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Testicular cancer

Pathology – Testicular cancer is a heterogeneous disease that occurs during or after puberty (Pyle & Nathanson, 2016). Most testicular cancers are germ cell tumors from the sperm and can be classified into two subtypes: seminomas, which are the most common, and nonseminomas, the more aggressive type.

Etiology – The cause of testicular cancer is unknown, but incidences are higher by genetics, typically, among close male relatives. It is the most common malignancy affecting males between the ages of 15-35.

Risk factors – Non-modifiable risk factors include gender, ages 15-35, family history, and genetic disorders including Klinefelter syndrome and Down syndrome (Pyle & Nathanson, 2016). Cancers can be caused by changes in chromosomes that turn off tumor suppressor genes which slow down cell division or turn on oncogenes which help cells grow and divide. Most testicular cancer cells have extra copies of a part of chromosome 12 which may be a contributing factor (Pyle & Nathanson, 2016). Men with a history of cryptorchidism and prior orchiopexy are also at increased risk. Some studies show a mild association between risk of testicular cancer and high intake of saturated fat, dietary cholesterol, and dairy products. Additionally, regular use of marijuana may increase the risk about twofold.

Signs/symptoms – Testicular tumors typically present as a nodule or swelling of one testicle that is typically painless. Male patients will report a dull ache or a heavy sensation in the lower abdomen, perianal area, or scrotum (Bjelaković et al., 2020). If it is metastatic, symptoms may vary depending on the site including neck mass, cough, or dyspnea related to pulmonary metastasis, anorexia, nausea, vomiting, and/or bone pain. Additionally, gynecomastia may occur due to a systemic endocrine manifestation of testicular germ cell tumors (Bjelaković et al., 2020). A testicular examination is essential as abnormalities of firm, hard, or fixed areas within the tunica albuginea should be considered suspicious. Testicular tumors are ovoid and may spread to the epididymis or spermatic cord.

Diagnostics – A physical examination is essential, in which both testicles should be examined and compared for size, tenderness, symmetry, and presence of nodules. A scrotal ultrasound is the gold standard for diagnosis, which is a rapid and reliable technique for suspected testicular tumor, as well as, to exclude hydrocele or epididymitis (Bjelaković et al., 2020). Radiographic testing and serum tumor markers, such as beta-human chorionic gonadotropin and alpha-fetoprotein, are helpful to determine the histologic type and extent of the disease. A CT is recommended if the metastatic disease involves the chest/peritoneum.

Treatment – Regardless of staging, radical orchiectomy is done initially. If cancer has spread, treatments including radiation or chemo should be considered.


Bjelaković, M. D., Vlajković, S., Bjelaković, G., & Antić, M. (2020). Testicular cancer stem cell hypothesis – diagnostic and therapeutic implications. Vojnosanitetski Pregled: Military Medical & Pharmaceutical Journal of Serbia, 77(11), 1210–1215. https://doi.org/10.2298/VSP170821197D

Pyle, L. C., & Nathanson, K. L. (2016). Genetic changes associated with testicular cancer susceptibility. Seminars in Oncology, 43(5), 575–581. https://doi.org/10.1053/j.seminoncol.2016.08.004


Acute Myeloid Leukemia (AML)

Acute myeloid leukemia the most common form of cancer in adults. As mentioned by (Tamamyan et al., 2017), the average age at diagnosis is 70. The disease is seen as more common in males than females, and prevalence is higher in withes than blacks. Treatment of the disease has progressed significantly. This was confirmed by (Tamamyan et al., 2017) wherein they mentioned that back in 1964, long-term survival was less than 5% and currently is nearing 30–40%.

Etiology: According to (Domino, 2020) the exact cause remains unknown, but there are many risk factors in developing the disease.

Modifiable and Nonmodifiable risk factors: There are many predisposing risk factors. Some may be adjustable such as environmental and lifestyle factors. Unfortunately, some are nonmodifiable such as genetic and blood disorders. As mentioned by (Tamamyan et al., 2017), the risk factors are genetic factors: Down’s syndrome and Klinefelter syndrome. Environmental factors and lifestyle: smoking alcohol use, tobacco use, and pesticide exposure. Drugs: Alkylating agents, chloramphenicol, and chloroquine. Antecedent blood disorders: myelodysplastic syndrome, aplastic anemia, and polycythemia vera. As stated by (Tamamyan et al., 2017), there is a noteworthy connection between tobacco smoking and AML.

Pathology: AML is a diversified and complex disease. (Tamamyan et al., 2017) explain the characteristics as a proliferation of immature, abnormal blast cells and impaired production of normal blood cells that are out of control. (Domino, 2020) add that these cells are unable to advance into more mature elements. This, in turn, progresses to bone marrow failure.

Pertinent signs and symptoms: The signs and symptomatology are not specific to the disease, but further workup will pinpoint towards the diagnosis. According to (Tamamyan et al., 2017), clinical manifestation is mainly related to pancytopenia and blast proliferation. A list of common signs and symptoms would include generalized weakness, fatigue, fever, easy bruising, bleeding, organomegaly (hepatomegaly and splenomegaly), and lymphadenopathy, dizziness, blurred vision, headache, and infections with difficulty clearing the same.

Diagnostics: The diagnosis process per (Tamamyan et al., 2017) is primarily dependent on bone marrow aspiration with the identification of 20% or more myeloid blasts in the bone marrow and/or peripheral blood. Initial testing, according to (Domino, 2020) would include a CBC that would identify abnormal RBCs, neutrophils, and platelets, ESR, LDH, and uric acid, which may be elevated. COAG’s profile may be normal, but in DIC will be prolonged. Imaging of the abdomen, such as ultrasound or CT scan, may elicit organomegaly. Confirmation of the disease is performed through bone marrow aspiration and biopsy. In agreement with (Domino, 2020) confirmations studies will show hypercellular bone marrow with effaced architecture and a blast count of 20% or more.

Treatment regimens to include both pharmacological and non-pharmacological: An oncologist will guide appropriate management of the disease. (Domino, 2020) asserts that the basis of the treatment is chemotherapy. (Ferri, 2021) summarizes the treatment by mentioning that immediate therapy will be offered to those presenting with Acute Promyelocytic Leukemia (APML) to correct metabolic, infectious, or hyperleukocytosis emergencies. Those without APML will begin with induction therapy to gain remission, defined as a blast count of <5% in the bone marrow, absolute neutrophil count of >1000/mcl, platelet count >100,000/mcl, and transfusion freedom. Consolidation therapies consist of intensive chemotherapy or stem cell transplantation with the intent to prevent relapses. Non-pharmacological management would include bone marrow transplantation. This is intended for high-risk patients, and as previously mentioned, stem cell transplantation to prevent relapses.

Nutritional approaches: As acknowledged by (Stauder et al., 2020), when patients with oncologic disease have co-existing malnutrition, the prognosis is poor, as it negatively affects their quality of life. The treatment plan may require modification which often leads to poor treatment outcomes and increased adverse events. With this said, (Domino, 2020) advises that each patient must maintain a balanced diet with adequate calorie and vitamin intake. If needs be, the patient may be started on total parenteral nutrition for aggressive support.


Domino, F. J. (2020). The 5-minute clinical consult (R. A. Baldor, J. Golding, & M. B. Stephens, Eds.; 28th ed.). Wolters Kluwer.

Ferri, F. F. (2021). Ferri’s clinical advisor 2021: 5 books in 1 (1st ed.). Elsevier.

Stauder, R., Augschoell, J., Hamaker, M. E., & Koinig, K. A. (2020). Malnutrition in older patients with hematological malignancies at initial diagnosis – association with impairments in health status, systemic inflammation and adverse outcome. HemaSphere4(1), e332. Retrieved May 12, 2021, from  https://doi.org/10.1097/hs9.0000000000000332

Tamamyan, G., Kadia, T., Ravandi, F., Borthakur, G., Cortes, J., Jabbour, E., Daver, N., Ohanian, M., Kantarjian, H., & Konopleva, M. (2017). Frontline treatment of acute myeloid leukemia in adults. Critical Reviews in Oncology/Hematology110, 20–34. Retrieved May 12, 2021, from  https://doi.org/10.1016/j.critrevonc.2016.12.004


Ovarian cancer (OC) is one of the most common gynecologic cancers that rank 7th among women and has a worse prognosis and highest mortality rate caused by being asymptomatic and secret growth of the tumor, delayed onset of symptoms, and lack of proper screening that results in its diagnosis in advanced stages. Most tumors appear to originate from other gynecological tissues and involve the ovary secondarily and low- and high-grade tumors arising from fallopian tube epithelium and other endometrioid tumors are genetically mutated and aggressive and differ histopathological and molecular subtype (Reid, Permuth, & Sellers, 2017). The majority of OC has an epithelial origin which is more invasive, and others have a non-epithelial origin which is less invasive, and epithelial OC may be mucinous and non-mucinous, non-mucinous are serous, endometrioid and clear cell and unspecified types (Momenimovahed, Tiznobaik, Taheri, & Salehiniya, 2019).

The non-modifiable risk factors are increasing age, locality such as European and Asian countries such as China, India, Singapore, Kazakhstan, and Brunei and in USA & Africa. Other non-modifying risk factors were pelvic inflammatory diseases, chlamydia trachomatis infection of GU tract, endometriosis, and tube ligation led to the upward trend of OC, family history of OC, BRCA mutations, Lynch syndrome (Momenimovahed, Tiznobaik, Taheri, & Salehiniya, 2019). The modifying risk factors were urban life, decreased pregnancy, duration of lactation, oral contraceptive pills, hormone replacement therapy, infertility treatments have a beneficial effect on ovarian cancer, consumption of high cholesterol diet with fewer vegetables, obesity and less physical activity, alcohol caffeine and cigarettes, reduced lactation and low income and low literacy all contributed to risk of OC.

According to Freij et al, (2018), the three highest known symptoms of OC recognized were extreme fatigue, back pain, and persistent pain in the pelvic area. Other general symptoms can be fever, loss of appetite, weight loss, nausea and vomiting, anemia, neutropenia, constipation, urinary frequency, and abdominal distension. Diagnosis of OC is by signs and symptoms and through detection of tumor markers such as CA125 and HE4, PRSS8, FOLR1, KLK6/7, GSTT1, and mi RNAs, and through trans vaginal ultrasonography, CT of abdomen pelvis and MRI, and tissue biopsy with histopathologic studies (Giampaolino et al, 2019). In my history taking going through risk factors, family history and symptoms and clinical examination will guide for my diagnostic tests in the patient. Once there the diagnosis made, a referral to a hematologist, oncologist surgery, and another rehabilitation team will be needed.

Frontline chemotherapy for endometrial OC is a combination of intravenous paclitaxel and carboplatin administered every 3 weeks has remained the standard of care and other alternative therapy intraperitoneal administration of chemotherapy and use of other antiangiogenic agent’s bevacizumab (Marth, Reimer, & Zeimet, 2017), immunotherapy, hormone therapy. Other non-pharmacological treatments are surgical removal of the tumor in combination with radiation and/or with chemotherapy along with nutritional therapy and another form of therapy like holistic healing. Correcting nutritional deficiency is an important part of the therapy to replenish electrolytes, protein, and vitamins and through enteral feeding tubes or TPN. Malnutrition leads to low-performance status, impaired quality of life, unplanned hospital admissions and reduced survival and hence oncologist and clinical nutritionist needs to plan the nutrition therapy and interventions for the success of the cancer therapy (Cotogni et al, 2019)


Momenimovahed, Z., Tiznobaik, A., Taheri, S., & Salehiniya, H. (2019). Ovarian cancer in the world: epidemiology and risk factors. International journal of women’s health11, 287. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6500433/

Reid, B. M., Permuth, J. B., & Sellers, T. A. (2017). Epidemiology of ovarian cancer: A review. Cancer biology & medicine14(1), 9. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5365187/

Giampaolino, P., Della Corte, L., Foreste, V., Vitale, S. G., Chiofalo, B., Cianci, S., … & Bifulco, G. (2019). Unraveling a difficult diagnosis: the tricks for early recognition of ovarian cancer. Minerva medica110(4), 279-291. Retrieved from https://europepmc.org/article/med/31081307

Marth, C., Reimer, D., & Zeimet, A. G. (2017). Front-line therapy of advanced epithelial ovarian cancer: standard treatment. Annals of oncology28, viii36-viii39. Retrieved from https://www.sciencedirect.com/science/article/pii/S0923753420346615

Freij, M., Al Qadire, M., Khadra, M., ALBashtawy, M., Tuqan, W., Al Faqih, M., … & Abd El-Razek, A. (2018). Awareness and knowledge of ovarian cancer symptoms and risk factors: A survey of Jordanian women. Clinical nursing research27(7), 826-840. Retrieved from https://journals.sagepub.com/doi/abs/10.1177/1054773817704749

Cotogni, P., Pedrazzoli, P., De Waele, E., Aprile, G., Farina, G., Stragliotto, S., … & Caccialanza, R. (2019). Nutritional therapy in cancer patients receiving chemoradiotherapy: Should we need stronger recommendations to act for improving outcomes?. Journal of Cancer10(18), 4318. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691712/



Pathology – Bronchiectasis is a chronic condition where the bronchi are thickened and scarred, and the injury of the airway prevents the clearing of the mucus. It can affect a section of the lungs or several areas of both lungs. Individuals with bronchiectasis may have exacerbations, and over time affects airway exchange leading to respiratory failure, atelectasis, and lung infections (Börekçi & Müsellim, 2021).

Etiology – Bronchiectasis can be congenital or acquired including childhood infections, such as whooping cough or measles. Though, it increases with age and is typically due to infections, airway obstruction, cystic fibrosis (CF), systemic diseases, allergic bronchopulmonary aspergillosis, connective tissue diseases, and/or pulmonary infections (Börekçi & Müsellim, 2021). Airway blockage of a tumor or an inhaled object may also lead to bronchiectasis.

Risk factors – Individuals with medical conditions, such as cystic fibrosis, immunodeficiency disorders, COPD, and asthma at increased risk for bronchiectasis (Choi et al., 2021). Repeated infections including COVID, pneumonia, tuberculosis, also increase risks; therefore, individuals should limit exposure. COPD patients should decrease exposure to infections and smoking to prevent exacerbations, which may worsen pulmonary function and accelerate the progression of disease (Choi et al., 2021).

Signs/symptoms – The classic clinical manifestation of bronchiectasis include cough with the production of mucopurulent and tenacious sputum that lasts months to years. Patients may also report dyspnea, pleuritic chest pain, and rhinosinusitis (Börekçi & Müsellim, 2021). Clinical findings include crackles, wheezing, and clubbing.

Diagnostics – Patients with persistent or recurrent production of purulent sputum should be suspected of bronchiectasis. Lab tests including CBC, immunoglobulin quantitation, sputum smear/culture, and rheumatoid factor can help identify the underlying cause that resulted in bronchiectasis. A chest radiograph may identify dilated and thickened airways, but a CT scan of the chest is the preferred imaging modality (Choi et al., 2021). Clinical features of bronchiectasis on CT include airway dilation which is detected as parallel lines or end-on ring shadows, bronchial wall thickening, mucus plugs, and cysts of the bronchial wall.

Treatment – Childhood vaccines for whooping cough and measles can prevent infections and reduce complications. Patients with COPD, asthma, and other respiratory conditions should avoid fumes, smoke, and other harmful substances.


Börekçi, Ş., & Müsellim, B. (2021). Decreasing rate of unknown bronchiectasis etiology: Evaluation of 319 adult patients with bronchiectasis. Turkish Thoracic Journal, 22(1), 18–23. https://doi.org/10.5152/TurkThoracJ.2021.19142

Choi, H., Yang, B., Kim, Y. J., Sin, S., Jo, Y. S., Kim, Y., Park, H. Y., Ra, S. W., Oh, Y.-M., Chung, S. J., Yeo, Y., Park, D. W., Park, T. S., Moon, J.-Y., Kim, S.-H., Kim, T.-H., Yoon, H. J., Sohn, J. W., & Lee, H. (2021). Increased mortality in patients with non-cystic fibrosis bronchiectasis with respiratory comorbidities. Scientific Reports, 11(1), 1–9. https://doi.org/10.1038/s41598-021-86407-8




The inflammation produced with TB infection is granulomatous, with epithelioid macrophages and Langhans giant cells along with lymphocytes, plasma cells, maybe a few polymorphonuclear leucocytes, fibroblasts with collagen, and characteristic caseous necrosis in the center. The inflammatory response is mediated by a type IV hypersensitivity reaction (Agyeman & Ofori-Asenso, 2017).


The association between poverty and TB is well-recognized, and the highest rates of TB were found in the poorest section of the community. TB occurs more frequently among low-income people living in overcrowded areas and persons with little schooling. Poverty may result in poor nutrition which may be associated with alterations in immune function. On the other hand, poverty resulting in overcrowded living conditions, poor ventilation, and poor hygiene-habits is likely to increase the risk of transmission of TB (Loddenkemper, Lipman, & Zumla, 2016).

Risk Factors

Specific risk factors include having lived in Asia, Latin America, Eastern Europe, or Africa for years; exposure to someone with infectious tuberculosis; residence in an institutional setting and homelessness. HIV infection Increases the risk for both progression to primary disease and reactivation of latent disease. In addition, active TB has been found to increase HIV viral loads (Loddenkemper, Lipman, & Zumla, 2016).

Signs and Symptoms

Cough for 2-3 weeks initially dry then later productive. Studies found that 50% of patients had cough over 2 weeks. Fever is usually low-grade and is less common in older population. Weight loss may be seen in patients with other suggestive symptoms (Agyeman & Ofori-Asenso, 2017). Malaise may be noticed in hindsight after treatment. Hemoptysis is present in <10% of patients typically with advanced disease. May be the result of sequelae such as bronchiectasis and is not represent in active disease (Loddenkemper, Lipman, & Zumla, 2016).


The possibility of TB should be considered in any person with risk factors for TB exposure, who has suggestive symptoms such as fever, malaise, pleuritic chest pain, cough longer than 2-3 weeks, night sweats, and weight loss, hemoptysis, psychological symptoms, clubbing, erythema nodosum or chest x-ray abnormalities (Loddenkemper, Lipman, & Zumla, 2016). Investigations for active infection include chest x-ray, 3 sputum samples obtained for acid-fast bacilli (AFB), nucleic acid amplification testing (NAAT), complete blood count, and electrolytes. Stained smears should be made from sputum specimens to identify AFB, as this is the first bacteriologic evidence of infection and gives an estimate of how infectious the patient is (Loddenkemper, Lipman, & Zumla, 2016). Sputum culture supports the diagnosis of TB, is more sensitive and specific than smear staining, facilitates identification of the mycobacterium species by nucleic acid hybridization or amplification, and evaluates drug sensitivity (Agyeman & Ofori-Asenso, 2017). CT of the chest, although not done routinely, may be of use to exclude other pathology for example cancer. It is recommended that all patients who have TB should be tested for HIV within 2 months of diagnosis. Investigations for latent infection in a person exposed to M. tuberculosis but without signs of active TB are based on the tuberculin skin test (TST) or interferon gamma release assays (IGRAs). The TST and IGRA measure the response of T-cells to TB antigens (Agyeman & Ofori-Asenso, 2017).


Treatment is initiated when TB is confirmed or strongly suspected and consists of an initial intensive phase and a subsequent continuation phase. The main goals are to cure the patient and to prevent further transmission of TB to others (Agyeman & Ofori-Asenso, 2017). Therapy for TB requires a minimum of 6 months of treatment except for culture-negative pulmonary TB. To reduce noncompliance rates, therapy can be given by a healthcare professional in conjunction with a local public health authority as DOT (Loddenkemper, Lipman, & Zumla, 2016). DOT can be given 5 days per week, or two or three times weekly, depending on the regimen and phase of treatment. Initial intensive phase treatment involves the preferred drugs of isoniazid, rifampin, pyrazinamide, and ethambutol, and lasts 8 weeks. Ethambutol may be discontinued immediately if the Mycobacterium tuberculosis isolate is sensitive to isoniazid and rifampin. If M. tuberculosis is sensitive to isoniazid and rifampin, in the continuation phase isoniazid and rifampin are given for 18 weeks, 26 weeks of total treatment (Agyeman & Ofori-Asenso, 2017).

Nutritional Approach

Reduced micronutrient intake, and especially intake of vitamins and minerals such as vitamins A, E, and C, zinc, and selenium, has been associated with an impaired immune response. There is evidence that at the time of diagnosis, patients with active TB have depressed blood concentrations of several micronutrients, including retinol, vitamins C and E, hemoglobin, zinc, iron, and selenium due to the immune system response to infection (Agyeman & Ofori-Asenso, 2017).

Food assistance is a potentially influential means for increasing adherence to TB treatment, reducing the costs to patients of staying in treatment, and for improving nutritional status. Food assistance may influence early case detection (encouraging patients to come sooner for diagnosis and treatment), and promote completion of the full course of treatment (Loddenkemper, Lipman, & Zumla, 2016). Both are important to decrease TB transmission. Periodic nutritional assessment, counseling on diet, nutritional management of symptoms and drug side-effects, may help TB patient maintain or increase their food intake and adhere to TB treatment (Agyeman & Ofori-Asenso, 2017).


Agyeman, A. A., & Ofori-Asenso, R. (2017). Tuberculosis—an overview. Journal of Public Health and Emergency, 1, 7–7. https://doi.org/10.21037/jphe.2016.12.08

Loddenkemper, R., Lipman, M., & Zumla, A. (2016). Clinical Aspects of Adult Tuberculosis. Cold Spring Harbor Perspectives in Medicine, 6(1). https://doi.org/10.1101/cshperspect.a017848


Restrictive Lung Disease

Restrictive lung diseases are a set of pulmonary disorders defined by restrictive patterns on spirometry, characterized by reduced distensibility of the lungs, compromising lung expansion, and lung volumes, particularly with reduced total lung capacity (King et al., 2019). Restrictive lung disease is often divided into two groups, depending on whether their cause is intrinsic or extrinsic.

I will focus on discussing interstitial lung disease (ILD), an intrinsic lung disease. ILD is an umbrella term used for a large group of diseases that cause scarring (fibrosis) of the lungs (King et al., 2019). ILDs are diffuse parenchymal lung diseases classified together because of similar clinical, radiographic, physiologic, or pathologic manifestations. The term “interstitial” reflects the pathologic appearance that the abnormality begins in the interstitium (King et al., 2019).

Pathology – Causes of ILD includes a broad range of diseases, exposures, and drugs, as well as idiopathic conditions (King et al., 2019). The most common identifiable causes of ILD are exposure to occupational and environmental agents, especially to inorganic and organic dusts, and drug-induced pulmonary toxicity (King et al., 2019). ILD can complicate the course of most rheumatic diseases (i.e., RA, lupus, and mixed connective tissue disease). Furthermore, idiopathic causes of ILD include sarcoidosis and idiopathic interstitial pneumonias.

Modifiable/nonmodifiable risk factors – Nonmodifiable risk factors include age and gender, family history, older age, autoimmune diseases and ethnic background (King et al., 2019). Some ILDs are more common in certain age groups or have a male or female predominance. Modifiable risk factors include smoking, prior medication use, radiation, chemotherapy, occupational and environmental exposures. Some ILD occur largely among current or former smokers, as well as some drugs having been reported to cause pulmonary toxicity (King et al., 2019).

Pertinent signs and symptoms – Patients with ILD commonly present with symptoms of progressive breathlessness with exertion (dyspnea) or a persistent nonproductive cough, chest discomfort, fatigue, and occasionally weight loss (King et al., 2019). They may have pulmonary symptoms associated with another disease, such as a connective tissue disease.

Diagnostics – Labs typically include BMP, CMP, CBC to evaluate hepatic and renal function, any evidence of anemia, polycythemia, leukocytosis, or eosinophilia (King et al., 2019). Chest x-ray is obtained to look for a reticular pattern, a common radiographic abnormality. Infectious processes can cause interstitial opacities on chest x-ray including fungal pneumonias, bacterial pneumonias, and viral pneumonias (King et al., 2019). Diagnostic approach to ILD relies on high resolution CT scan of the chest (King et al., 2019). Furthermore, I would obtain pulmonary function tests to assess spirometry and lung volumes as most ILDs have a restrictive defect with reductions in total lung capacity, functional residual capacity, and residual volume (King et al., 2019). The reductions in lung volumes become more pronounced as lung stiffness increases with disease progression.

Treatment regiments (pharmacological/nonpharmacological) – Approach to treatment varies based on the cause and type of ILD. Lung damage from ILDs is often irreversible and progressive, therefore treatment usually centers on relieving symptoms, improving quality of life, and slowing the disease’s progression (Distler et al., 2019). Medications, such as corticosteroids, can be used to decrease the amount of inflammation in the lungs. Oxygen therapy is another common treatment as it helps to make breathing easier for the patient. Lifestyle modifications should be included when treating these patients, such as smoking cessation, and reducing caffeine and carbonated beverage intake. A multidisciplinary approach is essential for diagnosis and treatment, particularly for patients with ILD related to autoimmune disease. Pulmonary rehab may be recommended in order to improve quality of life by giving patients techniques to improve lung efficiency, improve physical endurance and offer emotional support (Distler et al., 2019).


Distler, O., Highland, K., Gahlemann, M. (2019). SENSCIS Trial Investigators. Nintedanib for systemic sclerosis-associated interstitial lung disease. N Engl J Med, ;380(26):2518-2528. doi: 10.1056/NEJMoa1903076.

King, T., Flaherty, K., Hollingsworth, H. (2019). Approach to the adult with interstitial lung disease: Clinical evaluation. UpToDate. Retrieved from https://www.uptodate.com/contents/approach-to-the-adult-with-interstitial-lung-disease-clinical-evaluation?search=interstitial%20lung%20disease&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H5

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