Cassandra Case Study Nursing

Hi Roseann. Good Job. Your Unit 7 Initial Post is very informative. Her verbal report of fatigue, bilateral lower lobe crackles, skin is cool to touch, +2 edema in bilateral ankles, and heart rate of 112 are signs and symptoms of congestive heart failure. Her medical history of high blood pressure and coronary artery disease could also lead to heart failure. My focus would be is to teach her with CHF symptom management and to prevent exacerbation. To avoid hospitalization I would educate and give her a list of preventable measures such as avoiding salts, measuring her weight every morning, and fluid restrictions. I would advise S.P to notify her doctor with weight gain over 2 pounds. Medication compliance is also important in managing her

At this point, we do not know exactly what are the settings, we have previous requested pacemaker operative report from Regions. Unfortunately, from what he is telling today, his date of the birth was not correct as such dose report were not same. He noted that he thinks he came back from the hospital, he has not had similar complaint or concern or report of chest pain. It should be noted that hospital records, with a troponin that was negative, 12-lead EKG was similar to the one that was obtained here, essentially identifying sinus bradycardia with first-degree AV block, left ventricular hypertrophy with repolarization abnormality. QT was prolonged, similar EKG obtained at facility also identified pretty much the same abnormality pattern. Troponin was negative. Other workup included chest x-ray in the hospital were all unremarkable. Today he is not reporting any chest pain, no shortness of breath, no nausea or emesis. He has got healed ____ scar to the left chest from pacemaker implantation which is completely healed but slightly

According to the Bill of Rights, “Congress shall make no law respecting an establishment of religion, or prohibiting the free exercise thereof; or abridging the freedom of speech, or of the press; or the right of the people peaceably to assemble, and to petition the Government for a redress of grievances.” Nowhere in the First Amendment does it state that in times of war, the government can change the laws that have been made to protect the people of the United States. Although some thought President Wilson’s actions were just, he did not abide by the rules of the First Amendment, and because of that, he went too far in limiting people’s civil liberties during World War

Federal Reserve Chair, Janet Yellen, spoke at the Economic Club of New York yesterday. As a result of this speech, the stock market jumped and the dollar depreciated. Chelsey Dulaney of the Wall Street Journal reported that, "The WSJ Dollar Index, which measures the buck against a basket of 16 currencies, fell 0.4% to 86.65. The euro rose 0.3% to $1.13295." The key part of Janet Yellen's speech that triggered the dollar depreciation was when she said:

Electrocardiographic changes can include left ventricular hypertrophy with repolarisation changes with T wave inversion and deep Q waves. In family members carrying HCM gene mutations, the electrocardiogram may demonstrate only minor abnormalities. The presence of non-sustained ventricular tachycardia, a risk factor for sudden death, should be tested for by means of Holter monitoring (Maron et al., 2003). At present, the diagnosis of HCM relies on echocardiography revealing symmetric or asymmetric hypertrophy. Secondary causes of hypertrophy, including valvular disease or systemic hypertension, should be excluded. 2D imaging of the left ventricle by echocardiography can confirm the diagnosis in affected patients. The ejection fraction, a measure of left ventricular systolic function, is typically preserved but there is usually evidence of diastolic dysfunction. These can be measured by tissue Doppler ultrasonography, which can show diastolic dysfunction before the development of hypertrophy (Maron, 2002). Histologically, HCM is characterized by cardiac myocyte disarray and fibrosis. Myocyte death and myocardial scarring may be present and coronary arteries may have thickened walls. This pathology can promote ventricular tachycardia and ventricular fibrillation (Maron, 2002).

Crystal is a 20yo, G2 P1001, who was seen for a follow-up ultrasound assessment. The patient’s primary issue is the development of a postpartum cardiomyopathy after her 1st delivery in 2015. She also reportedly had an anti-M antibody but all of her antibody screens have been negative including one 3 weeks ago. She recovered from the cardiomyopathy and overall is asymptomatic. Her BP was normal today at 127/76 and her heart rate was 98. She states that she actually came to triage 3 weeks ago and had an echocardiogram and we obtained this record and ejection f4raciton is normal at 61.5% and no abnormalities were noted on the echocardiogram. She does have a history of a previous cesarean delivery and is interested in a repeat. In addition,

Maureen shows clinical manifestations such as hypotension (BP 80 mmHg systolic), tachycardia (HR 120 bpm and irregular), tachypnea (Resps 28 bpm), SaO2 unreadable, capillary refill time >4secs, temp 36.5°C (core) indicating the signs of hypovolaemia (Perner & Backer, 2014, p. 614). With the reference of Mrs. Hardy’s medical condition, such as arthritic knees and atrial fibrillation (INR 2.7), she is under diclofenac Acid 50mgs PO BD and warfarin 2mgs PO mane respectively (Jordan, 2010, p. 567; Zacher, et al., 2008, p. 930). Diclofenac is a

It is my impression/diagnosis that Salma had vasovagal episode without reaching syncope, which we discussed during last ER visit and advised Salma to improve her fluid intake. Also Selma had a complete right bundle branch block on ECG, despite having normal cardiac anatomy on echocardiogram and no prior cardiac surgeries. Although this is more often seen in congenital heart disease and post cardiac surgical repair of certain congenital heart defects, it could be also seen in ischemia, myocarditis , cardiomyopathy and valvular heart disease . All of which ,Selma doesn't have signs of on her physical exam, ECG or echocardiogram. In very small group, it could be a normal variant which could explains this findings in Salma.

Rationale for Priority: Jordan’s mother’s family has evident generational cardiac health problems. Donald died from a massive heart attack after years of HTN and CAD. Joyce currently has HTN and recently had a TIA. Shelia has HTN. Kim (Jordan’s mother) had PIH during her pregnancy with Jordan. Joyce and Shelia are on daily HTN medication (names unknown).

Tiffany is a 23yo, primigravida, who is currently 8 weeks 2 days as dated by a 6-week scan. She has a history of migraines that become somewhat worse in pregnancy, but are tolerable. She is also diagnosed with insulin resistance and is on metformin. She is planning to continue that throughout the pregnancy. She is obese with a BMI of 44. She was referred today to discuss a family history on the father of the baby’s side of Seckel syndrome. His brother was born with Seckel syndrome which includes significant dwarfism with occasional developmental delay. Tiffany met with our Genetic Counselor, Kristin Frazer, to discuss the inheritance pattern. They did a complete pedigree. We also performed an ultrasound.

According to the Encyclopædia Britannica (2014), a neural tube defect is “any congenital defect of the brain and spinal cord as a result of abnormal development of the neural tube.” This birth defect is “the most common congenital defect of the central nervous system, affecting the brain and/or spinal cord of 300,000 newborns worldwide each year” (Ricks et al., 2012, p. 391). The exact cause of these central nervous system defects is unknown, but there are many contributing factors that are evidenced to assist in the prevention of such a disorder. I will examine the varying types of neural tube defect, populations in which this defect is most prevalent, possible causes of the defect, and how this defect affects the healthcare system.

Rates are also higher among mothers with certain health problems, such as diabetes or seizure disorders (taking certain anticonvulsants), and significantly higher among couples in which at least one has SB, and couples who have already had a child with SB.” But, as “The HealthDay News” reporter Robert Preidt noticed: “Serious birth defects of the brain and spine called neural tube defects have fallen 35 percent in the United States since mandatory folic acid fortification of enriched grain products.” Since that moment, 1,300 fewer babies are born annually with neural tube defects. However, the Mayo Clinic Staff point out that doctors and researchers do not know for why SB occurs, they have identified few risk factors: race, some medications, and family history of neural tube defects which are defined early in the paragraph. Also, sex, folate deficiency, diabetes, obesity, and increased body temperature can be considered as risk factors of developing SB. First is sex, girls are effected more often. Second, folate (vitamin B-9) is important to the health development of a baby. The systemic form, found in supplements and fortified foods, is called folic acid. “The Genetics Home Reference” noticed that the gene called MTHFR (methylenetetrahydrofolate reductase) provides instructions for making a protein that is involved in processing the folate, and shortage (deficiency) of this vitamin

Recent onset of fatigue- Hypothyroidism is likely due to her weight gain, though this also may have happened due to her inactivity. It is possible that the patient is anemic, though her menstrual periods have not increased or extended and there is no sign of blood loss. Unlikely pregnancy due to a recent menses. Given the patient’s medical history of HTN and snoring, sleep apnea is possible, but her history with snoring for many years is not constant with her recent onset of fatigue. Her usage of HCTZ does not put the patient at higher risk.

Neural tube defects can be split into two different types: open and closed (Mitchell, 2005). The most common of the “open” NTDs are anencephaly and myelomeningocele. These two types of NTDs are when an end of the neural tube does not properly close. Anencephaly is when the brain end of the neural tube fails to close properly (Mitchell, 2005). Babies born with this defect are missing parts of their brain and skull and surrounding areas. There are both mental and physical problems associated with anencephaly. This neural tube defect is particularly devastating because babies born with this type of defect will certainly die shortly after being born. Below is an image of an example of what happens when a fetus is affected with anencephaly. This

Around 530 million years ago, the Cambrian explosion made a significantly fast appearance of main groups of complex organism. This was confirmed by the fossil record. Along the support by an apparent diversification of various living things, including phytoplankton, calcimicrobes and also animals. 580 million years before this, most life forms were basic, made out of individual cells occasionally sorted out into colonies. The Cambrian explosion can be said to happen in waves. The initial, a co-evolutionary transformative ascent in differing qualities as animals investigated specialties on the Ediacaran ocean bottom, trailed by a second development in the early Cambrian as they established in the waters column. The pace of advancement found in the Cambrian times of the explosion is not paralleled amongst the marine creatures: it changed all metazoan clades where Cambrian fossils were found. Later radiations, the fish in the Silurian and Devonian era, included less taxa, for the most part with basically the same body plans. Despite