Week 11 Discussion

Week 11 Discussion

Response # 2 to Melissa

Hello Melissa. Thank you for your interesting and informative post. As you mentioned in your

post, precocious puberty can affect proper growth and cause a child to have social issues and

embarrassment amongst peers. According Huether& McCance (2017), if precocious puberty is not

reversed and progresses to complete precocious puberty, progression of associated features like thelarche,

pubarche, and menarche can be challenging to treat. Unfortunately, complete precocious puberty also

causes long bones to stop growing before the child reaches normal height (Huether& McCance, 2017). On

the other hand, benign prostatic hyperplasia (BPH) varies greatly throughout the world and is highest in

the developed world (Huether& McCance, 2017). According Huether& McCance (2017), screening with

prostatic specific antigen (PSA) can amplify the incidence of prostate cancer and BPH by allowing for

detection of both BPH and prostatic lesions early. Although the BPH and or prostate lesions that are

detected early may meet the pathologic criteria for malignancy, they “have low potential for growth and

metastasis” (Huether& McCance, 2017, p. 865).

As you mentioned in your post, age is an important factor reproductive in both men and women.

My post was about testicular cancer and ovarian cancer. Just like in BPH and precocious puberty, age is

an important factor in both testicular cancer and ovarian cancer. According to the American Cancer

Society (2018), ovarian cancer is mainly discovered in women after menopause and rarely in women aged

below 40 years. Half of all ovarian cancers are found in women aged over 63 years. On the other hand,

testicular cancer occurs most commonly in men between the ages of 15 and 35 years (Huether&

McCance, 2017, p. 861).

References

American Cancer Society. (2018). Ovarian Cancer. Retrieved from

http://www.cancer.org/cancer/ovariancancer/

American Cancer Society. (2018). Testicular Cancer. Retrieved from

http://www.cancer.org/cancer/testicularcancer/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 11 Discussion

Response # 1 to Jessica

Hello Jessica. Thank you for your very interesting and informative post on benign prostatic

hyperplasia (BPH) and polycystic ovary syndrome (PCOS). It was interesting to read that the incidence of

BPH varies greatly throughout the world and is highest in the developed world (Huether& McCance

(2017). According Huether& McCance (2017), screening with prostatic specific antigen (PSA) can

amplify the incidence of prostate cancer and BPH by allowing for detection of both BPH and prostatic

lesions early. Although the BPH and or prostate lesions that are detected early may meet the pathologic

criteria for malignancy, they “have low potential for growth and metastasis” (p. 865).

As you mentioned in your post, age is an important factor for both BPH and PCOS. My post was

about testicular cancer and ovarian cancer. Just like in BPH and PCOS, age is an important factor in both

testicular cancer and ovarian cancer. According to the American Cancer Society (2018), ovarian cancer is

mainly discovered in women after menopause and rarely in women aged below 40 years. Half of all

ovarian cancers are found in women aged over 63 years. On the other hand, testicular cancer occurs most

commonly in men between the ages of 15 and 35 years (Huether& McCance, 2017, p. 861).

References

American Cancer Society. (2018). Ovarian Cancer. Retrieved from

http://www.cancer.org/cancer/ovariancancer/

American Cancer Society. (2018). Testicular Cancer. Retrieved from

http://www.cancer.org/cancer/testicularcancer/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 11 Discussion

Initial Post

Testicular Cancer

According Huether & McCance (2017), testicular cancer is one of the most common curable

cancers with cure rates greater than 90% and accounting for approximately 1% of all male cancers in the

United States (p. 861). For men with low-stage testicular cancer, the cure rate is as high as 100% (p.861).

Huether& McCance, (2017) states that the probability of developing testicular cancer in the United States

is 0.3% for white male but this rate is still 4.5 times higher than the incidence rate in African Americans

(p. 861). Testicular tumors are more common on the right side than on the left side (Huether& McCance,

2017). The first sign of this condition is usually a painless testicular enlargement that occurs gradually

and may be accompanied by a lump or swelling on the testicle, pain, breast growth or soreness, and

feeling of testicular heaviness or aching in the lower abdomen (American Cancer Society,

2016b,Huether& McCance, 2017).Symptoms of advanced testicular cancersinclude low back pain,

shortness of breath, chest pain, and headaches or confusion from cancer spread to the brain (American

Cancer Society, 2016b). Because of lack of symptoms, testicular mass is usually discovered by the

individual or by his sexual partner or it is found during medical check-up for other conditions (American

Cancer Society, 2016b, Huether& McCance, 2017).

Ovarian Cancer

According Huether& McCance (2017), globally, ovarian cancer is the seventh most common

cancer and the eighth cause of death from cancer in women (p. 825). It is considered one of the deadliest

cancers of the female reproductive system. Ovarian cancer is considered to be a generally silent disease

that develops with individuals not presenting with any early symptoms. There are no effective screening

techniques for this disease and by the time disease is detected, it is usually in advanced stages(Huether&

McCance, 2017). The early symptoms of ovarian cancer are described as vague and may include

abdominal distension, loss of appetite, pelvic pain. Advanced symptoms include abdominal pain,

abdominal swelling and distention, vomiting, abnormal vaginal bleeding(American Cancer Society, 2018,

Huether& McCance, 2017).

Age

According to the American Cancer Society, (2018), ovarian cancer is mainly discovered in womenafter

menopause and rarely in women below 40 years of age. Half of all ovarian cancers are found in women

aged 63 years or older.On the other hand, testicular cancer occurs most commonly in men between the

ages of 15 and 35 years (Huether& McCance, 2017, p. 861).

References

American Cancer Society. (2018). Ovarian Cancer. Retrieved from

http://www.cancer.org/cancer/ovariancancer/

American Cancer Society. (2018). Testicular Cancer. Retrieved from

http://www.cancer.org/cancer/testicularcancer/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 10 Discussion

Response # 2 to Tanya

Hello Tanya. Thanks for your very interesting and informative post on upper and lower

urinary truck infections (UTIs). According to Bethel (2012), diagnosis of pyelonephritis needs careful

consideration by the advanced nurse practitioner (NP) because there are other conditions that has similar

symptoms, some of which may be life threatening. These include: Ectopic pregnancy, appendicitis,

sexually transmitted infections, epididymitis, acute pancreatitis, renal calculi and symptoms of lower

UTIs. Bethel (2012) notes that symptoms confined to the lower urinary tract, with the absence of

significant pain, fever and systemic ill health in otherwise healthy sexually active young females may be

indicative of lower, uncomplicated urinary tract infection. However, for patients with pyelonephritis,

fever, flank pain and systemic features of ill health may be indicative of upper urinary tract or kidney

infection. Given the unreliability and inconsistency of clinical signs and symptoms of pyelonephritis,

certain diagnostic and investigative procedures like urinalysis and blood culture may be necessary to

enhance diagnostic accuracy (Bethel, 2012).

References

Bethel, J. (2012). Acute pyelonephritis: risk factors, diagnosis and treatment.<Nursing Standard,<27(5),

51–56. Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 10 Discussion

Response # 1 toAdenayo

Hello Adenayo. Thank you for your very interesting and informative post. According to Bethel

(2012), females are six times more likely to develop pyelonephritis than males for several reasons,

including the fact that females have a shorter urethra than males which makes it easier for bacteria to

reach the kidneys. The proximity of the urethral orifice to the perianal and anal region in females also

makes them more susceptible to urinary tract infections. Pregnancy is also associated with increased risk

of infection, which is partly due to hormonal changes that reduce urinary flow during pregnancy (Bethel,

2012 p. 51).

Bethel (2012) further describes that diagnosis of pyelonephritis can prove challenging in certain

patients, for example children, individuals with cognitive or sensory impairments and frail older adults,

who may have difficulty communicating their signs and symptoms. Diagnosis may also be difficult

because fever and dysuria, which are considered to be predominant markers of pyelonephritis, may be

present to varying degrees and are not specific to the condition. Up to one in three older patients may

develop pyelonephritis with absence of fever (Bethel, 2012). Onset of symptoms may vary from hours to

several days and even weeks in some cases. Severity of symptoms also varies from gradual onset of

comparatively mild symptoms to acute presentation of severe symptoms (Bethel, 2012).

References

Bethel, J. (2012). Acute pyelonephritis: risk factors, diagnosis and treatment.<Nursing Standard,<27(5),

51–56. Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 10 Discussion

Initial post

According to Couling (2008), urinary tract infections (UTIs) are the most common infection after

respiratory and gastro-intestinal infections. UTIs are also the most common cause of both community-

acquired and nosocomial infections for those admitted to hospitals. UTIS are more common in women

and “about 50% of womenwill be treated for UTI in their lifetime” with Escherichia coli being the most

common bacteria diagnosed as the cause. UTIs are also more common in sexually active women. Women

have shorter urethras than males which allows the migration of skin organisms into the bladder and

urethra causing cystitis and urethritis(Couling, 2008 p 486, Najar, Saldanha &Banday, 2009).

Lower urinary tract infection

The urinary tract is divided into the upper and lower sections. The lower urinary track is made up

of the urethra and the bladder.Lower urinary tract infections include acute cystitis which is the

inflammation of the bladder. The urinary tract is usually a sterile environment. Cystitis is the most

common UTI and is commonly caused by E. coli. In uncomplicated UTIs, cystitis occurs when there is a

bladder mucosal invasion, mostly by E. Coli which inhabits the peri- urethral vaginal introitus and

ascends into the bladder via the urethra (Brusch, 2016). In complicated UTIs pyelonephritis occurs when

host defenses, local leukocyte phagocytosis and renal production of antibodies kill bacteria in the

presence of complement. The three main mechanisms responsible for UTIs are colonization with

ascending spread, hematogenous spread, and peri urogenital spread (Brusch, 2016).Mild inflammation

causes redness in the bladder mucosa while more complicated cases lead to diffuse hemorrhage, pus

formation on the epithelial surface of the bladder. Severe cases of cystitis may lead to necrosis of the

bladder wall (gangrenous cystitis). Treatment for lower urinary tract infection is usually resolved with

oral course of antibiotics resolving in 1 to 5 days (Huether, & McCance, 2017).

Upper urinary tract infection (pyelonephritis)

The renal pelvis which receives urine from the renal tissue and to the ureters form what is called

the upper urinary tract. Upper urinary tract infection, also called pyelonephritis is a serious condition that

can lead to death if not treated. Infections in this area are often caused by E. coli, Proteus, or

Pseudomonas (Huether, & McCance(2017). Infection primarily affects the pelvis, calyces and medulla by

causing infiltration of white blood cells (WBC) with renal inflammation, renal edema and purulent urine.

In severe cases of infection, localized abscesses may form in the medulla, and may extend to the cortex

which can then lead to necrosis of the papillae. Although acute pyelonephritis rarely causes renal failure,

chronic pyelonephritis may lead to chronic kidney failure.<People with who are prone to pyelonephritis

include those who have anatomical abnormalities and those who are immune compromised. Immediate

treatment of pyelonephritis with intravenous antibiotics is necessary because patients can easily become

septic fast (Huether, & McCance, 2017).

Distinguishing between complicated and uncomplicated infections is important in being able to

correctly treat the infection. Complicated UTIs usually develop due to an abnormality in the urinary tract

system or in people who are immunocompromised such as those with HIV.Usually, uncomplicated UTI

develops in people with structurally normal urinary tracts. Distinguishing between complicated and

uncomplicated urine samples is important. Urine samples from an individual with complicated UTI is

often cloudy and malodorous. Dysuria, urinary frequency, and urgency are seen in both but fever, nausea,

vomiting, and pain in the costovertebral areas are suggestive of pyelonephritis. Diagnosis of UTIs that are

uncomplicated are usually done by analyzing the mainstream urine and blood count. Complicated UTIs

require, in addition to urinalysis and blood counts, pelvic ultrasounds, intravenous pyelogram, and

cystoscopy.

References

Brusch, J. L. (2016). Cystitis in females. Medscape. Retrieved

fromhttp://emedicine.medscape.com/article/233101-overview#a1

Couling R. (2008). Managing lower UTI in adults in the community.<Nurse Prescribing,<6(11), 485–489.

Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?

direct=true&db=rzh&AN=105593211&site=ehost-live&scope=site

Najar, M., Saldanha, C., &Banday, K. (2009). Approach to urinary tract infections.Approach to urinary

tract infections, 19(4), 129-139. Retrieved February 1, 2017.

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 9 Discussion

Response #2 to Anthony

Hello Anthony. Thank you for your very informative post. I agree with you that genetics have a

great effect on diabetes insipidus and diabetes mellitus (DM) type 1 and 2. Although individuals can’t

change genetic risk factors such as family history, age, or ethnicity, they can make lifestyle changes that

increase their chances of acquiring diabetes mellitus or it’s maintenance if they have it. As I mentioned in

my post, lifestyle and individual behavior play a major role in individuals with DM. Cutting weight and

not being obese by practicing portion control, eating less carbohydrate rich diet, exercising, blood sugar

monitoring, medications, insulin compliance, A1c and doctor’s visit are behaviors that an individual can

use towards effective management of DM (NIDDK, 2017, Huether& McCance, 2017).

References

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Retrieved from

http://diabetes.niddk.nih.gov

Week 9 Discussion

Response # 1 to Jessica

Hello Jessica. Thank you for your very interesting and informative post. I agree with you that

genetics and age are factors that influence the diagnosis and treatment on diabetes mellitus (DM) and

diabetes insipidus (DI). As I noted on my initial post, ethnicity and behavior are also important patient

factors. According to the American Diabetes Association, (2018), the prevalence of diabetes in American

Indians/Alaskan Natives is 15.1 percent, 12.7 percent in non-Hispanic blacks, 12.1 percent in Hispanics,

8.0 percent in Asian Americans and 7.4 percent in non-Hispanic whites (American Diabetes Association,

2018). As I noted on my post, lifestyle and individual behavior also plays a major role in individuals with

DM. Portion control and eating less carbohydrate diet, exercise, blood sugar monitoring, medications,

insulin compliance, A1c and doctor’s visit are behaviors that an individual can use towards effective

management of DM (NIDDK, 2017, Huether& McCance, 2017). Individuals with diabetes type 1 (DM1)

must take insulin from the time they are diagnosed since their body does not produce insulin.These

individuals must also observe the same behaviors as mentioned above for effective management of DM1.

Lifestyle changes like loss of weight, smoking and alcohol cessation are also necessary. All individuals

with DM are encouraged and expected to know how to use a glucometer to check their blood sugar whites

(American Diabetes Association, 2018). Behavior factor is important in management and treatment for

individuals with DI and depends on the level and the cause and may include ADH replacement, fluid

replacement, intranasal or oral synthetic vasopressin analog DDAVP administration (Huether& McCance,

2017).

References

American Diabetes Association. (2011). Diabetes statistics. Retrieved from:

http://www.diabetes.org/diabetes-basics/diabetes-statistics/

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.

Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes:

perspectives on the past, present, and future.<The Lancet, (9922), 1068. doi:10.1016/S0140-

6736(13)62154-6

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Retrieved from

http://diabetes.niddk.nih.gov

Week 9 Discussion

Initial post

According to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK,

2017), diabetes is a disease that occurs when the blood glucose, also called blood sugar, is too high.An

estimated 30.3 million people in the United States (US), have diabetes (NIDDK, 2017). This translates to

an estimated 9.4 percent of the US population have diabetes (NIDDK, 2017).

Diabetes Insipidus Pathophysiology

According Huether& McCance (2017), diabetes insipidus (DI) is an insufficiency of antidiuretic

hormone (ADH) activity. This insufficiency causes DI to manifest as presence of polyuria (frequent

urination) and polydipsia (frequent drinking). DI comes in two forms. The first one is neurogenic diabetes

insipidus which is caused by insufficient secretion of ADH. The second form is called nephrogenic

diabetes insipidus and is caused by inadequate response by the kidney’s renal tubules to ADH. The third

form of DI is described by Huether& McCance as a rare form called gestational diabetes insipidus which

is associated with pregnancy. In gestational DI, the level of the vasopressin-degrading enzyme

vasopressinase is increased (Huether& McCance, 2017).For people with DI, insufficient ADH activity

causes them to excrete large volumes of dilute urine. This causes the osmolarity of the osmolality of the

plasma to increase. For conscious individuals, this causes the thirst mechanism to be activated resulting in

polydipsia, usually in the form of craving for cold water. DI usually leads to dehydration if lost fluidsare

not replaced. Loss of water though polyuria leads to serum hypernatremia and hyperosmolality lost water

in urine is not replaced (Huether& McCance, 2017).

Diabetes Mellitus Pathophysiology

According Huether& McCance (2017), type 1 diabetes mellitus (DM1) is an autoimmune chronic

disease that is T cell-mediated and results from autoimmune destruction of the insulin producing

pancreatic beta-cells. DM1 progressesslowly,and leads to irreversible failure of insulin secretion.

Hyperglycemia starts occurring when 80 % to 90% of insulin secreting beta cells of the Langerhans are

destroyed (p. 473). Besides the decline in insulin secretion, secretion of amylin hormone, which is another

beta cell hormone which suppresses glucagon is also decreased. The compound effect of reduced

secretion of these two hormones is an increase of glucagon which further contributes to hyperglycemia in

people with DM1 (Huether& McCance, 2017).

According toKahn, Cooper, & Del Prato (2014), glucose metabolism is usually regulated by a

feedback loop that involves the islet β cells and insulin-sensitive tissues, especially the liver, muscles and

adipose. In type 2 diabetes mellitus (DM2), hyperglycemia is detected when β cells cannot release

sufficient insulin to counter the presence of insulin resistance in the insulin sensitive tissues mentioned

above(Kahn, Cooper, & Del Prato, 2014). As β-cell function and numbers progressively decreases, the

remaining β-cell develops exhaustion from increased demand for insulin. Just as with DM1, secretion of

amylin hormone is also decreased in DM2 with the same compounded effect of an increase of glucagon

which further contributes to hyperglycemia in people with DM2(Huether& McCance, 2017, Kahn,

Cooper, & Del Prato, 2014).

Similarities and differences between DI and Diabetes mellitus

As mentioned above, DI is caused by insufficiency of ADH activity which is produced by the

hypothalamus in the brain and stored in the posterior pituitary gland, which directs the kidneys on how

much<water<to conserve or excrete through urine (Huether& McCance, 2017). Diabetes mellitus (DM) on

the other hand is due to decreased beta insulin and amylin secretion, and increased alpha cell glucagon

secretion combined with increased resistance by insulin sensitive tissues mentioned above (Huether&

McCance, 2017).While DI is a disease in which the kidneys are unable to conserve water, DM involves

hyperglycemia. While DI is generally caused by hormonal imbalance, DM1 is an autoimmune disease

while DM2 a disease caused by several factors including lifestyles factors and over 60 genes(NIDDK,

2017, Huether& McCance, 2017, p. 474).Similarity of include thefollowing the fact that the kidneys and

the brain play major part in controlling the hormones involved in both diseases. In DM, the kidney

controls glucose reabsorption and glycogenesis (NIDDK, 2017, Huether& McCance, 2017).

Ethnicity and Behavior as patient factors

According to the American Diabetes Association, (2018), the prevalence of diabetes in American

Indians/Alaskan Natives is 15.1 percent, 12.7 percent in non-Hispanic blacks, 12.1 percent in Hispanics,

8.0 percent in Asian Americans and 7.4 percent in non-Hispanic whites (American Diabetes Association,

2018).Lifestyle and individual behavior play a major role in individuals with DM. Portion control and

eating less carbohydrate diet, exercise, blood sugar monitoring, medications, insulin compliance,A1c and

doctor’s visit are behaviors that an individual can use towards effective management of DM(NIDDK,

2017, Huether& McCance, 2017). Individuals with DM1 must take insulin from the time they are

diagnosed since their body does not produceinsulin.These individuals must also observe the same

behaviors as mentioned above for effective management of DM1. Lifestyle changes like loss of weight,

smoking and alcohol cessation are also necessary.All individuals with DM are encouraged and expected

to know how to use a glucometer to check their blood sugarwhites (American Diabetes Association,

2018).Behavior factor is important in management and treatment for individuals with DI and depends on

the level and the cause and may include ADH replacement, fluid replacement, intranasal or oral synthetic

vasopressin analog DDAVP administration (Huether& McCance, 2017).

References

American Diabetes Association. (2011). Diabetes statistics. Retrieved from:

http://www.diabetes.org/diabetes-basics/diabetes-statistics/

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.

Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes:

perspectives on the past, present, and future.<The Lancet, (9922), 1068. doi:10.1016/S0140-

6736(13)62154-6

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Retrieved from

http://diabetes.niddk.nih.gov

Week 8 Discussion

Response # 2 to Antonio

Hello Antonio. Thank you for your interesting and informative post. As I mentioned in my

previous post, Bull & Plummer (2015) states that although some symptoms of inflammatory bowel

disease(IBD) and irritable bowel syndrome (IBS) are common, most treatments for these disorders are not

similar. However, probiotics are indicated as successful in treating symptoms of both disorders. There is

no known cure for IBS, so treatment and symptom management arethe therapy goals. The fact that

patients with IBS can present with a wide array of symptoms like constipation and diarrhea, treatment and

symptom management should be tailored to each individual patient. Some of the strategies used in IBS

management include eliminate food known to exacerbate symptoms, laxatives, fiber, anti-diarrhea meds,

anti-spasmodic meds, anti-depressants and serotonin agonists and antagonists (American

Gastroenterological Association, 2014). I agree with you that treatment for IBD which depends on the

severity of the illness and is aimed at preventing exacerbation and achieving remission from inflammatory

ulcers. Medical management includes use of steroids, 5-aminosalicylates, and immunomodulatory agents.

In severe IBD, surgery to repair perforation or fistulas may be indicated (American Gastroenterological

Association, 2014, Huether and McCance, 2017).According to Huether and McCance (2017), both IBS

and IBD are more commonly diagnosed in younger people, at or before middle age. Those with

longstanding colonic disease require frequent cancer screenings through colonoscopy and endoscopy as

they are at high risk for adenocarcinoma of the colon even if they are still young (Huether and McCance,

2017).

References:

American Gastroenterological Association (2014). IBS 107: Understanding drugs to treat IBS. Retrieved

from: http://www.gastro.org/info_for_patients/understanding-drugs-to-treat-ibs-a-patient-guide

Bull, M. J., & Plummer, N. T. (2015). Part 2: Treatments for Chronic Gastrointestinal Disease and Gut

Dysbiosis. Integrative Medicine: A Clinician's Journal, 14(1), 25-33

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 8 Discussion

Initial post

According to the American Gastroenterological Association (2014), Irritable Bowel Syndrome

(IBS) is one of the most common gastrointestinal (GI) disorders with prevalence up to 15 percent of the

adult population in Northern America affected by it. IBS and Inflammatory Bowel Disease (IBD) are two

common GI disorders that can are hard to differentiate and that are often confused with each other

because they have similar symptoms. However, they have different clinical manifestations,

pathophysiology and treatment (American Gastroenterological Association 2014).

Pathophysiological Mechanisms of Inflammatory Bowel Disorder

and Irritable Bowel Syndrome

According to Huether and McCance (2017), Crohn Disease (CD) and Ulcerative Colitis (UC) are

both part of chronic and relapsing IBD that affects about 1.6 million people in the united states (p. 920).

According to Huether and McCance (2017), IBD occurs when the body’s immune response to intestinal

microflora becomes altered, likely by a lack of discrimination between normal flora and harmful

pathogens in the GI tract. This loss of ability to discriminate triggers dendritic cells that activate the T

cells in the lymph system. Activation of T cells causes production of cytokines, chemokines, tumor

necrosis factor (TNF), interleukins, toxic free radicals and interferon gamma which all cause damage to

the intestinal epithelium (Huether& McCance, 2017). UC causes ulcerations in the colonic mucosa,

mostly in the rectum and the sigmoid colon. These ulcerations can lead to small erosions that can then

develop into ulcers, which can then lead to formation of abscess and necrosis. These can then further lead

to edema and thickening of the muscularis mucosae which then narrows the bowel lumen. Common

symptoms of UC include diarrhea, passing mucous, cramping, rapid colonic transit time, bleeding, and

pain. (Huether& McCance, 2017). According to Huether and McCance (2017),CD can lead to

inflammation in any part of the GI tract. CD often spreads with discontinuous transmural involvement that

can extend into the lymphoid tissue and at times causes fistula formation with adjacent body structures.

Patients with CD often present with vague symptoms for several years and symptoms vary depending on

the location of the disease. Common symptoms include diarrhea, GI bleeding, anemia from poor

absorption of vitamin B12 and weight loss (Huether and McCance (2017).

According to Huether and McCance (2017),IBSpatients often experience abdominal pain,

diarrhea, bloating, constipation, and food intolerance. The difference between IBD and IBS is believed

to be that IBD is an inflammatory disorder, whereas IBS is a disorder of GI tract motility (Hammer &

McPhee, 2014). The pathophysiology of IBS is not well known and diagnosis is based symptoms and

exclusion of other disorders as there are no common distinct biomarkers for this disorder. According to

Huether and McCance (2017),the etiology of IBS is not fully understood even though it is believed to be

an organic disease that may be associated with trauma, stress, or epigenetic factors (Huether& McCance,

2017).

Common Treatments

According to Bull & Plummer (2015), although some symptoms of IBD and IBS are common,

most treatments of the disorders are not similar. However, probiotics are indicated as successful in the

treatment of the symptoms of both disorders. There is no known cure for IBS and treatment and symptom

treatment is the goal of therapy. The fact that patients with IBS can present with a wide array of

symptomslike constipation while others present with diarrhea,treatment and symptom management should

be tailored to the individual. Some of the strategies used in IBS management include food elimination,

laxatives, fiber, anti-diarrhea meds, anti-spasmodic meds, anti-depressants and serotonin agonists and

antagonists (American Gastroenterological Association, 2014). Treatment for IBD depends on the

severity of the illness and is aimed at preventing exacerbation and achieving remission from inflammatory

ulcers. Medical management includes use of steroids, 5-aminosalicylates, and immunomodulatory agents.

In severe IBD, surgery to repair perforation or fistulas may be indicated (American Gastroenterological

Association, 2014, Huether and McCance, 2017).

Age as a Factor for IBD and IBS

According to Huether and McCance (2017), both IBS and IBD are more commonly diagnosed in

younger people, at or before middle age. Those with longstanding colonic disease require frequent cancer

screenings through colonoscopy and endoscopy as they are at high risk for adenocarcinoma of the colon

even if they are still young (Huether and McCance, 2017).

References:

American Gastroenterological Association (2014). IBS 107: Understanding drugs to treat IBS. Retrieved

from: http://www.gastro.org/info_for_patients/understanding-drugs-to-treat-ibs-a-patient-guide

Bull, M. J., & Plummer, N. T. (2015). Part 2: Treatments for Chronic Gastrointestinal Disease and Gut

Dysbiosis. Integrative Medicine: A Clinician's Journal, 14(1), 25-33

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 7 discussion

Response #2 to Stella

Hello Stella. Thank you for your interesting and informative post on iron deficiency anemia (IDA)

and post-hemorrhagic anemia (PHA). As you mentioned, PHA is caused by sudden loss of blood,

andthereby loss of iron from the body. As you listed, a family history of certain disorders could put an

individual, especially women of child bearing age at risk for heavy blood loss during menstrual bleeding

(menorrhagia). According to Byams (2007), menorrhagia is a common clinical problem that affects 8%–

10% of women of reproductive age (p. 1249). The results of recent studies indicate that between 5% and

24% of women with menorrhagia may have undiagnosed von Willebrand disease (VWD), and as many as

2 million women in the United States may have either VWD or another type of bleeding disorder without

knowing it (Byams 2007(p. 1249), Hammer & McPhee, 2014, Huether& McCance, 2017).

References

Byams VR. (2007). Women with bleeding disorders.<Journal of Women’s Health (15409996),<16(9),

1249–1251. https://doi-org.ezp.waldenulibrary.org/10.1089/jwh.2007.CDC11

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 7 discussion

Response #1 toShareen

Hello Shareen. Thank you for your interesting and informative post. As you mentioned, Folate

deficiency anemia is a common anemia that progresses slowly and is brought about by folic acid

deficiency due to different factors like alcohol abuse, diet that is poor in vitamin B9, impaired absorption

from the intestines among many others. As in folate deficiency anemia, pernicious anemia (PA) is caused

by a vitamin deficiency. For PA, the cause is vitamin B12 deficiency mostly due to the absence of

intrinsic factor (IF) which is required for gastric absorption of dietary vitamin B12. Deficiency of IF could

be congenital or an autoimmune process that affects the gastric parietal cells. Vitamin B12 is an important

factor that is involved in DNA synthesis of erythrocytes (Hammer & McPhee, 2014, Huether& McCance,

2017).

References

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 7 discussion on Anemia

Initial post

According to Huether& McCance (2017), anemia is a reduction of the total count of erythrocytes

in blood circulation or a decrease in the quality or quantity of hemoglobin. The common causes of anemia

are; 1. Impaired erythrocyte production, 2. Acute or chronic blood loss, 3. Increased destruction of

erythrocytes or 4. A combination of the above listed causes (Huether& McCance, 2017). This discussion

will focus on the pathophysiological mechanisms of iron deficiency anemia (IDA) and pernicious anemia

(PA), a comparison of both and factors commonly associated with both. <

Pathophysiological mechanismsof IDA and PA

According to Hammer & McPhee (2014), the amount of iron stored in the body is generally

enough to last an individual for several years. Iron is absorbed in the duodenum and it is also recycled in

the body via macrophage phagocytosis and lysis. IDA can be as a result of dietary iron deficiency or as a

result of chronic iron loss due to blood loss either through gastrointestinal bleeding (GI) or loss of blood

through the genitourinary tracts. IDA can also be as a result of functional or metabolic disorders that

hinders iron delivery to the bone marrow or absorption of iron within the bone marrow. According to

Huether& McCance (2017), IDA develops slowly over time through three overlapping stages. In stage

one, the iron stored by the body for erythrocytes production and hemoglobin synthesis is depleted, but

erythrocytes production and hemoglobin content in erythrocytes remains normal. In stage two, an

insufficient amount of iron is transported to the marrow and production of iron-deficient erythrocytes

begins. In stage three, aged normal erythrocytes that have been destroyed are replaced by hemoglobin-

deficient erythrocytes. It is during this stage that manifestation of IDA appears (Hammer & McPhee,

2014, Huether& McCance, 2017).

According to Huether& McCance (2017), pernicious anemia (PA) is caused by vitamin B12

deficiency mostly due to the absence of intrinsic factor (IF) which is required for gastric absorption of

dietary vitamin B12. Deficiency of IF could be congenital or an autoimmune process that is affects the

gastric parietal cells. Vitamin B12 is an important factor that is involved in DNA synthesis of erythrocytes

(Hammer & McPhee, 2014, Huether& McCance, 2017).

Comparison

Both iron deficiency anemia and pernicious anemia are hemolytic conditions that that result in

decreased hemoglobin and thereby have the similar symptoms due to hemoglobin dysfunction. Both

conditions are associated with dietary malabsorption. In IDA, there is malabsorption of iron while in PA,

there is malabsorption of vitamin B12. The difference in the two conditions is that IDA is primarily due to

blood loss and malabsorption of iron while PA is caused by vitamin B12 deficiency and IF (Hammer &

McPhee, 2014, Huether& McCance, 2017).

Factors

Age and gender are major factors in IDA. Premenopausal women have the highest incidence of

IDA due to frequent menstrual blood loss. Premenopausal women who get pregnant are also at high risk

of developing IDA as they lose iron to the developing fetus which “efficiently extracts maternal iron for

use in its own hematopoiesis” (Hammer& McPhee, 2014, p. 127). In men and postmenopausal women,

IDA is usually as a result of gastro intestinal (GI) bleeding. Genetic is a major factor in pernicious anemia

(PA) as the autoimmune for of the disease has a has a genetic factor where twenty percent to thirty

percent of individuals related to people who have PA, also have PA (Huether& McCance, 2017).

Behavior factors like excessive alcohol, smoking and ingestion of hot tea can play a part in chronic

gastritis which can be a contributing factor in PA. PA commonly affects people of Northern European

descent older than thirty years, even though it has recently been found in all populations (Hammer &

McPhee, 2014, Huether& McCance, 2017).

References

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 Institutes of Health. (2017). Anemia. Retrieved from https://medlineplus.gov/anemia.html

Week 6 discussion

Response # 2 to Adedayo

Hello Adedayo. Thank you for your very interesting and informative post on acute bronchitis. I

agree with you that the advance nurse practitioner (NP) may have some difficulty in differentiating

between acute bronchitis and pneumonia because both conditions involve inflammation of the respiratory

airways and that both conditions cause cough and shortness of breath (Sign & Zahn, 2017). According to

Naktin&Babinchak (1999), diagnosis of acute bronchitis is based on exclusion. The amount or color of

the sputum does not aid in the diagnosis and there are no laboratory tests that are routinely used in the

diagnosis and management of acute bronchitis. However, physical assessment or chest x-ray should not

show any signs of consolidation. Before making a diagnosis of acute bronchitis, the NP should consider a

differential diagnosis of asthma, allergic aspergillosis, occupational exposures, chronic bronchitis,

sinusitis, pharyngitis, congestive heart failure, reflux esophagitis, bronchogenic tumor, and other

aspiration syndromes in (Naktin&Babinchak (1999).

References

Naktin J, &Babinchak T. (1999). Respiratory infections in the non-immunocompromised patient.<Topics

in Emergency Medicine,<21(4), 29–43. Retrieved from https://ezp.waldenulibrary.org/login?

url=https://search.ebscohost.com/login.aspx?direct=true&db=rzh&AN=107110594&site=ehost-

live&scope=site

Singh, A. and Zahn, E. (2017). Bronchitis, Acute. Retrieved from

https://www.ncbi.nlm.nih.gov/books/NBK448067/

Week 6 discussion.

Response #1 to Jennifer

Hello Jennifer.

Thanks for your very interesting and informative post on asthma. According to Hindley (2018),

asthma is one of the most common respiratory conditions and it affects 10% of pregnant women (p. 446).

Hindley points out that women who have well-controlled asthma, there is minimal risk of complications

during pregnancy, however, poorly controlled asthma is associated with a higher risk of dying. This risk

increased if the woman smokes. Some of the complications associated with asthma during pregnancy may

include gestational diabetes, pre-eclampsia and haemorrhage. Asthma also increases the risk of infection

and midwives need to be aware of these complications (Hindley, 2018).

References.

Hindley, C. (2018). Asthma in pregnancy: Physiology, management and recommendations for midwives.

British Journal of Midwifery, 26(7), 446–450.

https://doi-org.ezp.waldenulibrary.org/10.12968/bjom.2018.26.7.446

Week 6 Discussion

Main Post

Scenario 2

In scenario 2, Kelvin, a 6-year old boy presents with a profound cough that is described as really

deep. Cough is productive for mucus and he at times coughs so hard and sounds like he is barking. His

cough is bad enough that sometimes he actually vomits.His cough has been ongoing for approximately

one week. Kelvin has a low-grade fever. He has no history of asthma or RSV. Per Kelvin’s mother, they

moved around a lot in his first 2 years and the mother is not sure that his immunizations are up to date.

Pertussis (Whooping Cough)

According tothe Centers for Disease Control and Prevention (CDC, 2017), pertussis, also

commonly known as whooping cough is an acute and highly contagious upper respiratory disease caused

by a gram-negative bacterium called Bordetella pertussis.The disease is divided in three stages. Catarrhal,

the first stage of pertussis presents with clinical symptoms that can be dismissed as common cold

symptoms that usually include the following: Runny nose, sneezing, and a mild occasional cough and a

low-grade fever that may, or may not be there (Bentley, 2013, CDC, 2017, Spratling& Carmon, 2010).

The second stage called paroxysmal typically lasts between one to six weeks and is characterized by the

following symptoms:Violent cough, inspiratory whoop, post-tussive vomiting and a low-grade fever that

may or may not be there. The final stage of pertussis is called the convalescent stage and is characterized

by the cough gradually improving over a period of two to three weeks (Bentley, 2013, CDC, 2017,

Spratling& Carmon, 2010).

In diagnosing Kelvin with pertussis, the advanced nurse practitioner (NP) will consider the following:

Kelvin has a profound cough that has lasted about one week, has a deep cough that sounds like a bark.

Coughing so hard that patient sometimes actually vomits. No report of blood stains in the vomit. Low

grade fever. Unknown immunization status at age six years. No history of asthma or respiratory syncytial

virus (RSV). Kelvin’s clinical symptoms can be indicative of pertussis in its paroxysmal stage.

Confirmation of the diagnosis can be further supported if the patient has been in contact with a person

who is confirmed or suspected to have pertussis. Confirmation can also be done through culture and

isolation of B. Pertussis and/or detection of its deoxyribonucleic acid (Bentley, 2013, CDC, 2017,

Spratling& Carmon, 2010).

Pathophysiology

According to Dominguez (2005), pertussis is a highly contagious upper respiratory disease that is

caused by the gram-negative, coccobacillus Bordetella pertussis. Humans are the only known reservoirs

for this bacterium, and no animal or vector is known to exist. Transmission occurs through contact with

airborne droplets of respiratory secretions. The contagious period is seven days following exposure to the

organism and during the catarrhal stage. This period is usually two to three weeks after the onset of

symptoms. According to Dominguez (2005), two major non-fimbrial adhesions play an important role in

pertussis infection: filamentous hemagglutinin (FHA) and pertactin (PRN). Mutants lacking either of

these two are unable to attach to ciliated epithelial cells and cause colonization and cell damage.

According to Dominguez (2005), “Pertactin stimulates leukocytes to express integrins, which function as

receptors for FHA, leading to macrophage phagocytosis via CR3 avoiding oxidative burst and triggering

intracellular survival” (p. 234). After the attachment and onset of infection, adenylate cyclase (AC) toxin

plays an important role in cell damage and for causing impaired leukocyte function. The cytotoxic activity

of the AC results when the enzyme is activated by the host leading to “uncontrolled production of cAMP

altering the metabolism ofthe invaded cell. Tracheal cytotoxin and possibly dermonecrotic toxin are

involved in local damage to ciliated cells” (Dominguez 2005, p 234).

Behavior and Age Factors

According to Spratling (2010), pertussis is “primarily considered an illness of childhood” (p 239).

According to Bentley (2013), prior to the introduction of diphtheria, tetanus toxoid, and acellular pertussis

(DTaP) vaccination in the 1950s, pertussis was a leading cause of infants death with more than 120,000

deaths reported annually in the United Kingdom (UK) alone (p. 50). As in the case of Kelvin, human

behavior can affect whether a child gets vaccinated or not. Vaccination has led to a 99% decrease in

reported cases of pertussis, but recently, there has been an increase of reported cases particularly among

adolescents and adults (p. 50). Bentley (2013) reports that the World Health Organization (WHO)

reported that there were 16 million cases of pertussis reported globally in 2008 that resulted in the deaths

of approximately 195,000 children worldwide. This sadly means that pertussis remains a significant cause

of death for infants globally.

References

Bentley, J., Pinfield, J., & Rouse, J. (2013). Whooping cough: identification, assessment and

management.<Nursing Standard,<28(11), 50–57.

https://doi-org.ezp.waldenulibrary.org/10.7748/ns2013.11.28.11.50.e7911

Centers for Disease Control and Prevention. (2017). Pertussis (Whooping cough). Retrieved

from https://www.cdc.gov/pertussis/about/index.html

Domínguez D. (2005). The reemergence of pertussis in immunized populations: a case study.<Clinical

Laboratory Science,<18(4), 233–237. Retrieved from https://ezp.waldenulibrary.org/login?

url=https://search.ebscohost.com/login.aspx?direct=true&db=rzh&AN=106391335&site=ehost-

live&scope=site

Spratling R, & Carmon M. (2010). Pertussis: An Overview of the Disease, Immunization, and Trends for

Nurses.<Pediatric Nursing,<36(5), 239–243. Retrieved from https://ezp.waldenulibrary.org/login?

url=https://search.ebscohost.com/login.aspx?direct=true&db=rzh&AN=104928615&site=ehost-

live&scope=site

Week # 5

Late discussion post

Hello Dr Catherine. I am writing to you because I submitted my week 5 discussion late by one day. This

is not an excuse but a brief explanation of what happened prior to the assignment due date. While at work

on Tuesday Sept 25thnight, I felt a dull pain to the left upper side of my chest. The pain started gradually

and seemed to get worse when I made particular postures like turning my neck to the left or when I moved

my left shoulder. I checked all my vital signs and all were within normal parameters. A fellow nurse at

work did an EKG on me that came out as a normal regular rate, regular sinus rhythm. On Wednesday

morning, I considered going to our hospital ER department because the pain persisted. However, because

I didn’t have symptoms like shortness of breath or nausea, I drove myself to a nearby Care Now center

which is also owned by our hospital organization and charges our hospital employees a much lower rate.

After another EKG and a chest X-ray, I was diagnosed with Chondrocostal junction syndrome [Tietze].

The medications prescribed to me (Naproxen 500mg tabs and cyclobenzaprine5 mg tabs) made me very

drowsy. I was therefore unable to concentrate and finish my assigned discussion posts on Wednesday Sept

26th. The pain has gradually rescinded since then. I kindly request that you consider not subtracting marks

for my late submission.

Thank you.

Symonpeter Ndungu

Week #5 Discussion #2

Response #2 to Melissa

Hello Melissa. Thank you for a great post which I found very interesting and informative to read. I

agree with you that it is not a good idea to observe a patient suspected to be experiencing an anaphylactic

reaction in a clinical setting that is not equipped to handle an emergency that may require intubation to

protect the airway and intravenous medications. According to Santos_Longhurst& Watson (2018), all

anaphylactic reactions require an ER follow up even after initial treatment with epinephrine. It is also

important for people to understand that anaphylactic symptoms can rebound hours after the initial

treatment. I fount interesting to note that according to Santos_Longhurst& Watson (2018), one should

only administer epinephrine to a person who has a prescription for it. This becomes tricky because some

who get an anaphylactic reaction, such as the six-year old student in our case study has never had an

allergic reaction before, so, they never needed a prescription for epinephrine. However, considering that

an anaphylactic reaction is a life-threatening emergency, I agree with you that it is appropriate for the NP

to err on the side of ordering for administration of epinephrine intramuscularly and then send the patient

to the ER via ambulance(Santos_Longhurst& Watson, 2018).

References

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Santos-Longhurst, A. & Watson, S. (2018).< Healthline. Why Every Anaphylactic Reaction Requires a

Trip to the Emergency Room.< Retrieved from https://www.healthline.com/health/allergies/severe-

reactions-anaphylaxis-emergency-room

Week #5 Discussion #2

Response #1 to Stella

Hello Stella. Thanks for a great post. I found reading your post very interesting and informative. I

agree with you that all anaphylactic reactions require an ER follow up. According to Santos_Longhurst&

Watson (2018), it is important for people to understand that anaphylactic symptoms can rebound hours

after the initial treatment. The goal for all who get treated for an anaphylactic reaction should be to avoid

another one. It therefore is important for the advanced nurse practitioner (NP) to educate the individual to

stay away from their allergy trigger if it is known. If the allergy trigger is not known, the individual

should be referred to an allergist for a skin or blood test to identify their trigger (Santos_Longhurst&

Watson, 2018).

References

Santos-Longhurst, A. & Watson, S. (2018).< Healthline. Why Every Anaphylactic Reaction Requires a

Trip to the Emergency Room.< Retrieved from https://www.healthline.com/health/allergies/severe-

reactions-anaphylaxis-emergency-room

Week 5 Discussion # 2

Main Post

Pathophysiology of Anaphylactic Shock

Anaphylactic shock is an example of distributive shock that results from a severe hypersensitivity

reaction that is also known as anaphylaxis. According to Jevon (2010), anaphylaxis can also be described

as a severe, life threatening generalized or systemic hypersensitivity reaction. Common causes of

anaphylaxis include insect venoms, shellfish, peanuts, latex. Other common causes include drugs like

penicillin, muscle relaxants, antibiotics, non-steroidal anti-inflammatory (NSAIDs) and aspirin. When an

allergen is introduced to a predisposed individual, it initiates a vigorous humoral immune response that

results in degranulation of mast cells. The mast cells and basophils release histamine and a large number

of vasoactive mediators and inflammatory cytokines. This inflammatory response causes vasodilation

which causes hypotension and increased vascular permeability that causes edema due to peripheral

pooling. Besides the circulatory system, the inflammation process also affects the respiratory and the

gastrointestinal system. Other effects include decreased vascular tone, bronchospasm and pharyngeal and

laryngeal edema (Jevon, 2010, Huether& McCance, 2017).

Treatment

According to Huether& McCance (2017), the onset of anaphylactic shock is usually sudden and

progression to death can occur in a short time unless emergency treatment is administered. Besides

hypotension and altered mental status, other initial signs and symptoms of anaphylactic shock include

anxiety, dizziness, difficulty breathing, stridor, wheezing, abdominal cramping, pruritus with hives,

swollen lips and tongue.According to Jevon (2010), the initial treatment of anaphylaxis is basically the

same for adults and children. Initial treatment requires reassuring the patient and calling for help.The

patient should immediately be observed for any respiratory distress. If this happens in the hospital, then

protocol should be followed in calling in for help. If it happens outside the hospital, then asking someone

to call 911 is appropriate, even as one starts immediate interventions. If the probable cause for

anaphylaxis is visible, stop or remove it immediately. e.g. if a blood transfusion is in progress, stop it. If

oxygen is available, Jevon (2010) recommends administering high-flow oxygen at 15 liters/minute via a

non-rebreather mask. Jevon (2010) also recommends considering administering epinephrine

intramuscularly if there are clinical signs of shock or airway swelling. Patient should continue to be

monitored for oxygen saturation using a pulse oximeter.An electrocardiogram and blood pressure

monitoring should be done at the earliest opportunity. If available, IV fluids should be given with an aim

of reversing the relative hypotension.Epinephrine can be repeated after 5 minutes if there is no

improvement (Jevon, 2010, Huether& McCance, 2017).

Patient factors – Age and behavior

Factors that may impact anaphylactic shock include age and behavior.According to

Schub&Kornusky, (2016), food allergies are more likely to cause anaphylactic shock in children than in

adults. There is also an increased risk of children to having incidences of anaphylaxis due to poorly

controlled asthma (Schub&Kornusky, 2016). Anaphylaxis in older children and adolescents is more often

caused by medications, insect bites, and / or substance abuse.In adults aged 55-85, anaphylactic shock is

more likely as a result of drug induced allergies (Schub&Kornusky, 2016).

Anaphylactic shock can be prevented by patient’s behavior. If people are aware of their

allergies, learning to avoid the food or medications that cause an allergic reaction can go a long way in

avoiding incidences of anaphylactic shock (Schub&Kornusky, 2016). Individuals can reduce allergic

reactions if they learn to always read food labels. Those with allergies should also learn to make sure that

they inform their healthcare providers of their allergies. For those who are allergic to animal dander or

insects, they should learn to avoid such animals and they can also reduce their exposure to insects by

wearing long sleeved clothing, avoiding nests and hives, and avoiding use of perfumes. It is a good idea

for those who have allergies to wear medical alert bracelets. This would be important in medical

emergencies and may prevent incidences of anaphylactic shock from medications.

(Schub&Kornusky, 2016).

References

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.

Jevon P. (2010). Clinical focus. Recognition and treatment of anaphylactic reactions.<Nurse

Prescribing,<8(8), 362–368. Retrieved from

https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/login.aspx?

direct=true&db=rzh&AN=105085627&site=ehost-live&scope=site

Schub, T., &Kornusky, J. (2016). Shock, Anaphylactic. CINAHL Nursing Guide. Retrieve from

http://ezp.waldenulibrary.org/login?url=http://search.ebscohost.com/login.aspx?direct=tr

ue&db=rzh&AN=T701379&site=ehost-live&scope=site

Week 5 discussion

Response # 1 to

Hello Tanya. Thank you for your very interesting and informative post. As you mentioned, and I

agree with you, although heart murmurs in children are no an uncommon finding, the advanced nurse

practitioner (NP) should have done a more de

tailed assessment of the heart murmurs. As you mentioned, this case warranted referring the

patient to a pediatric cardiologist. Before sending the patient to the cardiologist, it would have been

important to order an echocardiogram anda 12-lead EKG. As I mentioned in my post, valvular aortic

stenosis (VAS) can be diagnosed via auscultation over the second right intercostal space at the sternal

border. On auscultation, one should hear a mid-systolic ejection murmur. In congenital aortic stenosis,

bicuspid valves rather than tricuspid valves are involved. VAS can be confirmed by echocardiography

which would show left ventricular hypertrophy and valve pathology which would typically show aortic

stenosis. By confirming the decreased valve area and increased peak flow, one can determine the severity

of the disease (Hull, 2012).

References

Hull, C. L. (2012). Treating Calcific Aortic Stenosis: An Evolving Science.<MEDSURG Nursing,<21(2),

82–88. Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 5 discussion

Initial post

Alterations of Cardiovascular function in Children

According to Huether& McCance (2017), congenital heart disease (CHD) is the most common

cause of cardiovascular alterations in children. CHD are classified based on whether they cause increased

or decreased blood flow to the lungs, whether they cause cyanosis and whether they cause an obstruction

of blood flow from the ventricles. In the scenario given in this week’s discussion, a 16-year-old male with

no significant medical or family history of sudden cardiac death (SCD) is assessed for a sports

participation examination by the advanced practice nurse (NP). The NP finds that the adolescent has a

grade II/VI systolic murmur heard loudest at the apex of the heart. All other physical findings were found

to be within normal limits. The NP cleared the him for activity without restriction. Sadly, later in the

season, the adolescent collapses on the field and dies.

Diagnosis and Treatment

On auscultation by the NP, the grade II systolic murmur at the apex of the heart could likely be

diagnosed as a valvular dysfunction due to stenosis (constriction or narrowing of the valve orifice) or

regurgitation (insufficient or incomplete valve). According to Huether& McCance (2017), valvular aortic

stenosis (VAS) is a serious defect because obstruction tends to get worse with time and may lead to

episodes of sudden myocardial ischemia that “can result in sudden death in late childhood or adolescence”

p. 657. According to Hull (2012), VAS can be diagnosed via auscultation over the second right

intercostal space at the sternal border. On auscultation, the NP should heat a mid-systolic ejection

murmur. In congenital aortic stenosis, bicuspid valves rather than tricuspid valves are involved. VAS can

be confirmed by echocardiography which would show left ventricular hypertrophy and valve pathology

which would typically show aortic stenosis. By confirming the decreased valve area and increased peak

flow, one can determine the severity of the disease (Hull, 2012).

Once the NP diagnoses VAS, he or she can refer the patient for specialized treatment by a

cardiologist. According to Hull, (2012), management for VAS is not perfected yet, and mortality increases

drastically when symptoms develop. Asymptomatic patients are monitored, and even mild to moderate

VAS does not require intervention or activity restriction. However, symptomatic patients should be

referred for specialized treatment. Treatment could be nonsurgical palliation or dilation of the stenotic

valve with balloon angioplasty. Surgical intervention for VAS depends on the severity of stenosis and

previous interventions, and the age of the child. Aortic valve replacement may be required if the valves

are severely damaged (Hull, 2012, Huether& McCance, 2017).

Patient Factor: Genetics

According to Huether& McCance (2017), the mechanism of causation of CHD is not known,

however, theincidence of CHD is three to four times higher among siblings of affected children. Children

with chromosomal defects like cri du chat syndrome, trisomy 13 syndrome, trisomy 18, trisomy 21

(Down syndrome), turner syndrome and Klinefelter variant have a relatively higher incidence of CHD.

References

American Heart Assocaition. (2016). Heart murmurs and valve disease. Retrieved from

http://www.heart.org/HEARTORG/Conditions/More/HeartValveProblemsandDisease/Heart-

Murmurs-and-Valve-Disease_UCM_450616_Article.jsp#.WVL1woqQzBI

Hull, C. L. (2012). Treating Calcific Aortic Stenosis: An Evolving Science.<MEDSURG Nursing,<21(2),

82–88. Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 4 discussion

Response # 2 to Edith

Hello Edith. Thank you for your informative post on myocardial infarction. As you mentioned, the

myocardium becomes cyanotic and cooler after 8 to 10 seconds of decreased blood flow and oxygen

reserves are quickly used. According to Huether& McCance (2017), although reperfusion is key to the

myocardium regaining full function, ischemic injury can be exacerbated by reperfusion injury once blood

flow is suddenly restored to the myocardium. Reperfusion can cause cell death when toxic oxygen free

radicals, calcium flux, and pH changes cause opening of mitochondrial permeability transition pores

(mPTPs). According to Vernma, Fedak, Weisel e.t al (2002), the myocardium is “stunned” by reperfusion

and requires prolonged period of time before regaining complete functional recovery. According to

Huether& McCance (2017), many innovative therapies are being explored to reduce reperfusion injury.

References

Vernma, S., Fedak, P. W., Weisel, R. D., Butany, J., Rao, V., Maitland, A., . . . Yau, T. M. (2002, May

21). Archive of all online content. Retrieved September 22, 2018, from

https://www.ahajournals.org/doi/abs/10.1161/01.cir.0000016602.96363.36

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

Week 4 discussion.

Response # 1 to Kristi

Thank you for your informative and interesting post on congestive heart failure (CHF). As you

mentioned, age and hypertension play a role in developing of CHF. According to the American Heart

Association (AHA, 2017), one in every three Americans have hypertension. If hypertension is not well

managed, it can lead to heart failure (HF). According to AHA (2017), more than six million Americans

are living with HF today, and it is predicted that this number will increase by 46% over the next 15 years.

Unfortunately, HF is a very costly condition and also interferes with an individual’s quality of life. It is

important that advanced nurse practitioners educate their patients that the treatment plan for HF may

include lifestyle changes and medication. According to AHA (2017), some lifestyle changes like quitting

smoking and eating a heart healthy diet can make significant changes in the outcome of those diagnosed

with HF. According to AHA (2017), HF costs Americans about $30 billion dollars each year. This cost is

expected to rise to almost $70 billion dollars by 2030, and 80% of these costs are due to hospitalization

(AHA, 2017).

References

American Heart Association, (2017). Understand Your Risk for Heart Failure. Retrieved from:

http://www.heart.org/en/health-topics/heart-failure/causes-and-risks-for-heart-failure/understand-

your-risk-for-heart-failure

Centers for Disease Control and Prevention. (2012). Heart disease facts. Retrieved

from<http://www.cdc.gov/heartdisease/facts.htm

Week 4 discussion. Initial post

Peripheral Artery Disease

Pathophysiology

According to Huether& McCance (2017), peripheral artery disease (PAD) is a disease that is

caused by atherosclerosis of the arteries that supply blood to the lower extremities. This disease affects

“an estimated 8.5 million Americans” agedover 40 years (p. 610). Atherosclerosis is a condition whereby

blood vessels become hardened and thickened due to accumulation of lipid-laden macrophages within the

arterial wall. This pathologic process can affect any vascular systems anywhere in the body. According to

Huether& McCance (2017), atherosclerosis begins when an injury occurs to the endothelial cells that line

the artery walls. This injury could be as a result of alterations caused by hypertension. Hypertension

increases shear stress on vessels and is known to contribute towards endothelial injury causing the risk of

atherosclerosis to increase by “twofold to threefold” (p. 612). An injury to the endothelial cells causes

infiltration of low-density lipoproteins (LDLs) into the subendothelial region. An injury to the endothelial

cells also causes inflammation which activates adhesion molecules that bind macrophages and other

inflammatory and immune cells to the site of injury. The inflammation process also generates toxic

oxygen free radicals that causes oxidation of LDL that has accumulated in in the subendothelial region

(Hammer & McPhee, 2014, Huether& McCance, 2017).

When macrophages engulf oxidized LDL, they become foam cells. An accumulation of these

foam cells causes lesions (fatty streaks) that are found in the walls of arteries of most people, even young

ones. These fatty streaks continue to produce more toxic oxygen free radicals that continue to recruit T

cells and causing more inflammation that leads to progressive damage of the blood vessel. Macrophages

continue to release growth factors that stimulate smooth muscle cell proliferation that produces collagen

over the fatty streak and thereby forming a fibrous plaque. This fibrous plaque can calcify and cause

hardening and thickening of the blood vessel which is called sclerosis. These fibrous plaques can cause

arterial obstruction in lower extremitiesand may lead to lower extremities ischemia. If this plaque

raptures, it leads to platelet aggregation and subsequent thrombus formation (Hammer & McPhee, 2014,

Huether& McCance, 2017).

Behavior risk factors

Some behavioral risk factors known for PAD include smoking, diabetes, hypertension and

dyslipidemia. According to Hammer & McPhee(2014), men who smoke a pack of cigarettes a day have a

70% increased risk of death from a cardiovascular disorder compared to nonsmokers. Smoking causes

carbon-monoxide hypoxia which causes endothelial damage. Quitting smoking is therefore a major way

of slowing down atherosclerosis. According to Hammer & McPhee(2014), diabetes is known to cause

complications that increase risks for atherosclerosis and is known to cause “severe circulatory deficiency

in the legs” that commonly results in gangrene (p. 310). According to Hammer & McPhee(2014),

hypertension causes an elevated blood pressure in the endothelium which increases shear stress. Shear

stress is a known factor for atherosclerosis. Managing blood pressure is therefore an important factor in

reducing PAD. According to Hammer & McPhee(2014), there is “overwhelming” evidence that lowering

plasma cholesterol and triglyceride levels while increasing high-density lipoproteins (HDL) in plasma

slows down, and in some cases, reverses the atherosclerosis process (Hammer & McPhee, 2014, p. 309).

References

Centers for Disease Control and Prevention. (2012). Heart disease facts. Retrieved

from<http://www.cdc.gov/heartdisease/facts.htm

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.

Laureate education, Inc. (Executive Producer). (2012a). Alterations of cardiovascular functions PPT

lecture. Baltimore, MD: Author.

Hello Shareen. Thank you for your very intersting and informative post. As you mentioned in your

post, research in genetics has discovered that subtle changes in DNA could partly explain the variation in

individual differences in pain and that various genes encoding for receptors are now known to play a

major role in the sensitivity, perception, and expression of pain (James, 2013). According to Lotsch

(2011), thereis a relation between a patient's genotype and pain phenotype which was first suggested

about 50 years ago. In that early report, the results of a basic genetics research study showed that the risk

of migraine is hereditary, with an emphasis on underlying molecular mechanisms. With the increasing

sophistication of genetic research, genotyping has become an effective scientific tool to identify specific

molecular causes underlying the susceptibility to pain, its intensity and its clinical development toward

either disappearance or chronification up to neuropathic pain. According to Lotsch (2011), there are new

pharmacological approaches to pain treatment currently under clinical studies. Functional genetic variants

may serve as substitutes for unavailable drugs by modulating the newly discovered molecular mechanism.

This would provide support for the successful development of pharmacological treatments targeting the

identified mechanism(Lotsch (2011).

References

Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO:

Mosby.

James, S. (2013). Human pain and genetics: some basics. British Journal of Pain, 7(4), 171–178.

http://doi.org/10.1177/2049463713506408

Lötsch, J. (2011). Genetic variability of pain perception and treatment-clinical pharmacological

implications.<European Journal Of Clinical Pharmacology,<67(6), 541-551. doi:10.1007/s00228-011-

1012-9

Neurological System: Pain

Week 3 Discussion: Initial Post

According to Huether & McCance (2017, p 336), pain is defined as “whatever the experiencing

person says it is, existing whenever he says it does.” According to CDC (2016), an estimated twenty

percent of patients presenting to a healthcare provider with noncancer pain symptoms or pain-related

diagnoses (including acute and chronic pain) receive an opiod prescription. As Advanced Nurse

Practitioners (APN) learning to treat patients with acute, chronic and refferred pain, it is important to learn

how to manage pain and monitor patients at risk or addicted to opiods (Center for Disease Control and

Prevention, 2016).

Pathophysiology

According to Huether& McCance (2017, p. 337), pain transduction begins when nociceptors are

activated by a noxious stimulus, causing ion channelson nociceptors to open and thereby creating

electrical pulses that travel through axions of two primary types of nociceptors that are transmitted to the

spinal cord, brain stem, thalamus, and cortex. The two primary types of nociceptors are A-delta fibers and

C fibers (Huether& McCance, 2017, p.337). A- delta fibers are largerand myelinated fibers that

quicklytransmitssharp, well localized fast pain sensations such as burn or pinprick. The spinal reflex that

causes a rapid withdrawal of the affected body part even before pain sensation is perceived is as a result

of activation of these fibers (Huether& McCance, 2017, p.337). Although the C fibers are the most

numerous, they are unmyelinated and are located in muscles, tendons, body organs, and in the skin. The

pain that they conduct is explained as dull, aching, burning, constant and is hard to localize (Huether &

McCance, 2017, p.337).

Acute Pain

According to Huether& McCance, (2017, p. 339), acute pain is described as a normal protective

mechanism for alerting an individual of an injury. The alert should prompt the individual to act in order to

relieve himself/herself from the pain. The pain is transient and usually lasts for seconds, days and up to

three months. The pain starts suddenly and it ends as soon as the chemical mediators that stimulate pain

receptors are removed. Acute pain can arise from an injury or as a response to inflammation or disease.

Physiological body reactions to pain may include increased heart rate, hypertension, diaphoresis and

dilated pupils(Huether& McCance, 2017, p.341).

Chronic Pain

According to Huether& McCance, (2017, p.340), chronic pain is described as pain lasting for

more than three to six months and well beyond the expected normal healing time. Chronic pain varies

with type of injury, serves no purpose, is poorly understood and often appears to be out of proportion with

any observable tissue injury. Chronic pain may be ongoing or intermittent. According to Huether&

McCance, (2017, p.337), it is thought that chronic pain is caused by changes to the peripheral and central

nervous systems that causes dysregulation of nociception and modulation processes. Neuro imaging

studies show that the brain changes in individuals with chronic pain causes cognitive deficits and

decreased ability to cope with pain. According to Huether& McCance (2017, p.340), the physiologic

responses to intermittent chronic pain is similar to acute pain, but the body allows for physiologic

adaptation to persistent pain, producing normal heart rate and blood pressure. Some chronic diseases like

osteoarthritis, rheumatoid arthritis causes chronic pain in individuals. Chronic pain does not resolve on its

own and without treatment, it can progress to and cause behavioral changes including depression,

difficulty eating and sleeping, and thereby can reduce the overall quality of life for individuals suffering

from it (Huether& McCance, 2017, p.340). (Huether& McCance, 2017).

Referred Pain

According to Huether& McCance, (2017, p.340), referred pain can be acute or chronic and is felt

in an area that is a distant from the affected area. The area where the pain is reffered to is served or

supplied by the same spinal segment of the actual pain site (Huether& McCance, 2017, p.340).The fact

that many cutaneous and visceral neurons converge on the same ascending neuron, the brain cannot

distinguish between different sources of pain(Huether& McCance, 2017, p.340).

Similarities and Differences

While acute can be described as short lasting, chronic pain is described as lasting for longer period

of time. Referred pain can be either chronic or acute. On treatment of the chemical or problem causing

acute pain, the acute pain eventually resolves and does not reappear. Chronic pain does not completely

resolve even with treatment. Acute pain is described as well defined, while chronic pain is not well

defined. Whether acute, chronic or referred, the same description of pain as described by Huether&

McCance (2017, p. 336) as “whatever the experiencing person says it is, existing whenever he says it

does” remains. Onset for acute pain is usually sudden while onset for chronic pain may be sudden or may

develop insidiously. While acute pain decreases over time, chronic pain increases over time (Huether&

McCance 2017, p. 341)

Age& Gender Factors

According to Epocrates (n.d.), increased age especially over forty-five years old increases the risk

of individuals developing with chronic pain (Epocrates, n.d.). With age, generally, individuals are at risk

of developing multiple comorbidities and age influences level of pain (Epocrates, n.d.).

Gender

According to Epocrates (n.d.), females generally are at a higher risk for chronic pain (Epocrates,

n.d.) and womenalso have greater pain sensitivity, enhanced pain facilitation, and reduced pain inhibition.

This places women at a higher risk than men for developing pain disorders.

Reference

Center for Disease Control and Prevention (March 18, 2016) CDC Guidelinesfro Prescribing Opiods for

Chronic Pain – United States, 2016. Retrieved from:

https://www.cdc.gov/mmwr/volumes/65/rr/rr6501e1.htm?CDC_AA_refVal=https%3A%2F

%2Fwww.cdc.gov%2Fmmwr%2Fvolumes%2F65%2Frr%2Frr6501e1er.htm

Epocrates. (n.d.). Chronic pain syndromes. Retrieved from:

https://online.epocrates.com/diseases/69421/Chronic-pain-syndromes/Definition

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.

Posta description of the pathophysiology of osteoarthritis and

rheumatoid arthritis, including the similarities and differences

between the disorders. Then explain how the factors you selected

might impact the pathophysiology of the disorders, as well as the

diagnosis of treatment for the disorders.

Main Post Jessica Hernandez

Week 2 Discussion 1

Response # 2 to Elaina

Hello Elaina. Thank you for your very interesting and informative post. As you mentioned, age is

an important factor in people developing psoriasis. As you mentioned, psoriasis can occur at any age, but

the onset generally occurs by age 40. Any onset of psoriasis at later stage in life is more related to co-

morbidities, like obesity, smoking, high blood pressure, and diabetes.<According to (Hammer & McPhee,

(2014, p 191), there is also evidence that genetic factors contribute to development of psoriasis disease.

As I mentioned in my post, there is documented high rate of concordance for psoriasis in monozygotic

twins and also an increased incidence among relatives of affected individuals. Gene products of specific

class I alleles of major histocompatibility complex (MHC) are overexpressed in patients with psoriasis.

However, psoriasis cannot be described as merely a genetic disorder because some susceptible individuals

never develop characteristic lesions. In predisposed individuals, a number of environmental factors like

infection, physical injury, stress and drugs can trigger development of psoriasis (Hammer & McPhee,

(2014, p 191)

References

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.

Discussion 2 Week 2

Initial post

Pathophysiology of Osteoarthritis

According to Huether& McCance (2017, p 1010), the primary defect in osteoarthritis (OA) is loss

of articular cartilage and is characterized by local areas of loss and damage of the articular cartilage,

inflammation, new bone formation of joint margins, subchondral bone changes, variable degrees of mild

synovitis and thickening of the joint capsule. OA can arise in any synovial joint but is most common in

the knees, hips, hands and, spine. In early stages of OA, the articular cartilage begins to look loose its

glistening appearance and becomes yellow-gray or brownish-gray. With progression of the disease, pieces

of the cartilage begin to flake off and deeper layers develop longitudinal fissures, resulting in a thin

cartilage and no cartilage at all in some areas.Loss of cartilage leaves underlying bones unprotected.

The unprotected bone becomes dense and hard. Cysts can then form cause further damage to the

cartilage. As pressure builds in the cysts, their contents are forced into the synovial cavity, thereby

breaking through the articular cartilage. This erodes the articular cartilage. As the articular cartilage

erodes, osteophytes may grow outward from the underlying bone and alter the joint anatomy. The spur-

like bony projections continues to enlarge until small pieces begin to break off in the synovial cavity

causing joint effusion or synovitis. This causes pain and may also cause limited range of motion as the

joint capsule becomes thickened and adhering to the bone. For weight bearing joints, pain relief may

occur when the joint is at rest. The primary signs and symptoms of OA are pain, stiffness, enlargement or

swelling, tenderness, limited range of motion, muscle wasting, partial dislocation and

deformity(Huether& McCance, 2017).

Pathophysiology of Rheumatoid Arthritis

According to (Huether& McCance, 2017), rheumatoid arthritis (RA) is a chronic,

systemicinflammatory autoimmune disease that causes joint swelling, tenderness and destruction of

synovial joints leading to disability and premature death. The first joint tissue to be affected by RA is the

synovial membrane. Though the initiating mechanisms of RA is unknown, some factor activates the

synovial fibroblasts (SFs) that line the joint cavity. This causes SF to undergo significant changes and to

develop an exaggerated immune response, thereby proliferating and producing proinflammatory

cytokines, enzymes, and prostaglandins that perpetuate the inflammatory process. Normal synovium in

the joints has a layer that is 1 to 2 cellsdeep. However, RA inflammation process increases the synovium

to a thickness 10 to 20 cells thick. The thickened synovial tissue called pannus invades the bone and acts

like a localized tumor, causing bone damage. Eventually, RA spreads through blood stream and causes

inflammation in other joints and fibrous joints.

According to, Huether& McCance, 2017), cartilage damage in RA is a result of neutrophils and

other cells in synovial fluid becoming activated thereby degrading the surface layer of articular cartilage.

Inflammatory cytokines, tumor necrosis factor-alpha, interleukin-7, and interleukin 21 induce enzymes

that break down the articular cartilage and bone. Meanwhile, T cells interact with SF and converts

synovium into pannus. Vascular changes also occur which can cause thrombosis. RA may

causesymptoms such as, fatigue, joint inflammation, pain, swelling, warmth, and stiffness.As RA

progresses, it can cause deformities in the joints. Early treatment can be effective in preventing the

systemic and joint abnormalities associated with this chronic disease (Hammer, & McPhee,

(2014),<Huether& McCance, 2017).

Similarities and Differences

Similarities in both osteoarthritis and rheumatoid arthritis include similar symptoms like joints

pain, swelling and stiffness. There is inflammation in both OA and RA. There also is destruction of

cartilage and the resulting synovitis in both OA and RA. According to (Hammer, & McPhee,

(2014),<Huether& McCance, 2017), the pathophysiology of both diseases includestumor necrosis factor

and interleukins aiding in the destruction of the cartilage. The exception is that RA affects joints

bilaterally. In both diseases, clinical presentation helps in their diagnosis.However, treatment for OA and

RA different. OAis treated with NSAIDs while RA is treated with steroids. While OA affects a single

joint, RA spreads through blood stream and causes inflammation in other joints and fibrous joints

throughout the whole body, thereby affecting more than onejoint (Huether& McCance, 2017).

Factors of Age and Gender

According to Huether& McCance (2017), OA is less common in people younger than 40 years of

age and its prevalence increases with age. Although other factors like obesity and trauma are well known,

age is a well-known common factor for OA and RA. However, although OA occurs in both men and

women, it is more prevalent in women after the age of 50 years (Huether& McCance, 2017, p 1009). The

same age factor applies in RA. RA is more common in patients in their 50’s or 60’s. According to

Hammer & McPhee (2014), RA is three times more likely to occur in women compared to men.

Hormones and menopause are believed to be a factor on why more women than men in the affected by

RA. Obesity is also a factor in both OA and RA. Weight adds strain on joints. As people age, they also

usually add weight, hence raising the prevalence of both OA and RA with age.(Huether& McCance,

2017).

References

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.

Arthritis Foundation. (2012). Retrieved from http://www.arthritis.org

Discussion Week 2

Response # 1 to Pamela

Hello Pamela. Thank you for your very interesting and informative post on Inflammatory bowel

disease (IBD) and Psoriasis. As you mentioned, the prevalence of IBD is about 1.6 million people in the

United States (Huether& McCance (2017). As you mentioned, the trigger for both IBD and psoriasis

remains unclear, but symptoms of both diseases are known to occur or can be exacerbated during or after

a stressful event. As I mentioned in my post, according to (Hammer & McPhee, (2014, p 372), though

genetics are not the only risk factors for IBD, newly recognized susceptibility genes for both Crohn

disease and ulcerative colitis have been discovered. Genetics as a risk factor is documented to increase

susceptibility of developing IBD by twenty to thirty percent. Studies found abnormalities in several

categories of susceptible genes in patients with IBD. This includes modulators for immune function,

autophagy and epithelial function that interacts with the body and microorganisms (Hammer & McPhee,

(2014, p 372).

According to (Hammer & McPhee, (2014, p 191), there is also evidence that genetic factors

contribute to development of psoriasis disease. There is documented high rate of concordance for

psoriasis in monozygotic twins and also an increased incidence among relatives of affected individuals.

Gene products of specific class I alleles of major histocompatibility complex (MHC) are overexpressed in

patients with psoriasis. However, psoriasis cannot be described as merely a genetic disorder because some

susceptible individuals never develop characteristic lesions. In predisposed individuals, a number of

environmental factors like infection, physical injury, stress and drugs can trigger development of psoriasis

(Hammer & McPhee, (2014, p 191)

References

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.

Main Post

Pathophysiology of Inflammatory Bowel Disease

According to Huether& McCance (2017, p 920-921), inflammatory bowel disease (IBD) consists

of two chronic diseases; Crohn disease(CD) and Ulcerative colitis (UC). The exact trigger for both

diseases is still unclear. The primary lesions of UC begin with inflammation at the base of the crypt of

Liebermakuhn in the large intestines. The disease begins in the rectum and may extend proximally to the

entire colon. The mucosa of those suffering from this disease is hyperemic, may appear to be red and

velvety, small erosions forms and turns into ulcers. This leads to abscess formation, necrosis and ragged

ulceration of the mucosa. The muscularis mucosae may narrow the lumen of the involved colon from

edema. Inflammation and destruction of the mucosa causes bleeding, cramping pain, frequent diarrhea

with passage of small amounts of blood and purulent mucus. Due to loss of the absorptive mucosal

surface and the rapid colonic transit time, this disease causes large volumes of watery diarrhea (Hammer

& McPhee, (2014, p 372), Huether& McCance (2017, p 920-921).

According to Huether& McCance (2017, p 921), Crohn disease is an idiopathic inflammatory

disease that can affect any part of the gastrointestinal track. The ascending colon and the transverse colon

are the most common sites of this disease, however, both the large and small intestines and especially the

ilium may be involved. Inflammation begins in the intestinal submucosa and spreads with discontinuous

transmural involvement. Typical lesions are granulomas that have a cobblestone appearance from

projections of inflamed tissue that is surrounded by ulceration. Perforation and fistulae may form in the

perianal area and can extend into the bladder, vagina, or the rectum. Strictures can also develop and cause

obstruction. Frank bleeding from the mucosal ulcerations can be insidious or massive. Smoking increases

the risk factors of developing this disease and inhibits its treatment(Hammer & McPhee (2014), Huether&

McCance, 2017).

Pathophysiology of Psoriasis

According to Huether& McCance (2017, p 1062), psoriasis is a chronic, relapsing and

proliferative inflammatory disease that involves the skin, scalp and nails. It can occur at any age and

ranges between mild, moderate and severe depending on the size, distribution and inflammation of

lesions. Psoriasis affects both the dermis and epidermis where they both become thickened due to cellular

hyperproliferation, altered keratinocyte differentiation, and expanded dermal vasculature.Usually, the

epidermis sheds in 14 to 20 days, however, with psoriasis shedding is reduced to every 3 to 4 days. This

leads to cell maturation and keratinization not occurring, the epidermis thickening, and the plaques

forming. Since keratinization does not occur, the loosely cohesive keratin gives the lesions a silvery

appearance and erythemawhich is caused by the rapid cell metabolism, capillary dilation, and increased

vascularization (Huether& McCance, 2017).

Maladaptive and Psychological Response

The immune responses in both IBD and psoriasis disease are very similar as they are both

inflammatory responses. In psoriasis,the inflammatory cascade involves complex interactions between

macrophages, fibroblasts, dendritic cells, natural killer cells, T helper cells, and regulatory T cells.

Macrophages are responsible for destroying cellular debris and microorganisms. These immune cells

trigger the secretion of numerous inflammatory mediators like interferon, tumor necrosis factor and

cytokines such as interleukin 12, 23, and 17. The inflammatory response is normally meant to promote

healing and to prevent further injury, but in the case these cases of psoriasis disease and IBD, the

inflammatory response is maladaptive and ends up hurting the body more.In IBD, environmental factors

are thought to alter the barrier functions of the mucosal epithelium thereby leading to loss of immune

tolerance to normal intestinal antigens. The loss of tolerance leads to activation of dendritic cells which

triggers their transport to the mesenteric lymph nodes where differentiation of T cells and T regulatory

cells is promoted. Production proinflammatory cytokines, chemokines, tumor necrosis factor, interleukins,

toxic oxygen free radicals, and interferon gamma leads to the damage of the intestinal epithelium.

However, chemokines are not secreted in psoriasis but are secreted in inflammatory bowel disease and are

responsible for attracting leukocytes to the site of inflammation. Natural killer cells which are not

produced in IBD are responsible for recognizing and eliminating infected cells(Huether& McCance,

2017).

Genetics Factor

According to (Hammer & McPhee, (2014, p 372), genetics are not the only risk factors for IBD,

however, newly recognized susceptibility genes for both Crohn disease and ulcerative colitis have been

discovered. Genetics as a risk factor is documented to increase susceptibility of developing IBD by twenty

to thirty percent. Studies found abnormalities in several categories of susceptible genes in patients with

IBD. This includes modulators for immune function, autophagy and epithelial function that interacts with

the body and microorganisms (Hammer & McPhee, (2014, p 372).

According to (Hammer & McPhee, (2014, p 191), there is evidence that genetic factors contribute

to development of psoriasis disease. There is documented high rate of concordance for psoriasis in

monozygotic twins and also an increased incidence among relatives of affected individuals. Gene

products of specific class I alleles of major histocompatibility complex (MHC) are overexpressed in

patients with psoriasis. However, psoriasis cannot be described as merely a genetic disorder because some

susceptible individuals never develop characteristic lesions. In predisposed individuals, a number of

environmental factors like infection, physical injury, stress and drugs can trigger development of psoriasis

(Hammer & McPhee, (2014, p 191)

References

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.

Response Post #1

Kristen,

Systemic Lupus Erythematosus (SLE) is actually able to be diagnosed with a laboratory test.

Although SLE is generally diagnosed based on having four of the ten clinical manifestations, it can also

be diagnosed with a positive blood test for antinuclear antibody or ANA. This is not entirely accurate for

diagnosis as only 98% of patients with SLE with have a positive ANA test (Huether& McCance,

2017).You bring up great points about the gender factor of inflammatory bowel disease and SLE. For this

discussion I chose the factor of behavior and have already addressed inflammatory bowel disease in my

main post. I would like to add to your post about SLE and its relations to behavior. Although SLE is not

very well known about the trigger of initiating the disease, it has been shown that genetics has the

strongest known risk factors. Studies have shown that drugs and viral infections can contribute to risk

factors. With that being said, avoiding drug use can minimize the risk of SLE development. In SLE flare

ups occur when an organism comes in contact with the antigen again the immune system responds.

Ultraviolet lights have been known to trigger the disease and provoke flare-ups (Hammer & McPhee,

2014). Staying away from tanning beds would be a behavior modification that can be done to avoid future

flare-ups.

References

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.

Response #2

Joshua,

For this post I chose the factor of behavior. Behavior and human immunodeficiency virus (HIV)

are very well correlated. HIV is a blood borne pathogen; therefore, it is easily spread to another through

the contact of blood. The most common ways HIV in acquired is through contact with blood, sexual

intercourse, intravenous drug abuse, and during birth from mother to baby. Babies can also contract the

disease from breast feeding (Huether, & McCance, 2017). With that being said there are many behavior

modifications that can occur to stop the transmission of HIV. First and foremost would be to remain

abstinent. Many people are unaware that even when using a condom there is still high risk for the

contraction of HIV (Huether, & McCance, 2017). The American Nurse Association (ANA) does not feel

it is ethical to require mandatory testing and disclosure of a person’s HIV status to prevent transmission.

The ANA does not support mandatory disclosure of HIV status to anyone (American Nurses Association,

2016). Basically everyone should take precautions to protect themselves against HIV/AIDS. New Jersey

does not require a person infected with HIV to report positive results to their partner. However if they

have unprotected intercourse and infect another person they potentially could be criminally persecuted,

although it is unlikely (The Center for HIV law and policy, 2012). This is why it is important to protect

yourself as in many states by law a person does not have to tell you they are infected. Saying no to drugs

or if using drugs, only use a clean needle and do not needle share can also be a behavior modification to

avoid contraction of HIV. As healthcare professionals it is important we always keep ourselves protected

when coming in to contact with blood as it is a daily part of our routine. Interestingly enough although

there has been much awareness raised about HIV the prevalence is still high and it was estimated in 2013

there were 2.5 newly infected people in the world (Huether, & McCance, 2017).

References

American Nurses Association. (2016). HIV testing. Retrieved from

http://nursingworld.org/MainMenuCategories/Policy-Advocacy/Positions-and-Resolutions/

ANAPositionStatements/Position-Statements-Alphabetically/HIV-Testing.html

Huether, S. E., & McCance, K. L. (2017).<Understanding pathophysiology(6th ed.). St. Louis,

MO: Mosby.

The Center for HIV law and policy. (2012). New Jersey. Retrieved from

http://www.hivlawandpolicy.org/states/new-jersey

Posta brief description of a patient scenario involving the disorder and the factor you selected.

Explain how the factor might impact your selected disorder, as well as potential associated

alterations and symptoms. Finally, explain the pathophysiology of the associated alterations,

including changes in cellular function.

Response # 1 to Tanya

Hello Tanya. Thank you for your very interesting and informative post on Parkinson’s disease

(PD). As you mentioned, the pathogenesis of Parkinson’s disease is unclear, however, age and gender

seem to be a common factor in most cases. You also mentioned that according to the National Institute on

Aging (n.d.), age is most strongly associated with the incidence of Parkinson’s disease and that 50 percent

more men than women are affected by this debilitating disease (National Institute on Aging, n.d.).

According to Hammer, & McPhee (2014, p 172), approximately 5% of PD cases are

familial.Genetic studies have identified causative mutations in five genes that provide important

information about molecular pathways involved in the disease. These genes include genes for alpha-

synuclein (PARK1), parkin (PARK2), DJ-1 (PARK7), ubiquitin-C-hydroselase-L1 (PARK5), and PTEN.

Mutations in alpha-synuclein on the chromosome 4q21-23 causes autosomal dominant PK. Alpha-

synuclein is listed as “the largest single genetic risk factor” for PD (Hammer, & McPhee, (2014, p 172).

Reference

Hammer, G. D. & McPhee, S. J., (2014). Pathophysiology of disease: An introduction to clinical

medicine. (7th Edition). New York, NY: McGraw-Hill Medical.

National Institute on Aging. (n.d.). Parkinson’s disease. Retrieved

fromhttps://www.nia.nih.gov/health/parkinsons-disease

Initial post - Week 1 Discussion

Factors that Influence Disease

Patient scenario.

I work in a psychiatric/mental health unit. Last year, we had to send a 66-year-old male patient to

the main hospital for further evaluation. The patient came to us for suicidal ideations with a plan to jump

from a high building. During the admission assessment, he told me that he usually has generalized lower

abdominal pain, and that his bowel habits had changed. He complained that he often has bright red blood

in his stool, and that the last time that happened was that morning. The patient had a past medical history

type II diabetes mellitus, smoked one pack of cigarettes every day, drank alcohol occasionally, was

obese,report his diet to be high in fat and low on fiber and denied involvement in any exercise. After

further evaluation in the main hospital, the patient was diagnosed with colorectal cancer (CRC).

According toUlbricht, C. (2013), CRC is the second-leading cause of cancer-related deaths in the United

States.

Impact of genetics on CRC and potential associated alterations and symptoms.

According to Huether& McCance (2012), CRC cases have familial history and can be an

outcome of complex multiple gene interactions, abnormal DNA methylation, or polyps.According to

Hammer, &McPhee (2014, p 98), the rare familial syndromes associated with predisposition to colon

cancer at an early age are known to result from germline mutations. Two examples of genetic factors in

this case are familial adenomatous polyposis (FAP) which is a result of mutations in the APC gene.

FAP is a rare disorder that causes people to develop multiple polyps in the colon or rectal lining. If left

untreated, FAP greatly increases the risk of developing CRC before age forty. Thehereditary

nonpolyposis colorectal cancer(HNPCC), also called Lynch syndrome if left untreated increases the

risk of developing CRC and other cancers in people before age fifty. HNPCC is associated with

germline mutations in the DNA repair genes such as hMSH2 and hMLH1 (Hammer, &McPhee, 2014).

According to Eskiocak et al. (2011), there are research findings that at least seventy genetic mutations 
are involved in formation of colon cancer. However, current CRC treatment targets one or two of the 
known genes. Eskiocak et al. suggests that CRC treatment should target multiple genes and pathways 
simultaneously. According toEskiocak et al., such treatment would prevent current outcomes of return 
of tumor growth.
With the understanding of how genes impact CRC, family members considered to be at a higher 
risk can be encouraged to participate in genetic testing and screening programs for hereditary non-
polyposis colon cancer (HNPCC). These family members should also be encouraged to have regular 
colonoscopy screenings, facilitation of removal of polyps and treatment of early tumors (McCann et al.).
The pathophysiology of the alterations, including changes in cellular function.
According to Hammer, &McPhee (2014, p 99), the earliest molecular defect in the pathogenesis of
colon cancer is the acquisition of somatic mutations in the APC gene in the normal colonic mucosa. 
Abnormalities in the regulation in cell proliferation causes defects in mechanisms that protect the genomic
stability. The resulting abnormal proliferation (growth) of cells to the lining of the colon wall leads to 
development of polyps. If polyps are left untreated, they continue to proliferate into malignant tumors that
can then invade the lining of the colon, leading to colon cancer(Hammer, &McPhee, 2014). According to 
Huether& McCance, (2017, p 940), some of the symptoms of CRC are pain, changes in bowel habits, 
bright red blood in stool, anemia, obstruction and abdominal distention. These clinical manifestations also
depend on the location, size, and shape tumors (Huether& McCance, 2014).
References
Center for Disease Control and Prevenction
Eskiocak U., Kim S. B., Ly P., Roig A. I., Biglione S., Komurov K., Cornelius C., (...), Shay J. W.(2011). 
Functional parsing of driver mutations in the colorectal cancer genome reveals numerous 
suppressors of anchorage-independent growth. Cancer Research, 71(13), 4359-4365. 
doi:10.1158/0008-5472.CAN-11-0794
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6thed.). St. Louis, MO: 
Mosby.
McCann, S., Macauley, D., Barnett, Y., Bunting, B., Bradley, A., Jeffers, L., & Morrison, P. (2009). 
Family communication, genetic testing and colonoscopy screening in hereditary non-polyposis 
colon cancer: A qualitative study. Psycho-Oncology, 18(11), 1208-1215. doi:10.1002/pon.1487
Hammer, G. D. &McPhee, S. J., (2014). Pathophysiology of disease: An introduction to clinical medicine.
(7th Edition). New York, NY: McGraw-Hill Medical.

Ulbricht, C. (2013). An integrative approach to colon cancer: A natural standard monograph. Alternative

& Complementary Therapies, 19(1), 44-48. doi:10.1089/act.2013.19101

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