HOMEWORK 4 Due Thursday, May 4, at the beginning of discussion 1. Write the Cayley table for the Dihedral group D8 with 8 elements. Why is D8 not isomorphic to Z/8Z? 2. Describe the following sets: • 4Z \ 6Z = {x 2 Z: x 2 4Z and x 2 6Z} • 4Z [ 6Z = {x 2 Z: x 2 4Z or x 2 6Z} • 4Z + 6Z = {h + k : h 2 4Z and k 2 6Z}. For each of set S, either prove that the set is a subgroup of (Z, +), or disprove the claim by means of a counterexample. 3. Let (G, ?) be a group and let H and K be subgroups of G. Prove or disprove each of the following statements. (If it is true, give a proof; if it is false, give a counterexample.) (a) H \ K = {x 2 G: x 2 H and x 2 K} is a subgroup of G. (b) H [ K = {x 2 G: x 2 H or x 2 K} is a subgroup of G. (c) (removed to be added to a later assignment) (d) Show that if (G, ?) is abelian, then H ? K is a subgroup of G. (e) If G = Z, H = 4Z and K = 6Z, find s, t 2 N such that H \K = sZ and H +K = tZ. How are s and t related to 4 an 6? In general, for H = mZ and K = nZ, make a conjecture about H \ K and H + K. 4. (postponed to a later assignment) (a) Compute the list of subgroups of the group Z/45Z and draw the lattice of subgroups. (prove that you really got all the subgroups) (b) How many subgroups does Z/2nZ have? 5. Let (G, ?) be a group and let G2 = {x 2 G: x ? x = e}. (a) Find G2 for G = (Z, +), (R � {0}, ·), (Z6, +6) and D6. (You may refer back to their group table.) (b) Disprove the following theorem: For every group G, G2 is a subgroup of G. (Make sure you explain why your counterexample disproves the theorem.) (c) Complete the theorem: If G is , G2 is a subgroup of G. Then prove your theorem. (d) (optional) Suppose G Is abelian. Is G3 = {x 2 G: : x ? x ? x = e} a subgroup as well? What about Gn (for n 2 N)? 6. Let GL2(R) be the group of 2⇥2 invertible matrices, with multiplication. (The elements of GL2(R) have real entries and non-zero determinant.) Consider the matrix: A = 1 1 0 1 ! . 1 a) Find the cyclic subgroup H of GL2(R) generated by the matrix A: H = hAi = {Ak : k 2 Z}. b) Find a familiar group isomorphic to H. Explicitly provide an isomorphism (and check that the given map is, indeed, an isomorphism). 7. Let (G, ?) and (K, �) be groups. Let �: G ! K be a group homomorphism (not neces- sarily an isomorphism). Prove that (a) �(eG) = eK, so � maps the identity of G into the identity of K. (b) Show that for all g 2 G, �(g�1) = [�(g)]�1. That is, � maps the inverse of g into the inverse of �(g). 2 Q-1 Bronchiectasis 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 acqu ...

1. HOMEWORK 4
Due Thursday, May 4, at the beginning of discussion
1. Write the Cayley table for the Dihedral group D8 with 8
elements. Why is D8 not
isomorphic to Z/8Z?
2. Describe the following sets:
• 4Z 6Z = {x 2 Z: x 2 4Z and x 2 6Z}
• 4Z [ 6Z = {x 2 Z: x 2 4Z or x 2 6Z}
• 4Z + 6Z = {h + k : h 2 4Z and k 2 6Z}.
For each of set S, either prove that the set is a subgroup of (Z,
+), or disprove the claim
by means of a counterexample.
3. Let (G, ?) be a group and let H and K be subgroups of G.
Prove or disprove each of the
following statements. (If it is true, give a proof; if it is false,
give a counterexample.)
(a) H K = {x 2 G: x 2 H and x 2 K} is a subgroup of G.
(b) H [ K = {x 2 G: x 2 H or x 2 K} is a subgroup of G.
(c) (removed to be added to a later assignment)
(d) Show that if (G, ?) is abelian, then H ? K is a subgroup of
G.
(e) If G = Z, H = 4Z and K = 6Z, find s, t 2 N such that H K =

2. sZ and H +K = tZ.
How are s and t related to 4 an 6? In general, for H = mZ and K
= nZ, make a
conjecture about H K and H + K.
4. (postponed to a later assignment)
(a) Compute the list of subgroups of the group Z/45Z and draw
the lattice of subgroups.
(prove that you really got all the subgroups)
(b) How many subgroups does Z/2nZ have?
5. Let (G, ?) be a group and let G2 = {x 2 G: x ? x = e}.
(a) Find G2 for G = (Z, +), (R � {0}, ·), (Z6, +6) and D6. (You
may refer back to their
group table.)
(b) Disprove the following theorem: For every group G, G2 is a
subgroup of G. (Make
sure you explain why your counterexample disproves the
theorem.)
(c) Complete the theorem: If G is , G2 is a subgroup of G. Then
prove your
theorem.
(d) (optional) Suppose G Is abelian. Is G3 = {x 2 G: : x ? x ? x
= e} a subgroup as
well? What about Gn (for n 2 N)?
6. Let GL2(R) be the group of 2⇥2 invertible matrices, with
multiplication. (The elements
of GL2(R) have real entries and non-zero determinant.)

3. Consider the matrix:
A =
1 1
0 1
!
.
1
a) Find the cyclic subgroup H of GL2(R) generated by the
matrix A:
H = hAi = {Ak : k 2 Z}.
b) Find a familiar group isomorphic to H. Explicitly provide an
isomorphism (and
check that the given map is, indeed, an isomorphism).
7. Let (G, ?) and (K, �) be groups. Let �: G ! K be a group
homomorphism (not neces-
sarily an isomorphism). Prove that
(a) �(eG) = eK, so � maps the identity of G into the identity of
K.
(b) Show that for all g 2 G, �(g�1) = [�(g)]�1.

4. That is, � maps the inverse of g into the inverse of �(g).
2
Q-1
Bronchiectasis
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

5. 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.
References
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
Q-2
Tuberculosis
Pathology
The inflammation produced with TB infection is granulomatous,
with epithelioid macrophages and Langhans giant cells along

6. 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).
Etiology
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).
Diagnostics

7. 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
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, &

8. 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).
References:
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

9. Aspects of Adult Tuberculosis. Cold Spring Harbor Perspectives
in Medicine, 6(1). https://doi.org/10.1101/cshperspect.a017848
Q-3
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,

10. 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 commo n
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

11. 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).
References
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=sear
ch_result&selectedTitle=1~150&usage_type=default&display_r
ank=1#H5
Q-1
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

12. 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

13. the chest/peritoneum.
Treatment – Regardless of staging, radical orchiectomy is done
initially. If cancer has spread, treatments including radiation or
chemo should be considered.
References
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
Q-2
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

14. 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

15. 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.
References
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. HemaSphere, 4(1), e332. Retrieved May 12, 2021,
from https://doi.org/10.1097/hs9.0000000000000332
Tamamyan, G., Kadia, T., Ravandi, F., Borthakur, G., Cortes,

16. J., Jabbour, E., Daver, N., Ohanian, M., Kantarjian, H., &
Konopleva, M. (2017). Frontline treatment of acute myeloid
leukemia in adults. Critical Reviews in
Oncology/Hematology, 110, 20–34. Retrieved May 12, 2021,
from https://doi.org/10.1016/j.critrevonc.2016.12.004
Q-3
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

17. 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)

18. Reference.
Momenimovahed, Z., Tiznobaik, A., Taheri, S., & Salehiniya,
H. (2019). Ovarian cancer in the world: epidemiology and risk
factors. International journal of women's health, 11, 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 &
medicine, 14(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 medica, 110(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 oncology, 28, viii36-viii39. Retrieved from
https://www.sciencedirect.com/science/article/pii/S0923753420
346615
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 research, 27(7),
826-840. Retrieved from
https://journals.sagepub.com/doi/abs/10.1177/105477381770474
9
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 Cancer, 10(18), 4318. Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691712/