of osteonecrosis characterized by sclerosis, lucency, and flattening of the femoral head. MRI will show subchondral lesions of variable signal intensity outlined by a low-signal rim on T1-weighted images along the anterosuperior aspect of the femoral head. A more specific sign is the double-line sign (an outer low-intensity rim and an inner high-intensity band) on T2-weighted images (Epocrates, 2020).

Bursitis is not a fatal disorder and most patients have a good outcome. The vast majority are managed as outpatients. However, patients who do not avoid the trigger or continue with the same activity tend to develop recurrences. Bursitis is very common in clinical practice. Once the diagnosis is made, the treatment in most cases is supportive. Most cases of non-infectious bursitis resolve on their own in a few weeks. However, if the fluid is infected, a consult should be obtained from the infectious disease specialist and orthopedic surgeon. After treatment, to restore functionality some patients may benefit from physical therapy. Patients should be educated to refrain from the same activities that triggered bursitis (Williams & Sternard, 2019)

Reference

Epocrates. (2020) Bursitis. Retrieved from https://online.epocrates.com/diseases/52335/Bursitis/Differential-Diagnosis

Williams, C., Sternard, B. (2019). Bursitis. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK513340/