WEEK 1
NURS 6501
Week 1 Discussion
Initial post
Factors that Influence Disease: Atherosclerosis
A forty-six-year-old woman comes to the emergency room complaining of pain when
walking, weakness of the left arm that happens often. The stated that these symptoms started
about three months earlier and are not getting better. She also claims of short of breath when
exercising. The patient says that the mother had atherosclerosis and died at the age of fifty-three.
In an article in NIH (2018), found that atherosclerosis is the result of hyperlipidemia and lipid
oxidation, it’s a disease in which all the vascular system from aorta to coronary arteries can be
involved. Nurse practitioners (NPs) are expected to know factors associated with any disease to
be able to manage it. As such, NPs to manage the disease process have to correctly diagnose the
patient and know (1) what a patient would complain of, (2) what to look for in a physical exam,
(3) diagnostic tests needed to confirm preliminary prognosis, (4) types of therapies essential to
treat a diagnosis, (5) information necessary in educating the patient, and (6) outcomes to evaluate
the effectiveness of medical interventions (Laureate Education, Inc. (Executive Producer),
2012d).
Genetics
“Understanding pathophysiology also entails the utilization of principles, concepts, and
basic knowledge from other fields of study including pathology, genetics, epigenetics,
immunology, and epidemiology” (Huether and McCance, 2017, p.xii). Knowledge how genes
are passed down from one generation to the next can disclose considerable amounts of
information about disease-causing genes, revealing treatment options, or genetic counseling.
Utilizing a pedigree chart, which depicts family members affected by a genetic disease and
summarizes family relationships is one tool in tracking transmission of a genetic disease
(Huether and McCance, 2017). Individuals are at risk for Atherosclerosis due to genetics have a
family history of hypertension, high cholesterol, early heart disease, or have elevated levels of C-
reactive protein (CRP) because CRP is a sign of inflammation in the body (National Institutes of
Health (NIH), 2016).
Atherosclerosis
When plaque (fatty deposits) clogs your arteries, that’s called atherosclerosis. These
deposits are made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin
(a clotting material in the blood).Arteriosclerosis is the thickening and hardening of blood vessel
causing lesions on the endothelial lining of a blood vessel wall (Huether and McCance, 2017).
Plaque is the formation of lesions from the accumulation of lipid-laden macrophages on the
artery wall and is an injury to the endothelial cells lining the arterial walls (2017). Plaque may
cause damage with enough accumulation, causing obstruction with thrombosis resulting in tissue
infarction often seen in transient ischemic events or stroke, or in coronary artery disease leading
to myocardial ischemia; furthermore, any area of the body may be affected by atherosclerotic
lesions (2017).
Clinical Manifestations of Atherosclerosis
Clinical manifestations are a result of inadequate tissue perfusion and are often linked to
stress or exercise causing significant pain or disability (Huether and McCance, 2017). The Mayo
Clinic (n.d.) describes atherosclerosis sign and symptoms to include leg pain when walking,
chest pain/pressure, hypertension; kidney failure signs of a stroke such as sudden weakness,
blurriness or loss of vision in one eye, difficulty with speech or slurring. Other symptoms
include arterial bruits because of diminished blood flow to tissues, and laboratory results may
contain high lipid, blood glucose, troponin, and CRP levels (Huether and McCance, 2017).
Atherosclerosis risk factors also include smoking, diabetes, and autoimmunity, infection and air
pollution (2017).
Pathophysiology of Atherosclerosis
The earliest visible lesion of?atherosclerosisis the fatty streak, which is an accumulation
of lipid-laden foam cells in the intimal layer of the artery. The?atherosclerotic?plaque is the
hallmark of?atherosclerosis.It starts with an injury or insult to the endothelial cells lining the
artery walls causing lesions which progress from endothelial damage to fatty streaks then on the
fibrotic plaque and finally to a complicated lesion when tissue ischemia is very likely (Huether
and McCance, 2017, p. 607). After an injury, endothelial cells become inflamed and
microRNAs or the “short pieces of RNA that regulate posttranscriptional gene expression” are
stimulated (2017, p. 607). Then inflamed endothelial cells express adhesion molecules, binding
macrophages to damage-associated molecular patterns (DAMPs), and other inflammatory and
immune cells including cytokines such as tumor necrosis factor-alpha, interferons, interleukin's;
C-reactive protein and enzymes that progress the injury to the vessel wall and release toxic
oxygen free radicals (2017). These free radicals cause oxidation and oxidize LDL causing
additional harm to the vessel wall, and the lipid-laden macrophages are called foam cells as they
accumulate and form lesions called fatty streaks. (2017). Fatty streaks generate more free
radicals and recruit T cells, which leads to progressive damage to the vessel wall (2017). Plaque
is formed by proliferation of the endothelial cells which produce collagen, which may calcify,
and obstruct blood flow or become unstable and rupture (2017). Plaque rupture occurs because
of the activation of proteinase and can cause a hemorrhage, or expose underlying tissue causing
platelet adhesion initiating thrombus formation, causing complicated atherosclerosis which leads
to tissue ischemia in conditions such as stroke or myocardial infarctions (2017).
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Laureate Education, Inc. (Executive Producer). (2012d).?Introduction to advanced
pathophysiology. Baltimore, MD: Author.
Mayo Clinic. (n.d.). Arteriosclerosis, Symptoms and causes. Retrieved from
http://www.mayoclinic.org/diseases-conditions/arteriosclerosis-atherosclerosis/
symptoms-causes/dxc-20167022
National Institutes of Health (NIH). (2016). Atherosclerosis. Retrieved from
https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis
National Institutes of Health (NIH). (2018). Atherosclerosis. Retrieved from
https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis
NURS 6501
Week 1
Response #1
Osteoporosis and gender differences
Mary,
Nice intervention. When speaking of gender differences, the etiology of osteoporosis
varies between men and women. According to an article written by Wolf, J. M., Cannada, L.,
Van Heest, A. E., O’Connor, M., & Ladd, A. L. (2015), one such belief to why women have an
increase occurrence in osteoporosis compared to men, is the difference in bone mass. During
bone growth in men, the periosteal expansion is greater. This establishes a gender difference in
bone at an early age. When individuals reach adulthood, a male’s bone mass is 35% to 42%
larger than that of a female, consistent with their larger body size. Once maturity is reached, a
male’s bones are generally wider and longer than that of the average female. Although,
trabecular bone loss is very similar for both genders, cortical absorption is 25% greater in
females compared to the 18% in males, unfortunately inadequate. Among patients in their 50s
who had an osteoporosis-related fracture, less than 50% of these patients had had a previous
diagnosis or treatment of osteoporosis (Lee et al, 2013, p.348). In particular, among the fracture
patients, the examination rate was 24.8% in men, which was significantly lower than 55.7% in
women. This is likely attributable to the incorrect perception that osteoporosis is a female
disease. Thus, it is necessary to accurately identify the nation-wide prevalence of osteoporosis
and to efficiently manage osteoporosis patients.
References
Jongseok Lee, Sungwha Lee, Sungok Jang, &Ohk Hyun Ryu. (2013). Age-Related Changes in
the Prevalence of Osteoporosis according to Gender and Skeletal Site: The Korea
National Health and Nutrition Examination Survey 2008-2010.?Endocrinology and
Metabolism, Vol 28, Iss 3, Pp 180-191 (2013), (3), 180. https://doi-
org.ezp.waldenulibrary.org/10.3803/EnM.2013.28.3.180
Wolf, J. M., Cannada, L., Van Heest, A. E., O’Connor, M., & Ladd, A. L. (2015). Male and
FemaleDifferences in Musculoskeletal Disease. Journal of the American Academy of
Orthopaedic Surgeons. 23(6), pg. 339-347. Doi: 10.5435/JAAOS-D-14-00020
NURS 6501
Week 1
Response #2
Hello Esther,
Nice intervention. I worked with a family that the child had Cystic fibrosis (CF). That
family needed so much education and other form of therapies for the management of the disease.
CF is the most common genetic condition in Caucasians, is generally identified through routine
newborn screening followed by other confirmatory diagnostic tests. Parents may find a diagnosis
of CF in their infant to be unexpected and confronting, and have little knowledge of the
ramifications of such a diagnosis on their families. Cystic fibrosis outpatient centers are
established in the major children’s hospitals; it is here that parents of infants newly diagnosed
with CF will receive initial education from the interdisciplinary team about the disease and its
management (Edwards et al. 2018). Many parents from regional, rural or remote locations will
need to attend a CF center located in the capital cities to receive this education, although ongoing
clinical management of their child may be undertaken on an outreach basis.
Physical activity is recommended as a component of the cystic fibrosis (CF) treatment
regimen. However, to date, there is limited research examining the effects of behavioral
counseling interventions aimed at increasing physical activity. Physical activity and exercise may
improve physical and psychosocial health as well as quality of life in people with cystic fibrosis
(CF). In addition to enhancing perceptions of wellness and quality of life, numerous studies have
found that exercise training is associated with notable physical benefits for people with CF (Mola
et al, 2017). Researchers have reported short-term improvements in physical and psychosocial
outcomes as a result of exercise training in young CF populations.The association between
aerobic fitness and survival is perhaps the most compelling rationale for the incorporation of
physical activity promotion within the care of people with CF.Physical activity, and exercise in
particular, may slow the rate of lung function de- cline over time and contribute toward survival.
References
Edwards, D. J., Wicking, K., Smyth, W., Shields, L., & Douglas, T. (2018). Information needs of
parents of infants diagnosed with cystic fibrosis: Results of a pilot study.?Journal of Child
Health Care,?22(3), 382–392.
https://doi-org.ezp.waldenulibrary.org/10.1177/1367493518760734
Moola, F. J., Garcia, E., Huynh, E., Henry, L., Penfound, S., Consunji-Araneta, R., & Faulkner,
G. E. J. (2017). Physical Activity Counseling for Children With Cystic
Fibrosis.?Respiratory Care,?62(11), 1466–1473.
https://doi-org.ezp.waldenulibrary.org/10.4187/respcare.05009
WEEK 2
NURS 6501
Week 2 Discussion
Initial post
Discussion 1
Systemic Lupus Erythematosus & Psoriasis
This discussion 1covers the pathophysiology of Systemic Lupus Erythmatosus (SLE) and
Psoriasis. The discussion will involve the compensatory mechanisms, maladaptive, and
physiological responses of the two disorders. The age inference with regards to the
pathophysiology of both SLE and Psoriasis will be reviewed.
Pathophysiology of Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is a prototypic multisystemic autoimmune disease,
withheterogeneous disease manifestations which could affect different organ
systems(Frostegård& al., 2018). It is a systemic autoimmune disease that occurs when your
body's immune system attacks your own tissues and organs. The inflammation caused by lupus
can affect many different body systemsincluding your joints, skin, kidneys, blood cells, brain,
heart and lungs.Lupus can be difficult to diagnose because its signs and symptoms often mimic
those of other ailments. The most distinctive sign of lupus a facial rash that resembles the wings
of a butterfly unfolding across both cheeks occurs in many but not all cases of lupus.During the
disease state, there is production of huge varieties of auto antibodies against nucleic acids (single
and double stranded DNA), erythrocytes, coagulation proteins, lymphocytes, platelets, and many
other self- proteins which causes inflammation, pain, and damage in various parts of the
body(Lupus Foundation of America, 2012). These autoimmune reactions are directed against
constituents of the cell nucleus that is antinuclear antibodies, particularly DNA, and as a result,
the circulating immune complexes containing antibody against DNA are deposited in the
basement membranes of capillaries in the kidneys, heart, skin, brain, and joints. Once the
complement is activated, inflammation occurs. It is imperative for advanced practice nurses to
know that the specific manifestations of SLE depends on type of cell or organs that is involved
(Lewis, Heitkemper, Dirksen, Bucher, & Camera, 2011).
Pathophysiology of Psoriasis
Psoriasis is a chronic dermatitis and relapsing inflammatory disease implicating overly
rapid turnover of epidermal cells.? During the inflammatory cascade of this disorder, there is
secretion of multiple inflammatory mediators(interferon, tumor necrosis factor- alpha), and
cytokines (interleukin-12, 13, 17) due to complex interactions between macrophages, fibroblasts,
dendritic cells, natural killer cells, T helper cells, and regulatory T cells (Huether? &McCance,
2017).
Variation in?Physiological Responses
SLE is extremely variable in its severity, ranging from a relatively mild disorder to a
rapidly progressive one affecting multiple body system due to accumulation of circulating
immune complexes (Lupus Foundation of America, 2012), whereas psoriasis can be mild,
moderate, or severe, depending on the size, distribution, and inflammation of the lesions
implicating mostly the dermis and epidermis due to cellular hyper-proliferation, altered
keratinocyte differentiation, and expanded dermal vasculature (Huether& McCance, 2017). The
most commonly affected tissues by the SLE are the skin and muscle, the lining of the lungs,
heart, nervous tissue, and the kidneys whereas psoriasis mostly affects the skin, scalp, and the
nails. ?Generalized complaints like fever, weight loss, arthralgia, and excessive fatigue may
precede an exacerbation of SLE activity, whereas a well-demarcated, thick, silvery, scaly
erythematous plaque surrounded by normal skin is the most common clinical manifestation of
psoriasis (Lewis et al., 2011). It is very crucial that advanced practice nurses should familiarize
themselves with this variation for proper diagnosis and treatment.
Variation in the adaptive responses of the SLE and Psoriasis
SLE is extremely variable in its severity, ranging from a relatively mild disorder to a
rapidly progressive one affecting multiple body system due to accumulation of circulating
immune complexes (Lupus Foundation of America, 2012), whereas psoriasis can be mild,
moderate, or severe, depending on the size, distribution, and inflammation of the lesions
implicating mostly the dermis and epidermis due to cellular hyper-proliferation, altered
keratinocyte differentiation, and expanded dermal vasculature (Huether& McCance, 2017). The
most commonly affected tissues by the SLE are the skin and muscle, the lining of the lungs,
heart, nervous tissue, and the kidneys whereas psoriasis mostly affects the skin, scalp, and the
nails. ?Generalized complaints like fever, weight loss, arthralgia, and excessive fatigue may
precede an exacerbation of SLE activity, whereas a well-demarcated, thick, silvery, scaly
Patient Factor: Age
According to Huether and McCance (2017), psoriasis can occur at any age, but the onset
is generally established by forty years of age. Any onset of psoriasis at later stage in life is less
familial and much secondary to co-morbidities, like obesity, smoking, high blood pressure, and
diabetes. With SLE, symptoms and diagnosis occur most often when women are in their
childbearing years, between the ages of 15 and 44. Symptoms of lupus will occur before age 18
in 15 percent of the people who are later diagnosed with the disease (Lupus Foundation of
America, 2012).
erythematous plaque surrounded by normal skin is the most common clinical
manifestation of psoriasis (Lewis et al., 2011). It is very crucial that advanced practice nurses
should familiarize themselves with this variation for proper diagnosis and treatment.
References
Frostegård, J., Hellström, C., Nilsson, P., Frostegård, A. G., &Ajeganova, S. (2018).
Autoantibody profiling reveals four protein candidate autoantigens associated with
systemic lupus erythematosus.?Lupus,?27(10), 1670–1678. https://doi-
org.ezp.waldenulibrary.org/10.1177/0961203318788153
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Lewis, S. L., Heitkemper, M.M., Dirksen, S. R., & Bucher, L., & Camera, I. (2011). Medical-
surgical nursing: Assessment and management of clinical problems (7th ed.). St. Louis,
Missouri: Mosby.
Lupus Foundation of America. (2012).What are the risk factors for developing lupus? Retrieved
from?http://www.lupus.org/answers/entry/risks-for-developing-lupus
Lupus Foundation of America. (2012).What happens in autoimmune diseases like lupus?
Retrieved from?http://www.lupus.org/answers/entry/what-happens-in-autoimmune-
diseases-like-lupus
NURS 6501
Week 2 Discussion
Initial post
Discussion 2
Osteoarthritis
Osteoarthritis (OA) is the result of mechanical and biologic events that destabilize the
normal process if degradation and synthesis of articular cartilage chondrocytes, extracellular
matrix, and subchondral bone. OA is equally prevalent in men and women, although women 50
and older are affected more severely, and the disorder is first commonly seen when people are in
their 50s and 60s (Huether& McCance, p.1009, 2017). Individuals whose joints are overloaded
and put under long-term mechanical stress, such as athletes or obese people, are especially prone
to OA (Huether& McCance, p. 1009, p.1011, 2017). Other risk factors for developing OA
include: a history of trauma, such as fractures and sprains; certain neurologic, hematologic, and
endocrine disorders; a history of inflammation or instability of the joints; and certain medications
that stimulate collagen-digesting enzymes in the synovial membrane (Huether& McCance,
p.1011, 2017).
Symptoms of OA usually begin with pain and stiffness in one or more of the weight-
bearing joints, such as knees or hips, and can be in the hands, neck, or lower back (Huether&
McCance, p. 1011, 2017). Other common signs include: mild swelling around the joint, stiffness
and limited range of motion that gets better with movement, and pain that is worse after activity
and at the end of the day (Arthritis Foundation, n.d.).
Pathophysiology of Osteoarthritis
As stated earlier, the primary cause of OA is the loss of articular cartilage, and in the
beginning stages, the cartilage begins to swell because of the increased production of
proteoglycans that are attempting to repair damage (Huether& McCance, p.1010, 2017). This
stage may last for years before the number of proteoglycans diminishes and the cartilage begins
to soften, lose elasticity, and layers begin to flake off and become thinner in some areas, which
leaves the underlying bone unprotected (Huether& McCance,p.1010, 2017). Over time, the loss
of cartilage leads to a loss of joint space. This process happens due to natural aging or long-term
excessive wear-and-tear on the joints. Eventually, the underlying bone becomes exposed,
abnormally altering the cellularity (Huether& McCance,p.1010, 2017).
Rheumatoid Arthritis
Rheumatoid Arthritis (RA) is an inflammatory autoimmune disorder in which the body
mistakenly attacks its own joints due to an abnormal immune response (Huether&
McCance,p.1012, 2017). 70 percent of RA sufferers are women, suggesting that female
hormones may play a role in the disease. Other risk factors include: genetics, obesity, smoking,
and exposure to physical or emotional trauma (Arthritis Foundation, n.d.).
Pain, stiffness, and swelling of the joints may be coupled with fatigue, loss of appetite,
and a low-grade fever (Arthritis Foundation, n.d.). RA is a systemic disease of chronic
inflammation, so it may affect other organs or body systems besides just the joints. For example,
eye and mouth dryness, rheumatoid nodules under skin on affected bony areas, anemia, and
inflammation of lung tissue and blood vessels that can lead to more serious complications
(Arthritis Foundation, n.d.).
Pathophysiology of Rheumatoid Arthritis
Rheumatoid Arthritis is caused by an abnormal immune response that activates B cells, T
cells, and innate immune effectors (Hammer & McPhee,p.1011, 2014). The pathological damage
occurs around the synovial linings of the joints, where thickened layers made up of activated
inflammatory cells form (Hammer & McPhee,p.1011, 2014). At the border of articular cartilage
and synovium, rheumatoid arthritis synovial tissue, known as pannus, attacks and destroys the
surrounding articular cartilage and bone (Hammer & McPhee, p.1011, 2014). RA is thought to
have genetic factors, and involve hormones, as it is most common in females. Environmental
factors include: smoking, diet, socioeconomic status, and area of birth (Huether&
McCance,p.1011, 2017).
Similarities and Differences Between Osteoarthritis and Rheumatoid Arthritis
Most joint diseases can be categorized as inflammatory or noninflammatory.
Osteoarthritis is considered noninflammatory while Rheumatoid Arthritis is inflammatory
(Huether& McCance, 2017). The biggest difference between the two is that OA is caused by
age/wear on the joints and RA is caused by an autoimmune reaction (Arthritis Foundation, n.d.).
OA is localized to specific joints. RA can affect multiple organs and systems, and has acute
onset. OA happens slowly over time and typically affects older people, and RA can happen over
weeks/months and occur at any time in life (Arthritis Foundation, n.d.). In OA, symptoms and
pain increase in the morning, at rest, while in people with RA pain increases with exercise. The
similarities between the two can be seen in some of the symptoms, such as pain and stiffness of
joints and limited range of motion (Arthritis Foundation, n.d.).
Diagnosis and Treatment of Both Disorders
OA is diagnosed by taking a medical history and assessment of current symptoms such as
pain, stiffness, limited range of motion, numbness, and tingling. Radiologic studies are done;
however, CT scans and MRI are usually not necessary (Huether& McCance,p.1012, 2017).
There is no cure for OA, so treatment involves managing the symptoms long-term, such as
weight management, appropriate physical activity, specific exercises to promote range of motion
and muscle tone, healthy diet, and sometimes pain medications. Braces may be used and surgery
is considered as a last resort (Huether& McCance, p. 112, 2017).
RA is diagnosed by taking a medical history and evaluation of current joint swelling,
pain, and stiffness. The practitioner should also check for low-grade fever and nodules on the
joints. Blood tests can indicate inflammation levels and antibodies (Arthritis Foundation, n.d.).
X-rays or ultrasound may help confirm the diagnosis. The patient may be referred to a specialist,
a rheumatologist, for further care (Arthritis Foundation, n.d.). Ideally, RA will be caught early,
when treatment can be more effective and the inflammation can be stopped so that the disease
will go into remission (Arthritis Foundation, n.d.). To slow the disease progression, anti-
rheumatic drugs such as methotrexate, sulfasalazine, and cyclosporine may be given (Huether&
McCance, 2017). Alternate pharmacologic treatment can be NSAID’s, glucocorticoids, and
steroid injections; while non-pharmacologic methods involve physical and occupational therapy
(Huether& McCance, 2017). Joint replacement surgery may be necessary in some cases.
References
Arthritis Foundation. (n.d.). Understanding arthritis. Retrieved on September 7, 2017 from
http://www.arthritis.org/about-arthritis/types/osteoarthritis/symptoms.php
Hammer, G.G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical
medicine (7th ed.). New York, NY: McGraw-Hill Education.
Huether, S.E., & McCance, K.L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Week 2 Discussion
Discussion 2
Response# 1
Osteoarthritis (OA), also referred to as degenerative joint disease or wearandtear arthritis,
is caused by the breakdown of joint cartilage. Primary OA is an idiopathic phenomenon,
occurring in previously intact joints, with no apparent initiating factor such as joint injury or
developmental abnormalities. It mostly affects women (Zhang et al., 2014).
Non-pharmacologic treatment includes patient education of the patient and controlling
join pain and stiffness, self-management, and exercise program (reassurance that exercise is not
harmful), physical and occupational therapy, knee brace, correct footwear, and patellar bracing
or taping for patellofemoral pain.
Pharmacology treatment can be done by using local analgesia, acetaminophen, or intra-
articular corticosteroid injection,
Rheumatoid arthritis (RA) is a chronic, inflammatory type of arthritis. RA is also classified as a
kind of autoimmune disease. arthritis in the elderly. Rheumatoid arthritis is a chronic,
inflammatory disorder that may affect many tissues and organs, but principally attacks flexible
(synovial) joints. RA affects 1% of the world’s population. Patients with RA not only have a
progressive and debilitating disease and severe functional impairment, but can also experience a
reduced life expectancy due to frequent involvement of the major organ systems(Huether&
McCance, p.1001, 2017). The disease is diagnosed clinically, laboratory and radiographic testing
provide prognostic information more often.
Patient with RA are usually started on DMARD such as leflunomide. Corticosteroids can be used
as well.
References
Huether, S.E., & McCance, K.L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Zhang, Q., Cheng, B., Yang, C.-X., & Ge, H.-A. (2014). Interaction relationships of
osteoarthritis and rheumatoid arthritis related genes.?European Review For Medical And
Pharmacological Sciences,?18(2), 179–184. Retrieved from
https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?
direct=true&db=mnh&AN=24488905&site=eds-live&scope=site
Week 2
Discussion 1
Response #2
Pathophysiology of HIV
The Human Immunodeficiency Virus (HIV) infects and destroys CD4+ T lymphocytes
that result in?poor?immune system functioning.??The virus enters the CD4 + T cells by binding to
CD4 and chemokine receptor sites on the cell surface. Many of the target cells used by HIV are
CD4 cells, bone marrow CD4 precursor cells and T-cells.??Inside the?cell,?the viral RNA
transcribes into viral DNA which enters the nucleus and incorporates itself into cellular genome
causing permanent cellular infection and a high level of virion production and CD4 cell death
(Nettina, 2014). The destruction of the T cell “suppresses the immune response against itself”
and results in the development of opportunistic infections and other abnormal tissue growth
leading to AIDS (Huether& McCance, 2015, p.182).
Maladaptive and Physiological Response HIV
Within the first month after HIV infection, some individuals develop acute HIV?with a brief flu-
like?symptom that may last for about two weeks. Symptoms at this stage include night sweats,
persistent swollen lymph nodes, diarrhea, fever, headaches, fatigue, weight loss, diffuse rash,
sore throat, body malaise and sometimes breathing problems. After the alleviations of
the?symptoms,?most people will experience a latent period for several years (Nettina,
2014).??With the decrease in the production of CD4 T?cells,?the viral load increases and the
immune system is weakened leading to susceptibility to?various?symptoms such as tuberculosis
and other chronic infections. HIV infection progresses gradually and if left untreated will turn
into AIDS (Huether& McCance, 2015).
Patient Factor- Behavior
HIV is a virus transmitted through contact with infected body fluid including blood,
semen, vaginal secretion, and breast milk and the most common mode of transmission is through
unprotected sexual contact with an infected partner (Nettina, 2014). Also, the use of intravenous
drugs through the sharing of needles and syringes exposes the?individual?to droplets of other
people’s blood and increase the risk for HIV. Men who?engage?in sexual intercourse with other
men have become the most common method of infection in males and heterosexual transmission
through anal, vaginal, and oral, has become the?common?method of transmission in women
(Lewis, Heitkemper, Dirksen, O’Brien, & Bucher,?2014).
5
References
Huether, S.E., &McCancee, K. L. (2015).?Understanding pathophysiology. St Louis,?MO.
Mosby, Inc.
Lewis, S.L., Heitkemper, M.M., Dirksen, S.R., O’Brien, P.G., & Bucher, L. (2014).??Medical-
surgicalnursing:Assessmentand management of clinical problems.St????????Louis, MO.
Mosby Inc.
Nettina, S.M. (2014).??Lippincott manual of nursing practice.?Baltimore, NY. Lippincott?William
& Wilkins
Discussion 2
Response # 2
Great job Krystal.
Factors genetic and behavior have been demonstrated to impact rheumatoid
arthritisRheumatoid arthritis (RA) is a chronic inflammatory disorder in which hypertrophy,
hyperplasia and angiogenesis of synovial tissue contribute to inflammatory joint destruction and
it affects 1% of the adults worldwide(Chatzikyriakidou et al., 2013). Both genetic and
environmental factors have been implicated in RA susceptibility. The main genetic factor for RA
is the HLA-DRB1 gene, but the HLA genes account only for one-third of the genetic liability to
the disease. Therefore, in order to understand what causes RA, the current genome-wide
association studies (GWAS) identified a number of single nucleotide polymorphisms (SNPs)
related to RA since they allow the unbiased test of hundreds of thousands of SNPs in large
groups of patients and controls.
It is well evidenced that higher levels of physical activity associate with improvement in
cardiovascular health, and physical function in rheumatoid arthritis (Sally et al., 2017). Sally also
proved that sedentary behavior is demonstrated to be adversely linked to several health outcomes
which are relevant to RA.
References
Chatzikyriakidou, A., Voulgari, P. V., Lambropoulos, A., &Drosos, A. A. (2013). Rheumatoid
Arthritis: Genetics in rheumatoid arthritis beyond HLA genes: What meta-analyses have
shown??Seminars in Arthritis and Rheumatism,?43, 29–38. https://doi-
org.ezp.waldenulibrary.org/10.1016/j.semarthrit.2012.12.003
Sally A. M. Fenton, Jet J. C. S. Veldhuijzen van Zanten, George D. Kitas, Joan L. Duda, Peter C.
Rouse, Chen-an Yu, & George S. Metsios. (2017). Sedentary behaviour is associated
with increased long-term cardiovascular risk in patients with rheumatoid arthritis
independently of moderate-to-vigorous physical activity.?BMC Musculoskeletal
Disorders, Vol 18, Iss 1, Pp 1-12 (2017), (1), 1.
https://doi-org.ezp.waldenulibrary.org/10.1186/s12891-017-1473-9
WEEK 3
NURS 6501
Week 3 Discussion
Initial post
Pain
Pain is an indication in the nervous system that something might be wrong in the body.
Pain is “an unpleasant, but protective phenomenon that is uniquely experienced by each
individual, and cannot be objectively measured by the observer” (Heuther, 2017, p. 336). It is a
complex experience that includes dynamic interactions between the physical, cognitive, spiritual,
emotional and environmental factors(Heuther, 2017, p. 336). Pain is subjective, only the person
who feels it can say it. Painis characterized as "unpleasant sensory and emotional experience
associated with genuine or potential tissue injury" (Arcangelo &Peterson, 2013).In the daily
basis, human being encounters three types of pain: acute, chronic, or referred.
Acute pain
Acute pain typically lasts less than three to six months, it is a type of pain directly related
to soft tissue damage such as sprain ankle, cut on the skin, ligaments, tendons, fibrous tissues,
fats, and synovial membrane. Acute pain has a sudden beginning, typically diminishes rapidly
and is described by sharp, localized sensations with an apparent cause (Arcangelo & Peterson,
2013). Acute pain was expressed to have a sharp,localized, or radiating quality while the chronic
pain was said to be dull (Pearson, 2012). When acute tissue damage occurs, neurochemical
reactions at the site of the injury activate the free nerves endings called nociceptors, which then
propagate through the peripheral nerves, traverse spinal tract, and land in the cerebral centers.
Acute pain can be sharp (burning, freezing, cutting, pricking, …etc).
Chronic pain
Chronic pain is any pain lasting more than three to six months. It is initially caused by an
injury such as back sprain or pulled muscle. Chronic pain develops after damage of a nerve. The
physiological response of acute pain is different from chronic pain. What is thought to prompt
chronic pain is changes in the peripheral and central nervous systems that cause dysregulation of
nociception and pain modulation processes. Chronic pain can be the result of depression, trouble
eating,and sleeping patterns, and worry with pain, …etc. Chronic pain can only be managed. The
common symptoms of chronic pain isthat is dull, persistent, aching, or diffuse.
Referred pain
The sensation of pain is perceived at a location other than the site of the painful stimulus.
It occurs because nerves from various parts of the body converge on their way to spinal cord. For
instance, the pain associated with a myocardial infarction is located in the mid or left side of the
jaw and into the left arm.
Factors: Age and gender
Age
Elderly individuals are more tolerant of pain than more youthful individuals. It could be
partially elderly individuals are used to pain. Pain is mutual among elderly individuals (Markman
& Narasimhan, 2014). An elderly individual that has been suffering from back pain or arthritis
pain for an extendedperiod has acquired tolerant to pain. Most elderly individuals mistakenly
think that pain is an inevitable part of aging and therefore limit them complains about pain, or
only do not report pain (Markman & Narasimhan, 2014). The skin sensation decreases with age,
that’s why it is imperative to constantly assess elderly’s skin and take into consideration the
following characteristics: facial expression, inactivity, change in range of motion, change in the
ADLs performance, …etc.
Gender
Women as all the more eager to report pain, less able to tolerate pain, and more delicate
to pain than men (Wandner, Scipio, Hirsh, Torres, & Robinson, 2014). The distinction in men
not reporting pain might be the saying men’s that stated, "men guessed cry." Be that as it may,
pain is the thing that the individual encountering pain says it is, gender apart. Women will
complain of pain if they are feeling pain, versus men attempting to tough it out. Given the study
was done on pain sensitivity amongst men and women. "The average woman was rated as being
more sensitive to pain than the average man. Likewise, the typical woman was rated as being
more sensitive to pain than the member (Wandner et al., 2014).
References
Arcangelo, V. P., & Peterson, A. M. (Eds.). (2013). Pharmacotherapeutics for advanced
practice:
A practical approach (3rd ed). Ambler, PA: Lippincott Williams & Wilkins
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Markman, J., & Narasimhan, S. (2014). Overview of Pain. -Brain, Spinal Cord, & Nerve
Disorder. Retrieved from http://www.merckmanuals.com/home/brain,-spinal-cord,-and-
nerve-disorders/pain/overview-of-pain
Pearson, N. (2012). Acute versus Chronic Pain: Understanding the difference and
choosing
appropriate treatment. Retrieved from https://www.orionhealth.net/2012/01/acute-and-
chronic-pain/
Wandner, L. D., Scipio, C. D., Hirsh, A. T., Torres, C. A., & Robinson, M. E. (2014). THE
PERCEPTION OF PAIN IN OTHERS: HOW GENDER, RACE, AND AGE
INFLUENCE PAIN EXPECTATIONS. Journal of Pain, (13(3): 220-227.
Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294006/.
DOI: http://dx.doi.org/10.1016/j.jpain.2011.10.014
NURS 6501
Week3
Response #1
How Genetics and ethnicity Impact Pain
Genetics and ethnicity can have a very big impact on how pain is perceived, diagnosed
and treated. Pain perception is the awareness of pain which occurs in the reticular and limbic
systems and the cerebral cortex (Huether, 2017). Some individuals have some type of genetic
mutation that can make them feel no pain, which is not a good response. It has been discovered
that there are some possible gene variants that are prevalent to each pain group. In a study done
it was noticed that the gene DRD1 was associated with low pain tolerance, COMT and OPRK
was associated with moderate pain, and DRD2 was seen with high pain levels (Pain and genetics,
2017). Its also noted that opioid system is an important source for the study of genetics and pain
perception. There hasn’t been a lot of studies done on the effect of genetics and medication
regimen for pain.
Ethnicity also plays a vital role in pain perception, diagnosis and treatment. Many
cultures view pain differently and react to it differently. For example, African-Americans report
greater pain compared to whites in the following conditions such as migraines, post-op pain,
joint pain, etc. (Campbell, 2012). I remember working on the postpartum unit and having
patients from various backgrounds and watching the way they respond to pain. My patients of
Asian-Pacific Islander would report not having any pain and not wanting to take the medication
that was offered to them, whereas my African-American patients didn’t shy away from receiving
their medications and often made sure they knew the schedule of when the medication was due.
Pain is a hard thing to treat because the practitioner never really knows how much pain someone
truly has.
References
Campbell, C. &. (2012). Ethnic differences in pain and pain management. Pain Management,
219-230. doi:https://dx.doi.org/10.2217%2Fpmt.12.7
Huether, S. &. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Elsevier.
Pain and genetics. (2017). Pain Pathways Magazine. Retrieved from
https://www.painpathways.org/pain-and-genetics/
NURS 6501
Week 3
Response #2
I read an article talking about gene that affects pain in patients with total knee
replacement. Total knee replacement (TKR) is the treatment option of choice for the millions of
individuals whose osteoarthritis pain can no longer be managed through noninvasive methods
(Belfer et al., 2014). Over 500,000 TKRs are performed annually in the United States (Belfer et
al., 2014). Although most patients report improvement in pain and functioning following TKR,
up to 30% report persistent pain that interferes with daily function. However, the reasons for
poor outcomes are not clear. Pain management should be individualized based upon patient’s
genetic, proteomic as well as clinical variables. It is expected that identification of these
variables will lead to development and implementation of novel and more tailored preventive
strategies in patients at risk. For example, behavioral interventions tailored to patients’
psychosocial, clinical, and demographic presentation as well as genetic makeup may prevent
post-TKR pain. Such targeted interventions in patients at risk may reduce the burden of pain and
significantly improve quality of life post TKR. Genes are selected based on their reported role in
human pain perception in general, and in acute and chronic postsurgical pain in particular.
Genetic data from this study may provide evidence on the contribution of genetic factors to pain
phenotypes related to TKR and could lead to a larger multicenter study that would use the
developed methodology and collect comprehensive pain phenotypes in a very large cohort.
Another study showed that chronic widespread pain is linked to genetics. Chronic
widespread pain (CWP) is defined as “pain on the left side of the body, pain on the right side of
the body, pain above the waist, pain below the waist and axial skeletal pain (cervical spine or
anterior chest or thoracic spine or low back) for at least 3 months. Besides a genetic
predisposition to CWP, physical and psychological stress, affective disorders, and alterations in
the central nervous system have shown to be potential risk factors for the condition (Kerr
&Burri, 2017). CWP is almost always associated with a set of psychosocial correlatesand shows
strong comorbidity with depressive and anxiety disorders.Based on evidence from previous
studies suggesting a genetic contribution, this literature review addresses the current state of
genetic and epigenetic research on CWP. Genes shape our neural
structures,immunological,endocrinologicalprocesses, and subsequently our behavior and
experiences (Kerr &Burri, 2017). However, this is not just a one-way effect; the environment can
also have an impact on our genes and alter gene expression (epigenetics).There is increasing
evidence that social experiences and contextual factors (eg: stress and abuse) can have long-
lasting effects on an organism by impacting on gene expression and consequently manifesting
themselves in behavioral changes.
References
Belfer, I., Greco, C. M., Lokshin, A., Vulakovich, K., Landsittel, D., Dai, F., … Chelly, J. E.
(2014). The design and methods of genetic studies on acute and chronic postoperative
pain in patients after total knee replacement.?Pain Medicine,?15(9), 1590–1602.
https://doi-org.ezp.waldenulibrary.org/10.1111/pme.12487
Kerr JI, &Burri A. (2017). Genetic and epigenetic epidemiology of chronic widespread
pain.?Journal of Pain Research, Vol Volume 10, Pp 2021-2029 (2017), 2021. Retrieved
from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?
direct=true&db=edsdoj&AN=edsdoj.19490b4bbd49079659018817549433&site=eds-
live&scope=site
WEEK 6
Week 6 discussion
Respiratory System
Main Post
Respiratory Alterations in Children
It is essentialfor a healthcare practitioner to fully understand the pathophysiology of
respiratory disorders in order to appropriately diagnose and treat their patients. For the sake of
this discussion, I am going to describe the disorder and the underlying respiratory alteration
associated with the type of cough in scenario two. Then, I am going to explain the
pathophysiology of the respiratory alteration. Lastly, I am going to explain how the factors of
gender and genetics might impact the disorder.
The second scenario for this week’s discussion, Kevin is a 6-year-old boy who is brought
in for evaluation by his parents.?The parents are concerned that he has a really deep cough that he
just can’t seem to get over. The parents are concerned that about a week ago, Kevin developed a
profound cough that is deep and sounds like he’s barking. Kevin also has occasional vomiting
with productive cough. Additionally, his symptoms also include a low-grade temperature.
The symptoms the 6 years old has are of croup. According to Huether& McCance (2017),
croup is an acute laryngotracheitis and almost always occurs in children between 6 months and 5
years of age. In the case of Kevin, I believe he has a diagnosis of spasmodic croup since
spasmodic croup occurs mainly in older children (Huether& McCance, 2017). The clinical
manifestations of croup are rhinorrhea, sore throat, and low-grade fever for a few days, and then
develop a harsh barking cough, inspiratory stridor, and hoarse voice (Huether&McCance, 2017).
Although Kevin was up to date with his vaccines, some of the causes of croup can be viral, such
as RSV, rhinovirus, adenovirus, rubella virus, or atypical bacteria (Huether& McCance, 2017).
The Pathophysiology of Croup
Croup is a respiratory illness characterized by inspiratory stridor, cough, and hoarseness.
These symptoms result from inflammation in the larynx and subglottic airway. The viruses that
cause croup typically infect the nasal and pharyngeal mucosal epithelia initially and then spread
locally along the respiratory epithelium to the larynx and trachea.A barking cough is the
hallmark of croup among infants and young children, whereas hoarseness predominates in older
children and adults. Although croup usually is a mild and self-limited illness, significant upper
airway obstruction, respiratory distress, and, rarely, death, can occur.
According to Huether& McCance (2017), the pathophysiology of viral croup is caused
primarily by subglottic inflammation and edema from the infection. The mucous membranes of
the larynx are tightly adherent to the underlying cartilage, whereas those of the subglottic space
are looser and thus allow accumulation of mucosal and sub-mucosal edema (Huether&
McCance, 2017). Spasmodic croup also causes obstruction but with less inflammation and
edema; an increased resistance to airflow leads to increased work of breathing that generates
more negative intra-thoracic pressure that, in turn, may exacerbate dynamic collapse of the upper
airway (Huether& McCance, 2017).
The Factors of Gender & Genetics
Genetics plays a role in the development of croup disease.ccording to Huether&
McCance (2017), approximately 15% of affected children have a strong family history of croup.
Another study performed by Pruikkonen, Dunder, Renko, Pokka, &Uhari (2009), also confirmed
that a family history of croup among the siblings and parents of the index cases was the most
important risk factor for croup and its recurrence.
As far is gender is concerned, croup is most common in boys than girls (Rennie et al.,
2013).
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Pruikkonen, H., Dunder, T., Renko, M., Pokka, T., &Uhari, M. (2009). Risk factors for croup in
children with recurrent respiratory infections: a case-control study.?Paediatric And
Perinatal Epidemiology,?23(2), 153-159. doi:10.1111/j.1365-3016.2008.00986.x
Rennie, D. C., Karunanayake, C. P., Chen, Y., Nakagawa, K., Pahwa, P., Senthilselvan, A.,
&Dosman, J. A. (2013). CD14 gene variants and their importance for childhood croup,
atopy, and asthma.?Disease Markers,?35(6), 765-771. doi:10.1155/2013/434920
Week 6 Discussion
Response #1
The symptoms of acute bronchitis are due to acute inflammation of the bronchial wall, which
causes increased mucus production along with edema of the bronchus. This leads to the
productive cough that is the hallmark of a lower respiratory tract infection. In acute
bronchitis,smaller air\way consolidation and infiltrates are absent normally seen in pneumonia
(Blush, 2013).
While the infection may clear in several days, repair of the bronchial wall may take
several weeks. During the period of repair, patients will continue to cough. Pulmonary function
studies of patients with acute bronchitis demonstrate bronchial obstruction similar to that in
asthma. As the symptoms of acute bronchitis abate, pulmonary function returns to normal.
Half of all patients with acute bronchitis continue to cough for more than 2 weeks.?In a quarter of
patients, cough may last for more than 1 month. Cough is the cardinal symptom in patients
presenting with acute bronchitis. By definition, the cough lasts at least 5 days, although, in most
patients, it persists for 1 to 3 weeks, with a median duration of 18 days. For most patients with
acute bronchitis, symptoms are self-limited, resolving in about one to three weeks. Reassurance
and symptom control are the cornerstones of care. Antibiotics are not recommended for routine
use.Most cases of acute bronchitis are viral infections. However, there is insufficient evidence to
support the use of antibiotics to treat acute bronchitis in the general adult population and the
potential adverse effects of antibiotics should be considered when making treatment decisions
(Tanner &Roddis, 2018).
The most common viruses implicated in acute bronchitis are the same as those that cause
URIs and include coronavirus, rhinovirus, respiratory syncytial virus, and adenovirus. In some
younger populations of military recruits and college students, other pathogens such as?Chlamydia
pneumoniae?and?Mycoplasma pneumoniae?have been isolated from patients with acute
bronchitis. However, these pathogens have been identified in only a minority of patients with
acute bronchitis, and it is unclear if these agents are involved in causing the symptoms.
Several medications or environmental exposures can also cause acute cough. These
include the use of ACE inhibitors or occupational exposures to dusts or chemicals. In many of
these cases, such as ACE inhibitor use, the cough is nonproductive. In occupational exposures,
symptoms are generally restricted to the cough, without any other systemic symptoms such as
fever, headaches, or lethargy.
References
Blush, R. R., III. (2013). Acute bronchitis: evaluation and management.?The Nurse Practitioner,
(10), 14. Retrieved from
https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?
direct=true&db=edsgea&AN=edsgcl.346810673&site=eds-live&scope=site
Tanner, M., &Roddis, J. K. (2018). Antibiotics for acute bronchitis.?Nursing Standard,?32(27),
41–43. https://doi-org.ezp.waldenulibrary.org/10.7748/ns.2018.e11123
WEEK 4
NURS 6501
Week 4 Discussion
Initial post
Cardiovascular diseases combine many diseases that affect the heart, responsible for
pumping blood in the circulation. It is the leading cause of morbidity and mortality in the United
States (National Institute of Health, 2016). The cardiovascular disease chosen for the current
week discussion is Myocardial Infarction (MI). The pathophysiology, behavior, and delineated
on how it can confer the pathogenesis would be analyzed. Myocardial Infarction otherwise
called, a heartattack is the death of heart muscle because of prolonged oxygen deficiency
(Hammer & McPhee, 2014). The occluding blockage is typical because of ulceration or rupture
and thrombosis of wabbly plaque from atherosclerosis and is a combination of proteins,
cholesterol, fat, calcium,and white blood cells (Huether, & McCance, 2017). Additional causes
of ischemia and possible infarction are because of reduced blood flow and oxygen, for example,
anemia, coronary spam, dysrhythmia, hypotension, and hypoxemia (Huether, & McCance,
2017). And the impacts of dyslipidemia will as well be analyzed and discussed on how it could
prompt a Myocardial Infarction.
Pathophysiology of Myocardial Infarction
At the point when there is a deficiency of blood flow in the body, it causes a myocardial
infarction (American Heart Association, 2018). There are two categories of Myocardial
Infarction, for example, STEMI: A mutual name for ST-elevation myocardial infarction, a type
of heart attack caused by a complete blockage in a coronary artery. NSTEMI: A non-ST-elevated
myocardial infarction, a kind of heart attack in which an artery is partially blocked and severely
reduces blood flow (American Heart Association, 2012).
When someone has a Myocardial Infarction, numerous changes start happening within the cells
and myocardium. Anaerobic metabolism starts and supplies just sixty-five percent of glycolysis
while adenosine triphosphate is being less produced. The body begins to go into an acidotic
state,and the myocardial tissues are also compromised. Alongside a diminished oxygen supply,
the cells start to go into a condition of electrolyte imbalances with a reduction in calcium,
potassium, and magnesium. The directing capacity of the heart is additionally compromised and
loses contractility. Ischemia results from the myocardium and makes the cells discharge
catecholamines causing dysrhythmias and heart failure. Free unsaturated fats ascend within one
hour which could likewise detrimentally affect the cells. Additional damaged results in
reperfusion damage because of the release of free radicals and calcium flux. Apoptosis happens
following twenty minutes and results in the release of creatinine phosphokinase (CPK-MB) and
troponins inside the circulatory system. The inflammatory response is activated thru a
Myocardial Infarction and results in a repair process causing proliferation of fibroblasts,
degradation, and formation of scar tissue (Huether& McCance, 2017).
Behavior and Dyslipidemia
Human behavior assumes a role in health maintenance. Preventive measures for changing
behaviors could incredibly decrease cardiovascular disorders. The most widely recognized
reason for a Myocardial Infarction is atherosclerosis (Shenoy, Shenoy, & Rao, 2015).
Atherosclerosis is when fatty deposits clog arteries. These deposits are comprised of cholesterol,
fatty substances, cellular waste products, calcium and a clotting material in the blood.
As plaque builds up, the wall of the blood vessel thickens. This constricts the channel
within the artery, which decreases the flow of blood. That, sequentially, decreases the amount of
oxygen and other nutrients reaching the body (American Heart Association, 2012).
Atherosclerosis is hastened when someone eats a diet high in fat, use tobacco and lives an
inactive way of life (Pratico, Patterson, & Wang, 2015). One main causative factor of
atherosclerosis is dyslipidemia. Dyslipidemia is a disorder of the lipoprotein metabolism. It
shows by an intensification in total serum cholesterol, low-density lipoprotein cholesterol,
triglyceride concentrations, with a reduction in high-density lipoprotein cholesterol
concentration. Dyslipidemia assumes a crucial role in the development of cardiovascular
disorders (Shenoy et al., 2015).
Reference
American Heart Association. (2018). About heart attacks. Retrieved from
http://www.heart.org/HEARTORG/Conditions/HeartAttack/AboutHeartAttacks/About-
Heart-Attacks_UCM_002038_Article.jsp#.Wbrn48h95PY
Hammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical
medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
National Institute of Health, MedlinePlus. (2016). Heart diseases. Retrieved from
https://medlineplus.gov/heartdiseases.html
Pratico, D., Patterson, C., & Wang, H. (2015). Atherosclerosis: Risks, mechanisms, and
therapies. Retrieved from Walden University Library databases
Shenoy, C., Shenoy, M. M., & Rao, G. K. (2015). Dyslipidemia in dermatological disorders.
North American Journal of Medical Sciences, 7(10), 421–428.
http://doi.org/10.4103/1947-2714.16865743
Week 4
Response #1
Great post Kemi
Although any one person suffering from heart disease has an increased chance of dying
compared to any other cause, certain racial groups are at a greater risk than others. These differences
appear to be correlated with an increase incidence in elevated blood pressure, diabetes and obesity
compared to white Americans. Genetic differences do exist (Harvard Health Publishing, 2015).
In the United States, nearly half of all black adults have some form of cardiovascular disease,
compared with about one-third of all white adults. It is believed that individuals who lived in equatorial
Africa developed a genetic predisposition to being salt sensitive. This means that their bodies are able
to retain more sodium than others. When an individual retains salt, blood volume increases, which in
turn raises blood pressure. This salt sensitivity allowed for their bodies to conserve water which was
beneficial in the hot and dry climate that they lived in. Even generations later, their decedents
remained disproportionately salt sensitive.
References
Harvard Health Publishing. (2015). Race and ethnicity: Clues to your heart disease risk?
HarvardHealth Letter. Retrieved from https://www.health.harvard.edu/heart-health/race-and-
ethnicity-clues-to-your-heart-disease-risk
Inamdar, A. A., & Inamdar, A. C. (2016). Heart Failure: Diagnosis, Management andUtilization. Journal
of Clinical Medicine, 5(7), 62. http://doi.org/10.3390/jcm5070062
Week 4
Response # 2
Factor genetic in peripheral artery disease
Christina, nice post,
Peripheral artery disease (PAD) is a complex disorder and is attributed to multiple risk
factors such as age, smoking, diabetes mellitus, dyslipidemia, and hypertension (Shimamura et
al., 2013). Certain genetic markers may predispose to the development or progression of PAD.
Some earlier studies indicate a genetic component for development of PAD.?A genetic marker
for PAD can identify individuals at risk for PAD, or those with PAD at risk for poorer outcomes.
In addition, genetic determinants of PAD may also uncover key molecules/pathways implicated
in the pathogenesis of PAD, thereby identifying new therapeutic targets for more definitive
therapies (Hazarika & Annex, 2017). Peripheral artery diseases (PAD), ischemic stroke, and
coronary artery diseases refer to arterial stenosis caused by atherosclerosis and thrombosis.
Critical limb ischemia (CLI) is a complication of PAD and causes pain on walking
(claudication), pain at rest, and nonhealing ulcers. Although patients with CLI are treated with a
combination of risk factor modification, such as statins, antiplatelet drugs, and angioplasty, these
treatments are occasionally insufficient to recover sufficient blood flow to maintain normal tissue
function.
References
Hazarika, S., & Annex, B. H. (2017). Biomarkers and Genetics in Peripheral Artery
Disease.?Clinical Chemistry, (1), 236.
https://doi-org.ezp.waldenulibrary.org/10.1373/clinchem.2016.263798
Lung-An Hsu, Semon Wu, Jyh-Ming Jimmy Juang, Fu-Tien Chiang, Ming-Sheng Teng, Jeng-
Feng Lin, … Yu-Lin Ko. (2017). Growth Differentiation Factor 15 May Predict Mortality
of Peripheral and Coronary Artery Diseases and Correlate with Their Risk
Factors.?Mediators of Inflammation, Vol 2017 (2017). https://doi-
org.ezp.waldenulibrary.org/10.1155/2017/9398401
Shimamura, M., Nakagami, H., Koriyama, H., &Morishita, R. (2013). Gene therapy and cell-
based therapies for therapeutic angiogenesis in peripheral artery disease.?Biomed
Research International,?2013, 186215.
https://doi-org.ezp.waldenulibrary.org/10.1155/2013/186215
WEEK 5
NURS 6501
Week 5
Discussion 1
Main post
Heart Murmurs
A hearth murmur is an extra sound that MD and nurses hear when they listen to the heath
with a stethoscope. Normal heartbeat sound is made as the heart valves open as blood flows
through the heart. The heart valves are structures that keep blood flowing in only one direction.
The heart murmur happens when the sounds of the blood flowing through the heart or blood
vessels is loud enough to be heard. On the other side, some heart murmurs are abnormal, they are
caused by a heart condition. Common causes of abnormal heart murmur are the following:
The heart valves can leak too much and let blood flow backward, or they can get stuck and not
open well.
Heart problems that people are born with, such as a hole inside the whole of the heart.
Diagnosis
Differential diagnosis is needed to definitely find out if the heart murmur is innocent or
abnormal. Heart murmurs occur due to turbulence in blood flow which is caused by passing of
high velocity blood from a narrow cross-section (Khalilian et al., 2016). The most common test
used for diagnosis is echocardiogram, which uses sound waves to create a picture of the heart as
it beats. It shows the size of the heart chamber, how well the heart is pumping, and how well the
valves are working. But Echocardiography is the key to detection but it remains a relatively
scarce resource (Draper & Chambers, 2016).?
To check whether the murmurs are innocent or abnormal, the following questions are
answered:
How loud is the murmur? This is rated on the scale from 1-6, 6 being the loudest.
Where in the heart is the murmur located? Can it be heard on the neck or back?
What is the pitch? Low, medium, or high?
Does the exercise or body position affect the sound?
When does it occur? For how long?
Additional tests are the following: Chest X-Ray, echocardiogram, cardiac catheterization.
Treatment
If the murmur is serious, the treatment might involve surgery; if not, the condition will be
monitored. If it gets worse, a treatment will be done.
Medications
Anticoagulants such as aspirin, coumadin, clopidogrel.
Water pills such as Lasix.
Statins, to help lower blood cholesterol.
Beta blockers
Surgery
Valve repair
Balloon valuloplasty, performed to relieve a narrowed valve
Annuloplasty, tightening the tissue around the valve by implanting an artificial ring
Valve leaflet repair
Valve replacement
Open-heart surgery
Transcatheter aortic valve replacement
Behavior factor and heart murmur
Having high cholesterol seems to worsen some heart valve problems, including some heart
murmurs.
References
Draper, J., & Chambers, J. (2016). Detecting heart valve disease: can we do better??The British
Journal Of General Practice: The Journal Of The Royal College Of General
Practitioners,?66(644), 156–157.
https://doi-org.ezp.waldenulibrary.org/10.3399/bjgp16X684181
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Khalilian, M. R., Malekian, A., Aramesh, M. R., Dehdashtian, M., & Maryam, T. (2016).
Innocent versus Pathologic Murmurs: A Challenge of Neonatal Examination.?Journal of
Clinical Neonatology,?5(3), 174. Retrieved from https://ezp.waldenulibrary.org/login?
url=https://search.ebscohost.com/login.aspx?
direct=true&db=edb&AN=119017073&site=eds-live&scope=site
NURS 6501
Week 5
Discussion 2
Main post
Anaphylactic shock
Anaphylaxis is an acute, potentially lethal multisystem syndrome resulting from the
sudden release of mast cells and basophil-derived mediators into the circulation. Anaphylactic
shock begins with exposure of a sensitized individual to an allergen. It most often results from
immunologic reactions to foods, medications, and insects’ stings, although it can also be induced
through nonimmunologic mechanisms by any agent capable of producing a sudden, systemic
degranulation of mast cells or basophils.
The lifetime prevalence of anaphylaxis is 0.5 – 2% (Heuther, 2017, p.644). The basic
physiology alteration are vasodilation and relative hypovolemia, leading to decrease tissue
perfusion and impaired cellular metabolism. Anaphylactic shock is characterized by other effects
that rapidly involve the entire body. Common allergens known to cause these reactions are insect
venoms, shellfish, peanut, latex, and medication such as penicillin.
The onset of anaphylactic shock is usually sudden and death can occur very quick, within
minutes, unless emergency rescue medication is given. The primary clinical manifestations of
anaphylaxis include anxiety, dizziness, difficulty breathing, stridor, wheezing, pruritis with hives
(urticaria), swollen lips and tongue, and abdominal cramping; a rapid fall in blood pressure
occurs, followed by impaired mentation. Other signs include systemic vascular resistance, with
high or normal cardiac output, and oliguria. The diagnosis can be confirmed by a number of
serum markers such as plasma histamine and tryptase. Treatment begins with removal of antigen
if possible. Epinephrine is then administered IM to cause vasoconstriction and reverse airway
constriction, supplementation by high dose corticosteroids, antihistamines, intravenous fluids,
airway management.
Outpatient – based of anaphylaxis
Educate staff and patients
Prepare anaphylaxis emergency cart
Develop an office action plan for anaphylaxis management to maintain proficiency
At the onset of the anaphylaxis:
Administer epinephrine intramuscularly in the mid-outer thigh
Remove the itching allergen if possible
Quickly assess airway-Breathing-Circulation, and mentation
Start if needed, cardiopulmonary resuscitation
After administering epinephrine, notify EMS for patient having severe anaphylaxis and
/or patients not responding to epinephrine.
After administration of epinephrine, maintain patients on supine position and pregnant women
on the left side to maintain hemodynamic circulation.
Emergency care for anaphylaxis
Patients will be sent for Emergency care if not responding to IM epinephrine treatment.
Factor gender and anaphylactic shock
Sex steroid hormones, primarily estrogens, have been suggested to be
responsible for the sex- dependent differences in the prevalence and clinical
pictures of allergic diseases, which can be confirmed by the following
observations based on epidemiological studies (Nittner-Marszalska, Liebhart, &Dor-
Wojnarowska, n.d., p.187). Some studies have shown slight female predominance. Episodes of
anaphylaxis to IV muscle relaxants, aspirin, and latex are more common in women, whereas
insects sting anaphylaxis is more common in men. These sex discrepancies are likely a function
of exposure frequency. a survey reporting on severe allergic reactions defined by the necessity of
medical care showed a higher incidence of food allergy in females (Just et al., n.d., p.1603).
References
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Just, J., Elegbede, C. F., Deschildre, A., Bousquet, J., Moneret-Vautrin, D. A., Crepet, A., &
Mirabel Study Grp. (n.d.). Three peanut-allergic/sensitized phenotypes with gender
difference.?CLINICAL AND EXPERIMENTAL ALLERGY,?46(12), 1596–1604.
https://doi-org.ezp.waldenulibrary.org/10.1111/cea.12791
Nittner-Marszalska, M., Liebhart, J., &Dor-Wojnarowska, A. (n.d.). Sex-related clinical aspects
in insect venom anaphylaxis.?INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY
AND PHARMACOLOGY,?28(2), 187–193.
https://doi-org.ezp.waldenulibrary.org/10.1177/0394632015586143
Week 5
Discussion #1
Response #1
In controversy to other studies, low socio-cultural level is associated to a higher risk for
pathological heart murmur. This may be related to consanguinity and exposure to environmental
risk factors in these categories. There are 7 variables that proved their implication as risk factors
for pathological heart murmur: Age<1 years old, North region, Consanguinity, Family History of
CHD, low socio-economic status, presence of other malformations and associated symptoms
leading the diagnosis of murmur (Insight Medical Publishing, n.d.). Living in the North of
Lebanon seems to be a major factor for pathological heart murmurs. This is mainly due to high
rate of consanguinity, low socio-economic and cultural levels and family history of CHD,
present in this region.
Taking certain medications or illegal drugs during pregnancy.?Use of certain medications,
alcohol or drugs can harm a developing baby, leading to heart defects (Mayo Clinic, n.d.).
References
Heart Murmur among Lebanese Children: A Retrospective Study to Evaluate Epidemiological
Features and Risk Factors | Insight Medical Publishing. (n.d.). Retrieved from
http://pediatric-cardiology.imedpub.com/heart-murmur-among-lebanese-children-a-
retrospective-study-to-evaluate-epidemiological-features-and-risk-factors.php?aid=17406
Heart murmurs - Symptoms and causes - Mayo Clinic. (n.d.). Retrieved from
https://www.mayoclinic.org/diseases-conditions/heart-murmurs/symptoms-causes/syc-
20373171
Week 5
Discussion # 1
Response #2
Genetics seem to play a major risk factor for pathological heart murmur (HM). Both
consanguinity and family history of CHD reflect a higher risk for pathological HM: in
consanguine marriages 75.5% of the children with heart murmur seem to have a CHD while
81.5% of children with a family history of CHD also have a pathological HM(Insight Medical
Publishing, n.d.). While reviewing literature, consanguinity was incriminated as risk factor due
to hereditary transmission of some CHD. For example, there is an autosomal dominant
transmission for some polymalformative syndrome associated with birth defect and family
history of CHD is thereby also a risk factor. Furthermore, we have only determined 10% of CHD
etiologies, hereditary factors account of 3% of all identified causes. Nevertheless, 90% of
undetermined etiologies are probably due to more genetic factors not yet established(Insight
Medical Publishing, n.d.).
Atrial septal defect (ASD) is anatomically characterized by a defective interatrial
septum, which allows communication between the left and right sides of the heart. ASD
represents 30 to 40% of congenital heart defects (CHDs) and is the third most common type
of CHD (Ruo-Hao et al., 2018). Most ASD is sporadic with no specific cause and often
encountered in genetic syndromes such as Noonan syndrome, Holt-Oram syndrome, and
Down’s syndrome (Ruo-Hao et al., 2018).
References
Heart Murmur among Lebanese Children: A Retrospective Study to Evaluate Epidemiological
Features and Risk Factors | Insight Medical Publishing. (n.d.). Retrieved from
http://pediatric-cardiology.imedpub.com/heart-murmur-among-lebanese-children-a-
retrospective-study-to-evaluate-epidemiological-features-and-risk-factors.php?aid=17406
Ruo-hao Wu, Dong-fang Li, Wen-ting Tang, Kun-yin Qiu, Yu Li, Xiong-yu Liao, … Luo.
(2018). Atrial septal defect in a patient with congenital disorder of glycosylation type 1a:
a case report.?Journal of Medical Case Reports,?12, 1. Retrieved from
https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?
direct=true&db=edb&AN=127588031&site=eds-live&scope=site
Week 5
Discussion # 2
Response #1
Anaphylaxis and genetics
Allergies and asthma tend to run in families and there is believed to be a genetic
predisposition to them. People with allergies to the common triggers of anaphylaxis are more at
risk.?You could develop anaphylaxis in future exposures to the allergen even if your usual
reaction is mild, such as a rash.?If you previously had an anaphylactic reaction, you are at greater
risk of having one again. Future reactions may be even more severe.People with even mild
asthma are more at risk of severe allergic reactions, including anaphylaxis. If you are allergic to
foods, medications, or insects, you need to take extra precautions if you also have asthma. The
same is true for people with other chronic lung diseases as the respiratory symptoms will be
more severe during anaphylaxis. Poorly-controlled asthma raises the risk that you could die
during anaphylaxis.Mastocytosis is a rare condition that develops due to a mutation in a gene. In
most cases, this mutation happens during the production of mast cells in an individual and is not
inherited or passed on to their children. With mastocytosis,?you have more mast cells, which are
the immune cells that store histamine and other chemicals. These cells can accumulate in the
skin, internal organs, and bones. If triggered by an allergen, you are more at risk of anaphylaxis
because of the number of cells releasing these chemicals. If you have a poorly-controlled
cardiovascular disease you are more at risk of death is you have an episode of anaphylaxis.
People with cardiovascular disease who are taking beta-blockers or alpha-adrenergic blockers are
at further risk if they develop anaphylaxis because those medications reduce the effects of
epinephrine, which is given to stop the anaphylactic reaction. Anaphylaxis treatment with
epinephrine carries more risk for people over age 50 as it can produce heart complications
including atrial fibrillation and myocardial infarction.
In their study, Wang and her colleagues analyzed DNA samples from 2,759 participants
(1,315 children and 1,444 of their biological parents) enrolled in the Chicago Food Allergy
Study. Most of the children had some kind of food allergy. They scanned approximately 1
million genetic markers across the human genome, searching for clues to which genes might
contribute to increased risk of developing food allergies, including peanut. They found that a
genomic region harboring genes such as HLA-DQ and HLA-DR and located on chromosome six
is linked to peanut allergy. ?This study suggests that the HLA-DR and -DQ gene region probably
poses significant genetic risk for peanut allergy as it accounted for about 20 percent of peanut
allergy in the study population.??
References
Anaphylaxis: Causes and Risk Factors. (n.d.). Retrieved from
https://www.verywellhealth.com/anaphylaxis-causes-risk-factors-82703#genetics
Do Genes Play a Role in Peanut Allergies? New Study Suggests Yes - 2015 - News Releases -
News - Johns Hopkins Bloomberg School of Public Health. (n.d.). Retrieved from
https://www.jhsph.edu/news/news-releases/2015/do-genes-play-a-role-in-peanut-
allergies-new-study-suggests-yes.html
Week 5
Discussion # 2
Response # 2
Anaphylaxis and age
The age- specific trend showed a decreasing trend from infants to schoolchildren, a
gradually increasing trend from adolescents to middle ages, and finally a declining trend towards
the older ages (Jeong et al., 2018). The prevalence of anaphylaxis was considerably higher in the
middle-aged groups from 45 to 65 years in each year of the study period (Jeong et al., 2018).
Among children and adolescents up to 18 years, the prevalence of anaphylaxis was markedly
higher in the youngest age group (0–2 years) in each year of the study period (Jeong et al., 2018).
The overall prevalence of anaphylaxis increased by 1.7-fold during the 5 years, with the most
noticeable increment being in young children (Jeong et al., 2018).
The prevalence of emergent anaphylaxis was generally higher in patients in their fifties and
sixties and lower in children and adolescents. However, the increase in the prevalence of
emergent anaphylaxis was greater in young children, specifically those in the 0–2 year and 7–12-
year age groups (Jeong et al., 2018).
The percentage of in- hospital epinephrine administration among anaphylaxis patients was
approximately 10% in 0–6-year-olds, between 25 and 35% in young and middle-aged adults,
and decreased to 17% in those aged 80 years and older ((Jeong et al., 2018). The age group with
the highest average percentage of in- hospital epinephrine administration was 50–59 years.
Compared to 2010, the percentage of in-hospital epinephrine administration in 2014 increased
significantly, particularly in the younger age groups, by 2.5-fold in the 0–2 year and by 2.6-fold
in the 3–6-year age groups (Jeong et al., 2018). The percentage increase was also high in those
aged 75 years and older.
Death from food anaphylaxis remains a rare but tragic event . The majority of fatal food
anaphylaxis involves children and young adults. In most fatal cases there is a combination of
several known risk factors, which often could have been individually mitigated. The purpose of
this review is to highlight known factors that increase the risk for severe allergic reactions to
food and to present, in a practical and visual manner, strategies that can be used to identify and
deal with these factors when taking a history, examining and planning management for
individuals with food allergy.
References
Jeong, K., Lee, J.-D., Kang, D. R., & Lee, S. (2018). A population-based epidemiological study
of anaphylaxis using national big data in Korea: trends in age-specific prevalence and
epinephrine use in 2010-2014.?Allergy, Asthma & Clinical Immunology, (1). https://doi-
org.ezp.waldenulibrary.org/10.1186/s13223-018-0251-z
Risk multipliers for severe food anaphylaxis. (n.d.). Retrieved from
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4657220/
&
Week 6
Week 6 discussion
Response # 2
Great post Meghan
Respiratory syncytial virus (RSV) is a major cause of infectious lower respiratory disease in
infants and the elderly (Johnson et al., 2014). RSV causes seasonal outbreaks throughout the
world. In the northern hemisphere, these usually occur from October or November to April or
May, with a peak in January or February. In the southern hemisphere, wintertime epidemics
occur from May to September, with a peak in May, June, or July. In tropical and semitropical
climates, the seasonal outbreaks usually are associated with the rainy season. The epidemic
peaks are not as sharp as in temperate climates, and in some settings RSV can be isolated in as
many as eight months of the year.In the United States between 1997 and 2006, the annual
average rate of RSV hospitalization among children <5 years of age was 6.7 per 1000 (95% CI
5.3-8.1) (UpToDate, MD). Although the RSV hospitalization rate was greatest among infants <3
months (48.9 per 1000), 42 percent of total hospitalization occurred in children >6 months
(UpToDate, MD).
Hospitalization for RSV infection also may occur in children >5 years, but these children
typically have underlying medical problems (neurologic disease, immunodeficiency, etc).
Children with Down syndrome are at increased risk for severe RSV disease. In addition, studies
evaluating potential genetic predisposition to severe RSV disease have revealed associations
with polymorphisms in cytokine- and chemokine-related genes including interleukin (IL)-4 and
its receptor, IL-8, IL-10, IL-13, and chemokine receptor (CCR)5 (UpToDate, MD). Genetic
polymorphisms in genes related to potential virus-cell surface interactions or cell signaling such
as toll-like receptor (TL)-4, chemokine receptor 1 (CX3CR1), surfactant protein (SP)-A, and SP-
D also have been associated with severe RSV disease.
References
Johnson, T. R., Rangel, D., Graham, B. S., Brough, D. E., & Gall, J. G. (2014). Original Article:
Genetic Vaccine for Respiratory Syncytial Virus Provides Protection Without Disease
Potentiation.?Molecular Therapy,?22, 196–205.
https://doi-org.ezp.waldenulibrary.org/10.1038/mt.2013.142
UpToDate. (n.d.). Retrieved from https://www.uptodate.com/contents/respiratory-syncytial-
virus-infection-clinical-features-and-diagnosis/print
WEEK 8
NURS 6501
Week 8
Main post
Inflammatory bowel diseases
Irritable bowel diseases (IBD) are classified into 2 categories, Crohn’s Disease (CD) and
Ulcerative Colitis (UC). Pathologically, CD and UC share comparable indications, comprising of
diarrhea, hematochezia, and abdominal pain, though the location and depth of inflammation, as
well as impediments and occurrence can vary (Kim &Cheon, 2017).
Pathophysiology
Crohn’s Disease
Current theories about the pathophysiology of Crohn’s Disease (CD) indicate a role for
infectious, immunologic, environmental, dietary, and psychosocial factors in a genetically and
immunologically susceptible person.The initial lesion starts as an inflammatory infiltrate around
intestinal crypts that subsequently develops into ulceration of the superficial mucosa. The
inflammation progresses to involve deeper layers and forms noncaseating granulomas. These
granulomas involve all layers of the intestinal wall and the mesentery and regional lymph nodes.
The finding of these granulomas is highly suggestive of CD, yet their absence does not exclude
the diagnosis.Early endoscopic findings include hyperemia and edema of the inflamed mucosa.
This progresses to discrete deep ulcers located transversely and longitudinally, creating a
cobblestone appearance. These lesions are separated by healthy areas known as skip lesions. CD
affects the large intestine as well as small intestine.IBD is distinguished from infectious disease
processes by recurrent episodes of mucopurulent bloody diarrhea that lacks positive cultures for
known microbial pathogens and failure to react to antibiotics only (Hammer & McPhee, 2014).
The clinical presentation of CD and the order of investigations performed varies based on the
involved part of the gastrointestinal (GI) tract, the degree of inflammation, and presence of
complications. CD may involve any portion of the GI tract from mouth to perianal area. The
diagnosis of CD is suggested by a typical history supported by physical findings, especially
perianal involvement.Patients present with a constellation of abdominal findings including right
lower quadrant abdominal tenderness, and palpable abdominal mass. In addition, oral inspection
for ulcers; perineal inspection for perianal skin tags, fistulae, abscesses, and sinus tracts; and
digital rectal examination for occult blood and exclusion of a mass should be performed.?
Treatment choices are influenced by:5
Patient age
Site and activity of disease (CD is a highly heterogeneous disease with many different
phenotypes, such as ileocecal, colonic, upper gastrointestinal [GI], perianal disease)
Behavior of the disease
Previous drug tolerance and response to treatment
Previous relapses on treatment
The presence of extraintestinal manifestations.
Surgical treatment is appropriate for:5
Neoplastic or preneoplastic lesions
Obstructing stenoses
Suppurative complications
Fistulizing disease
Medically intractable disease.
Symptomatic therapy
Symptomatic treatment includes managing diarrhea, abdominal pain, and malabsorption.
Antidiarrheal agents should be avoided in patients with active colitis, given the risk of
developing toxic megacolon. Abdominal cramps can be effectively treated with oral
antispasmodics.
Patients with terminal ilea disease develop secretory diarrhea due to inability to absorb bile
acids. Bile acid sequestrants are helpful in this situation.
Ulcerative colitis
Macroscopically, most cases of ulcerative colitis (UC) arise in the rectum, with some
patients developing terminal ileitis (i.e., extending up to 30 cm) due to an incompetent ileocecal
valve or backwash ileitis. The bowel wall is thin or of normal thickness, but the presence of
edema, the accumulation of fat, and hypertrophy of the muscle layer may give the impression of
a thickened bowel wall. The term "proctitis" is used when the inflammation is limited to the
rectum.Microscopically, UC usually involves only the mucosa, with the formation of crypt
abscesses and a coexisting depletion of goblet cell mucin. In severe cases, the submucosa can be
involved, and in some cases, the deeper muscular layers of the colonic wall can also be affected.
Further microscopic changes include inflammation of the crypts of Lieberkuhn and abscesses.
Ulcerated areas are soon covered by granulation tissue. The undermining of mucosa and the
excesses of granulation tissue form polypoidal mucosal excrescences, known as inflammatory
polyps or pseudopolyps.?
Early disease manifests as bleeding, petechial hemorrhages, and hemorrhagic
inflammation with loss of the normal vascular pattern. Edema is present, and large areas become
denuded of mucosa. Undermining of the mucosa leads to the formation of crypt abscesses, which
are the hallmark of the disease.
Acute severe colitis can result in a fulminant colitis or toxic megacolon, which is characterized
by a thin-walled, dilated colon that can eventually become perforated.
Treatments
UC can be classified both by severity and by extent.?Treatment is guided by both factors.
Distal disease (proctitis and left-sided disease, below splenic flexure) is generally amenable to
topical therapies. Extensive disease (pancolitis, beyond splenic flexure) requires systemic
therapy. Treatment differs also between management of acute flare-ups (severe or fulminant
disease) and maintenance of remission (mild-to-moderate disease). Fulminant disease is
managed as an emergency to prevent life-threatening complications such as toxic megacolon and
perforation.
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is a practical bowel disorder described as a chronic or
recurring abdominal pain associated with relief or exacerbation by excretion, or change in bowel
routine (Holtmann, Ford, Talley, 2016). Most patients can be categorized, conferring to the
prevalent stool pattern they have, into IBS with diarrhea, IBS with constipation, and those who
have both diarrhea and constipation, known as mixed-stool-pattern IBS (Holtmann, Ford, Talley,
2016). IBS is one of the most extensively recognized functional bowel disorders, with more than
“10%” of the worldwide adult populace reporting signs well-matched with the condition in
population-based surveys (Holtmann, Ford, Talley, 2016). In clinical practice, a diagnosis of IBS
is made on the basis of typical symptoms and the use of investigations is often constrained to a
particular panel of tests that help to omit known organic diseases that present with comparable
symptoms, such as inflammatory bowel disease or coeliac disease (Holtmann, Ford, Talley,
2016).
IBS is the most common cause of referral to the gastroenterologist, although it has an
unknown pathophysiology and no specific biomarkers, there are multiple theories to explain the
disorder; such theories include visceral hypersensitivity, abnormal gastrointestinal permeability,
motility, and secretion; post inflammatory, alteration in gut microbiota, food allergy or
intolerance, and psychosocial factors (Huether& McCance, 2017).
Similarities & Differences
There are several comparisons and variances when discoursing IBD and IBS. IBS is
categorized by a disordered gut-brain axis, but can progress following an enteric infection, and is
linked with tenacious immune activation that is a feature of IBD (Rani, Ali, & Lee, 2016).
Likewise, IBD, which includes CD and UC, is branded by chronic deteriorating inflammation
and immune activation; yet, new evidence also points to altered gut microbiota and disturbed
psychology, which are features of IBS, being important, both in the development and
maintenance of the disease (Rani, Ali, & Lee, 2016). Apart from similarities in symptoms and
signs, there are several other pathophysiological similarities between IBD and IBS. These can be
generally considered in four main sections, comprising of the brain-gut axis, genetic factors,
microbiota, and the epithelial barrier, among others (Rani, Ali, & Lee, 2016).
Distinguished variances were also seen amid IBD and IBS, some are as follows: In IBD, mucosal
inflammation is usually ongoing and slow to resolve, even in clinically asymptomatic patients.
IBD in diminution still displays a higher level of TNF-α and intraepithelial lymphocytes likened
to IBS patients (Rani, Ali, & Lee, 2016). In dissimilarity, IBS patients manage to display low
grade, alterable, or even vague mucosal inflammation (Rani, Ali, & Lee, 2016). Essentially, IBD
is an organic disease, as evidenced by mucosal inflammation, whereas IBS lies more in the
spectrum of a functional disorder, with no evidence of organic disease (Rani, Ali, & Lee, 2016).
Also, with fecal calprotectin it is possibly simpler to differentiate between IBD, IBS, with its
low-grade inflammation (Rani, Ali, & Lee, 2016).
Age Factor
Nearly “60,000” different cases of IBD are identified annually and the uppermost rates of
IBS are seen in individuals who are in middle adulthood, younger than 45 (Crohn’s & Colitis
Foundation of America, 2014). IBD can happen at any age, but is normally diagnosed in
individuals between the ages of 15 and 35 (Huether& McCance, 2017). Both forms of IBD affect
young adults, with disease onset frequently happening between ages 15 and 30 years, and less
frequently between 50 and 70 years of age for ulcerative colitis (Crohn’s & Colitis Foundation of
America, 2014). Crohn’s disease is diagnosed most commonly in people from most commonly
20 to 30 years of age; It does not discriminate between men and women as it affects them
similarly (Crohn’s & Colitis Foundation of America, 2014).
IBS appears to be more predominant in women than men and more common in those
with a family history of IBS. There are studies that propose there is a psychological factor, such
as anxiety and depression that can increase one’s risk for development of this disorder
(Huether& McCance, 2017). Irrespective of the disease all are unsettling to the individual’s
lifestyle. Health care providers should be mindful that in order to effectively treat these
conditions, they must comprehend the similarities and differences to correctly treat the patient.
References
Crohn’s & Colitis Foundation of America. (2014). Inflammatory bowel disease and irritable
bowel syndrome. Retrieved from http://www.crohnscolitisfoundation.org/assets/pdfs/ibd-
and-irritable-bowel.pdf
Hammer, G. D., & McPhee, S. J. (2014). Pathophysiology of disease: An introduction to clinical
medicine (7th ed.). New York, NY: McGraw-Hill Medical.
Holtmann, G., Ford, A.C., & Talley, N. (2016). Pathophysiology of irritable bowel syndrome.
The Lancet Gastroenterology and Hepatology, 1(2),133–146. doi:
https://doi.org/10.1016/s2468-1253(16)30023-1.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Kim, D. H., &Cheon, J. H. (2017). Pathogenesis of inflammatory bowel disease and Recent
Advances in biologic therapies. Journal of Immune Network, 17(1),25–40. doi:
10.4110/in.2017.17.1.25
Rani, R. A., Ali, R. A., & Lee, Y. Y. (2016). Irritable bowel syndrome and inflammatory bowel
disease overlap syndrome: pieces of the puzzle are falling into place. Intestinal Research
Journal, 14(4), 297–304. https://doi.org/10.5217/ir.2016.14.4.297
NURS 6501
Week 8
Response # 1
As environmental conditions, in contrast to genetic risk factors, can be influenced,
knowledge on those risk factors becomes crucial to modulate disease incidence, disease course or
clinical presentation. It is obvious that prevention of environmentally triggered disease flares
would be a goal most relevant for IBD patients (Gerhard et al., 2016).
Studying the relationship between environmental factors and IBD may provide the missing link
to increasing our understanding of the etiology and increased incidence of IBD in recent years
with implications for prevention, diagnosis, and treatment. Environmental factors are
heterogeneous and genetic predisposition, immune dysregulation, or dysbiosis do not lead to the
development of IBD in isolation.
Cigarette smoking is the earliest environmental risk factor that has been consistently
shown to be associated with IBD. The mechanism by which smoking exerts its effect in IBD is
poorly understood. However, putative mechanisms by which smoking modulates the immune
system in UC may involve the reduction in tumor necrosis factor (TNF alpha) production?via?the
action of nicotine on the nicotinic acetylcholine receptor a7 subunit, increased production IL-10
in response to carbon monoxide in cigarette smoke, increased mucin synthesis, decrease in IL-8
expression, hypoperfusion of the rectum and acutely damaged colonic tissue. In CD, increased
carbon monoxide from cigarette smoke may cause impairment in vasodilation capacity in
chronically inflamed micro vessels, resulting in ischemia, and perpetuating ulceration and
fibrosis. Decreased total radical-trapping antioxidant potential and abnormalities of the
microvasculature, and a defect in bacterial clearance or macrophage deficiency may also play a
role.
If you live in an industrialized country, you're more likely to develop IBD. Therefore, it
may be that environmental factors, including a diet high in fat or refined foods, play a role.
People living in northern climates also seem to be at greater risk (Mayo Clinic(n.d.).
Diet?Recommendations for Crohn's Disease Flare. Follow a low residue?diet?to relieve abdominal
pain and diarrhea. If you have strictures, it is especially important to avoid nuts, seeds, beans and
kernels. Avoid foods that may increase stool output such as fresh fruits and vegetables, prunes
and caffeinated beverages.
Foods to Avoid in an IBD Diet
Fatty, fried foods.
Spicy foods.
Meats.
Creamy sauces.
High-fiber foods including raw fruits and vegetables.
Nuts, seeds, and beans.
Caffeinated beverages.
Sweets including candy, soda, and juice.
References
Evidence based literature review. (n.d.).Environmental risk factors for inflammatory bowel
diseases: Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4945988/
Mayo Clinic(n.d.). Inflammatory bowel disease (IBD) - Symptoms and causes - Retrieved from
https://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/symptoms-
causes/syc-20353315
Rogler, G., Zeitz, J., &Biedermann, L. (2016). The Search for Causative Environmental Factors in Inflammatory
Bowel Disease.?Digestive Diseases (Basel, Switzerland),?34 Suppl 1, 48–55. https://doi-
org.ezp.waldenulibrary.org/10.1159/000447283
NURS 6501
Week 8
Response #2
Inflammatory bowel disease (IBD) has predominantly affected whites, particularly
Ashkenazi Jews. Over the last 2 decades, IBD has "emerged" in minorities. Inflammatory bowel
disease (IBD) is now increasingly recognized in diverse ethnic populations. In the United States,
IBD among the minority populations, especially Mexican Americans, has not been extensively
studied. Apart from the known genetic influences that differ among the IBD subtypes [ulcerative
colitis (UC) vs. Crohn's disease (CD)], serologic markers may differentiate UC and CD,
including perinuclear antineutrophilic cytoplasmic antibody (p-ANCA) and anti-Saccharomyces
cerevisiae antibody (ASCA) in UC and CD.
Epidemiologic studies suggest an increasing incidence and prevalence of IBD in
developed countries. Although there are fewer epidemiological data from developing countries,
there appears to be a similar trend, fueling its emergence as a global disease. Some studies
reported on a change in migrants moving from developing low incidence countries to developed
high incidence countries, whereby they exhibit the incidence of the adopted country. This
phenomenon is worth exploring further for several reasons. Firstly, it implies there may be an
environmental trigger for the disease as the onset is too rapid to be accounted for by genetic
changes. Secondly, the demographics over the last 50 years have changed due to globalization
and significant migration to developed countries. Disease presentation following migration offers
a unique opportunity to further examine how environmental factors might influence disease
expression in migrants.
Inflammatory bowel disease (IBD) has become a global disease with a rising incidence in
both developed and developing countries. In the United States, nearly 1.5 million patients are
affected with IBD, with approximately equal distribution of Crohn’s disease (CD) and ulcerative
colitis (UC). Epidemiological studies are mostly in Caucasian populations in North America and
Europe, and similarly large efficacy trials, hospitalizations rates, and surgery outcomes have also
included data from predominantly Caucasian populations?
References
Google Search. (n.d.). The Impact of Racial and Ethnic Differences in Inflammatory Bowel
Disease Phenotype in the United States - Retrieved from
https://www.google.com/search?
client=safari&channel=iphone_bm&source=hp&ei=Pj1BXKWHIeGigge444_gBg&q=T
he+Impact+of+Racial+and+Ethnic+Differences+in+Inflammatory+Bowel+Disease+Phe
notype+in+the+United+States&btnK=Google+Search&oq=The+Impact+of+Racial+and
+Ethnic+Differences+in+Inflammatory+Bowel+Disease+Phenotype+in+the+United+St
ates&gs_l=psy-ab.3...7523.7523.9497...0.0..1.106.209.0j2......1....2j1..gws-
wiz.....0.38ciG2XGerg
Inflammatory bowel disease (IBD) - Symptoms and causes - Mayo Clinic. (n.d.). Retrieved
from https://www.mayoclinic.org/diseases-conditions/inflammatory-bowel-disease/
symptoms-causes/syc-20353315
WEEK 9
NURS 6501
WEEK 9
Initial post
Endocrine system
Although Diabetes Insipidus and Diabetes Mellitus share a common first name they are
very different diseases. DI is uncommon, although the exact prevalence in the general population
is difficult to estimate. For both central DI and nephrogenic DI, there are no clear differences in
prevalence between genders or among ethnic groups.?Inherited causes for both central and
nephrogenic DI account for approximately 1% to 2% of all cases.Diabetes insipidus (DI) is a
disorder in which polyuria due to decreased collecting tubule water reabsorption is induced by either
decreased secretion of antidiuretic hormone (ADH; central DI) or resistance to its renal effects
(nephrogenic DI). In most patients, the degree of polyuria is primarily determined by the degree of ADH
deficiency or resistance. Both disease states are related to inefficiencies of hormones in the
endocrine system.
Diabetes Insipidus
DI is a result of insufficient ADH release and DM is a lack of insulin or a deficit or
resistance to insulin. Ironically, the clinical manifestations are similar regardless of the
differences of the hormones involved. In individuals suffering from DI or DM they will
demonstrate polyuria and polydipsia. Diabetes insipidus (DI) is a disease of the posterior
pituitary. DI may be transient or permanent depending on the type and causation. There is central
or nephrogenic DI. Central DI may be hereditary or acquired and is a result of an absence of
ADH (Huether& McCance, 2012).?Patients with untreated central diabetes insipidus (CDI) typically
present with polyuria, nocturia, and, due to the initial elevation in serum sodium and osmolality,
polydipsia. They may also have neurologic symptoms related to the underlying neurologic
disease.?Acquired DI includes idiopathic, traumatic, resulting from cancer, ischemic,
granulatomas disease, infectious or autoimmune (McPhee& Hammer, 2010).?Nephrogenic types
result from an inadequate response of the kidneys to respond to ADH (Huether& McCance,
2012). Nephrogenic types may be hereditary or acquired due to hypokalemia, hypercalcemia,
post renal obstruction, drugs, sickle cell disease, amyloidosis or pregnancy (McPhee & Hammer,
2010).?Regardless of the reason for DI the clinical manifestations remain the same. There is a
substantial increase in urine output, a low urine specific gravity due to the inability to
concentrate urine. McPhee & Hammer, (2010)?describes the hallmark of DI as dilute urine in the
face of hypernatremia.
The evaluation for DI includes water deprivation testing. However, this may be risky due
to the risk for circulatory collapse if the individual loses more than 3% of the pretest body weight
ADH (Huether& McCance, 2012). Other testing includes serum osmolality and plasma ADH
levels (Huether& McCance, 2012). It is important to differentiate between central and
nephrogenic types of DI. This can be accomplished by the injection of vasopressin. In central DI
there will be an increase in urine volume and osmolality, but in nephrogenic DI there will be
little to no change (McPhee & Hammer, 2010).
Treatment for DI is related to the individual’s ability to maintain hydration. IN
cases where there is a complete ADH deficiency synthetic vasopressin (DDAVP) may be
prescribed (Huether& McCance, 2012).
Diabetes Mellitus
Diabetes Mellitus (DM) is a group of disorders rather than a single type of disease. There
are multiple types of DM. The most common are type 1 where there is an absolute insulin
deficiency, Type 2 which involves insulin resistance or a secretory deficit, and Gestational
Diabetes which is present during pregnancy (Huether& McCance, 2012).
The pathophysiology of DM Type 1 is an autoimmune response in which there is a
selective destruction of pancreatic beta cells by T lymphocytes targeting ill defines B cell
antigens which results in the pancreas ability to produce insulin (McPhee & Hammer, 2010).?The
pathophysiology in type 2 is not as clearly defined. Obesity has been proven to be a predisposing
factor which leads to insulin resistance. Decreased beta cell responsiveness to plasma glucose
along with abnormal glucagon secretion is also known to play a large part in DM type 2
(Huether& McCance, 2012).
Clinical manifestations include polydipsia and polyuria along with increased serum
glucose are present in all types of DM. Type 1 commonly presents in childhood and onset of
symptoms are acute. Because Type 1 DM has an acute onset and affects the metabolism of fat,
protein and carbohydrates, the initial symptom may be diabetic coma (Huether& McCance,
2012). This is a result of metabolic acidosis from ketoacidosis resulting from increased
metabolism of fats and proteins resulting in high levels of circulating protein (Huether&
McCance, 2012). Clinical manifestations for DM type 2 are much less specific and less acute
than inn type 1. They include recurrent infections, puritis, visual changes, paresthesias and
fatigue (Huether& McCance, 2012). Gestational diabetes develops during pregnancy and is a
result of glucose intolerance rather than resistance or absence of insulin.
Treatment for DM is related to the type identified. In type 1, individuals must be given
insulin in accordance with their baseline blood glucose and dosed according to the number of
carbohydrates ingested. Type 2 diabetes management begins with lifestyle modification
including weight loss, dietary changes, and exercise. After lifestyle changes are initiated, oral
hypoglycemic may be needed and only when treatments are ineffective insulin is used (McPhee
& Hammer, 2010).?
Behavior Influences
An individual’s lifestyle is directly responsible for the majority of cases of DM type 2.
However, trauma or drug use are the only lifestyle factors that predispose any individual for
developing DM type 1 or DI.
Conclusion
Diabetes insipidus and diabetes mellitus share a common root word but are completely
different diseases resulting from inappropriate or lack of hormone secretion. Health care
professionals must be able to identify the differences in the two disease states as the hallmark
symptoms are generally very similar. Failure to intervene promptly and correctly could result in
coma or even death.
Bridgette,
I found your post very though provoking. I agree that behavior plays a large part in the
development and predisposition for DM type 2. I found it interesting that many cases of the
nephrogenic form of DI were present at birth. The majority cases I encountered were related to a
neurogenic form. What percentage of cases does the inherited form account for? The
nephrogenic form would more commonly the result of kidney damage or medications. However,
McPhee & Hammer, (2010) drug-induced nephrogenic DI only occurs in 12-30% of individuals
treated with lithium, fluoride and other salts.
Stacy
References
McPhee, S. J., & Hammer, G. D. (2010).?Pathophysiology of disease: An introduction to clinical
medicine(Laureate Education, Inc., custom ed.). New York, NY: McGraw-Hill Medical.
Huether, S. E., & McCance, K. L. (2012).?Understanding pathophysiology?(Laureate custom
ed.). St. Louis, MO: Mosby.
WEEK 10
NURS 6501
Week 10
Initial Post
Renal & Urologic Systems
Urinary Tract Infections
According to Huether& McCance (2017), urinarytract infection (UTI) is an
“inflammation of the urinary epithelium usually caused by bacteria from gut flora”. UTI can be
caused in any part of the system — your kidneys, ureters, bladder and urethra (Mayo Clinic,
2017). UTI is categorized into lower and upper. Lower UTI includes cystitis and upper UTI
include pyelonephritis (Huether& McCance, 2017). As a health care practitioner, it is imperative
to know how to diagnose and treat these infections in a timely manner.
Pathophysiology of Lower and Upper Urinary Tract Infections
According to Huether& McCance (2017), acute cystitis is an inflammation of the bladder
and is the most common site of UTI. The most common infecting microorganisms are uropathic
strains of Escherichia coli and second most common is Staphylococcus saprophyticus (Huether&
McCance, 2017). Less common microorganisms include Klebsiella, Proteus, Pseudomonas,
fungi, viruses, parasites, or tubercular bacilli and schistosomiasis is the most common cause of
parasitic invasion of the urinary tract on a global basis, infecting more than 200 million people
(Huether& McCance, 2017). The contamination of the sterile urine usually occurs by retrograde
movement of gram-negative bacilli into the urethra and bladder and then to the ureter and
kidneys (Huether& McCance, 2017). The infections caused by these bacteria initiates an
inflammatory response and the symptoms of cystitis; the inflammatory edema in the bladder then
stimulates discharge of stretch receptors initiating symptoms of bladder fullness with small
volumes of urine and producing the urgency and frequency of urination associated with cystitis
(Huether& McCance, 2017).
Acute pyelonephritis, on the other hand, is an infection of one or both upper urinary tracts
(ureter, renal pelvis, and interstitium) (Huether& McCance, 2017). In comparison to acute
cystitis, the microorganisms involved in acute pyelonephritis include E. coli, Proteus, or
Pseudomonas (Huether& McCance, 2017). These microorganisms also split urea into ammonia,
making alkaline urine that increases the risk of stone formation (Huether& McCance, 2017).
According to Huether& McCance (2017), the ascending uropathic microorganisms along the
ureters probably spread the infection; however, dissemination may also occur by the way of the
bloodstream. Pyelonephritis causes medullary infiltration of white blood cells with renal
inflammation and edema, and purulent urine (Huether& McCance, 2017). The inflammatory
process of acute pyelonephritis is usually focal and irregular, and primarily affects the pelvis,
calyces, and medulla (Huether& McCance, 2017).
The Factors of Gender & Genetics
In all my years of nursing, I have seen that women are more likely to be diagnosed with
UTI than men. According to Huether& McCance (2017), cystitis is more common in women
because of the shorter urethra and the closeness of the urethra to the anus that increases the
chances of bacterial contamination. Huether& McCance (2017), further explain that
approximately fifty percent of women may suffer from lower UTI at some point of their life. As
far as genetics is concerned, some women may be genetically susceptible to certain strains of E.
coli attachment (Huether& McCance, 2017). According to a study performed by Zaffanello et al.
(2010), recent advances have suggested that a deregulation of candidate genes in humans may
predispose patients to recurrent UTI.Zaffanello et al. (2010) further explain that, in particular, the
HSPA1B, CXCR1 & 2, TLR2, TLR4, TGF-1 genes seem to be associated with an alteration of
the host response to UTIs at various levels.
In general, at risk for UTI’s are premature newborns; prepubertal children; sexually
active and pregnant women; women treated with antibiotics that disrupt vaginal flora; spermicide
users; estrogendeficientpostmenauposal women; individuals with urinary catheters; and persons
with diabetes mellitus, neurogenic bladder, or urinary tract obstruction (Huether& McCance,
2017). In the case of pyelonephritis, most of the cases are also found mainly in women than men
(Huether& McCance, 2017).
Diagnosis and Treatment
In the case of acute cystitis, the infections in symptomatic individuals are diagnosed by
urine culture of specific microorganisms with counts of 10,000/ml or more from freshly voided
urine (Huether& McCance, 2017). Urine dipstick testing that is positive for leukocyte esterase or
nitrite reductase can be used for the diagnosis of uncomplicated UTI’s (Huether& McCance,
2017). If there is bacteria found in the urine culture and antibiotic sensitivity testing then
treatment is to be done with microorganism-specific antibiotics (Huether& McCance, 2017).
Most commonly, a 3 to 7 days course of antibiotics may be prescribed for uncomplicated UTI
and a 7 to 14 days of antibiotic therapy is required if the infection is relapsing (Huether&
McCance, 2017).
Pyelonephritis, on the other hand, is diagnosed by a combination of tests - urine culture,
urinalysis, and clinical signs and symptoms the patient is having (Huether& McCance, 2017). If
the health care practitioner suspects a case of complicated pyelonephritis, the diagnosed is made
with blood cultures and urinary tract imaging (Huether& McCance, 2017). Pyelonephritis may
also be treated with the help of antibiotics. A course of 2 to 3 weeks of microorganism-specific
antibiotic therapy is usually needed to treat this infection (Huether& McCance, 2017). Follow up
urine cultures are also advised 1 to 4 weeks post treatment (Huether& McCance, 2017).
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Mayo Clinic, (2017). Urinary tract infections. Overview. Retrieved from
https://www.mayoclinic.org/diseases-conditions/urinary-tract-infection/symptoms-
causes/syc-20353447
Zaffanello, M., Malerba, G., Cataldi, L., Antoniazzi, F., Franchini, M., Monti, E., &Fanos, V.
(2010). Genetic risk for recurrent urinary tract infections in humans: a systematic
review.?Journal Of Biomedicine & Biotechnology,?2010321082.
doi:10.1155/2010/321082
Week 10
Response # 1
Urinary Tract Infections
Great post. I really enjoyed reading your post and you have provided some great
information. According to Huether& McCance (2017), a urinary tract infection (UTI) is an
“inflammation of the urinary epithelium usually caused by bacteria from gut flora”. Lower UTI
includes cystitis and upper UTI include pyelonephritis (Huether& McCance, 2017). I think
elderly population takes the biggest hit from UTI’s. Almost every elderly patient I have seen
diagnosed with UTI was confused in some way. According to Huether& McCance (2017),
cystitis is more common in women because of the shorter urethra and the closeness of the urethra
to the anus that increases the chances of bacterial contamination. Huether& McCance (2017),
further explain that approximately fifty percent of women may suffer from lower UTI at some
point of their life. What makes matters complicated is when women are pregnant as healthcare
practitioners have to be more careful. A drug named nitrofurantoin is being used to treat pregnant
women suffering from UTI’s (Jean & Mari, 2010). Jean & Mari (2010) further explain that
nitrofurantoin has been consideredto be the preferred antibiotic for bacteriuria suppression, as
bothampicillin and cephalosporinscan interfere with the normal gastrointestinalflora. Thus,
nitrofurantoin is usedextensively in pregnant women.
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Jean, M., Shailendra, P., & Mari, E. (2010). Treating UTIs in reproductive-age women—Proceed
with caution.?The Journal Of Family Practice, (4), 220.
NURS 6501
Response #2
Urinary Tract Infections
Great post. I really enjoyed reading your post and you have provided some great
information. According to Huether& McCance (2017), a urinary tract infection (UTI) is an
“inflammation of the urinary epithelium usually caused by bacteria from gut flora”. Lower UTI
includes cystitis and upper UTI include pyelonephritis (Huether& McCance, 2017).
To add to your factor of age, according to my experience, the older the patient more the
complications related to UTI. I have seen elderly patients getting very confused because of UTI.
Some patients get so confused that we have to restrain them for their own safety. And to add to
the factor of gender, according to Huether& McCance (2017), cystitis is more common in
women because of the shorter urethra and the closeness of the urethra to the anus that increases
the chances of bacterial contamination. Huether& McCance (2017), further explain that
approximately fifty percent of women may suffer from lower UTI at some point of their life. Did
you know that, women treated with antibiotics that disrupt vaginal flora; spermicide users;
estrogen deficient post menauposal women are at the highest risk for UTI infections (Huether&
McCance, 2017). One thing that most patients fail to perform is a follow up urine cultures that
are advised 1 to 4 weeks post treatment (Huether& McCance, 2017).
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
WEEK 11
NURS 6501
Week 11
Initial post
Reproductive disorders
Endometriosis
Endometriosis is a problem affecting a woman’s uterus, the place where a baby grows
when a woman is pregnant. Endometriosis is a common disorder affecting 10-25 % of women of
reproductive age (Huether& McCance, 2017, p. 642). Endometriosis is when the kind of tissue
that normally lines the uterus grows somewhere else. It can grow on the ovaries, behind the
uterus, on the bowels, or on the bladder. Rarely, it grows in other parts of the body.This
“misplaced” tissue can cause pain, infertility, and very heavy periods. The pain is usually in the
abdomen, lower back, or pelvic areas. Some women have no symptoms at all, and having trouble
getting pregnant may be the first sign they have endometriosis.
Endometriosis typically affects women of reproductive age, but a wide spectrum of age at
diagnosis exists. Premenarcheal girls presenting with chronic pelvic pain should be evaluated for
endometriosis as this condition has been reported in this young cohort.?Furthermore,
endometriosis can present in menopausal women.The prevalence is thought to be higher in white
women and in those with a lower body mass index.?
Fibroids
The true incidence and prevalence of uterine fibroids in the general female population are
unknown because the condition is frequently asymptomatic and therefore not identified.
Incidence increases with age during the reproductive years such that cases occur in 20% to 50%
of women older than 30 years (Epocrates Online. n.d.).Uterine fibroids (leiomyomata) are benign
tumors of the uterus primarily composed of smooth muscle and fibrous connective tissue.They
range in size from seedlings to large uterine tumors. Grossly, these tumors are round, firm, and
well-circumscribed nodules located just under the uterine serosa (subserosal), within the
myometrium (intramural) or just below the endometrium (submucosal). There are often multiple
tumors in a single uterine specimen.?Microscopically, these nodules are made up of spindle-
shaped cells with no mitotic activity or remarkable nuclear atypia.
Similarities and differences
Both involve abnormally growing tissue, however uterine?fibroids?are benign growths
that appear on?or within uterine walls, and?endometriosis?is caused by the tissue that is normally
found in the uterus; when endometrial tissue extends beyond the uterus and attaches to the
nearest organs, such as the large intestine.
If females have the following symptoms, they need to consult a doctor to confirm or deny the
diagnosis.
Severe abdominal cramping and shooting pain
Painful menstruation
Heavy menstrual bleeding
Painful sex
Irregular bowel movements / diarrhea during menses
However, sometimes endometriosis has several distinctive symptoms. It can be characterized by
bleeding from the rectum or bladder instead of bleeding through the vagina.
Endometriosis can also lead to infertility or difficulties getting pregnant. Much like uterine
fibroids, endometriosis can be asymptomatic for a long time and start bothering you in late stages
References
Endometriosis Emerging Therapies - Epocrates Online. (n.d.). Retrieved from
https://online.epocrates.com/diseases/35543/Endometriosis/Emerging-Therapies
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Week 11
Response #1
The clinical definition of male factor infertility is the presence of abnormal semen
parameters in the male partner of a couple unable to achieve conception after 1 year of
unprotected intercourse. The World Health Organization defines male factor infertility as the
presence of ≥1 abnormality in the semen analysis or the presence of inadequate sexual or
ejaculatory function.
The causes of male factor infertility include abnormal spermatogenesis; reproductive tract
anomalies or obstruction; sexual and ejaculatory dysfunction; and impaired sperm motility.
Altered spermatogenesis is probably the most common reason for male infertility and is of
unknown etiology in most cases. Factors that alter spermatogenesis through low testosterone
levels include obesity, endocrinopathies, and exposure to medication or environmental
toxins.?Other factors that have a direct deleterious effect on spermatogenesis include varicocele,
increased scrotal heat, systemic diseases, smoking, history of undescended testicles, and alcohol
intake.?Y chromosome deletions and other chromosomal anomalies, such as Klinefelter
syndrome (XXY), are less common causes. Testicular torsion and trauma can also affect sperm
production.
Ejaculatory duct obstruction may be congenital, such as congenital bilateral absence of
vas deferens, related frequently to a mutation in the cystic fibrosis transmembrane regulator
gene, or acquired secondary to epididymal or prostatic infections, vasectomy, or complications
of surgical procedures (e.g., inguinal hernia repair or orchiopexy for testicular undescended).
Prostatic surgery and some pharmaceuticals may be associated with retrograde ejaculation.
Erectile and ejaculatory dysfunction may be associated with psychological factors,
hypogonadism, spinal cord disease, and metabolic and vascular conditions such as diabetes.
Sperm motility can be reduced in the immotile cilia syndrome (Kartagener syndrome) or in the
presence of antisperm antibodies.Male fertility requires normal sperm production and sperm
transport, and adequate sexual performance. For instance, for conception to occur, the ducts for
sperm transport must be patent and ejaculation must occur so the sperm can be delivered near the
female’s cervix (Huether& McCance, 2017, p. 656).These functions require normal levels of
testosterone. Testosterone is produced by the testicular Leydig cells under the influence of LH.
Spermatogenesis is controlled directly by testosterone and FSH. FSH is believed to act on the
Sertoli cells, which support spermatogenesis in the seminiferous tubules. The pituitary
production of FSH and LH is controlled by the hypothalamic GnRH. GnRH and FSH production
by the hypothalamus and pituitary are negatively controlled directly by testosterone levels and
through its aromatization to estradiol at the central or peripheral levels. Inhibin is produced by
Sertoli cells and has a negative effect on FSH secretion. Circulating testosterone is bound mainly
to the sex hormone-binding globulin (SHBG) and albumin. Levels of SHBG affect the active
portion of circulating testosterone or free testosterone. Hyperprolactinemia has a negative effect
on GnRH secretion.The presence of an intact Y and 1 copy of the X chromosome is essential for
the differentiation of the embryonic gonads into testicles and for the later development of
adequate spermatogenesis. Normal fertilization of the oocyte requires many motile sperm with
intact acrosomal reaction.Sperm production is negatively affected by endocrine effects of
obesity, increased local testicular heat, and exposure to environmental toxins or endocrine
disruptors.?[8]?Smoking and alcohol also have a toxic effect on sperm production. A variety of
medications or metabolic conditions can alter testosterone production or have an antitestosterone
effect at the receptor level. Other medications or environmental exposures can directly alter
spermatogenesis or sperm motility.
References
Huether, S. E., & McCance, K. L. (2017).?Understanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Male factor infertility Etiology - Epocrates Online. (n.d.). Retrieved from
https://online.epocrates.com/diseases/49724/Male-factor-infertility/Etiology
NURS 6501
Response # 2
Ovarian cancer is the most common cause of cancer death from gynecologic tumors in
the United States(Green, 2017). Per Huether& McCance (2017) it is the deadliest cancer of the
female reproductive system and is often difficult to diagnose and treat due to indistinct
symptoms in the early stage. Huether& McCance (2017) go on to explain that diagnosis is
usually made at a later stage when the prognosis is poor and treatment often ineffective. Early
ovarian cancer causes minimal, nonspecific, or no symptoms(Green, 2017). The patient may feel
an abdominal mass. Symptoms associated with later-stage disease include gastrointestinal
symptoms such as nausea and vomiting, constipation, and diarrhea(Green, 2017). Per the
American Cancer Society (2016a) it ranks fifth in cancer deaths and mainly develops in older
women. Although the cause is unknown, it is estimated that it may be related to ovulation
mechanisms and exposure of cancer-causing substances passing through the vagina reaching the
fallopian tubes and ovaries (Huether& McCance, 2017).
About half of testicular cancers occur in men between the ages of 20 and 34. But this
cancer can affect males of any age, including infants and elderly men per Huether and McCance
(2017). The risk of developing ovarian cancer gets higher with age. Ovarian cancer is rare in
women younger than 40. Most ovarian cancers develop after menopause. Half of all ovarian
cancers are found in women 63 years of age or older.
References
American Cancer Society. (2016a). Ovarian cancer. Retrieved from
http://www.cancer.org/cancer/ovariancancer
American Cancer Society. (2016b). Testicular cancer. Retrieved from
http://www.cancer.org/cancer/testicularcancer/
Green, A. E. (2017). Ovarian cancer. Retrieved from
http://emedicine.medscape.com/article/255771-overview
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
