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MSN570 NURSING LATEST FINAL STUDY GUIDE- UPDATED
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MSN570 NURSING LATEST FINAL STUDY GUIDE- UPDATED WELL SUMMARIZED FOR EASE OF REVISION TO YOUR BEST SCORES DOWNLOAD FOR BEST REVISION AND GREAT SCORES
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MSN 570 UPDATED LATEST FINAL GUIDEDiabetes Mellitus Type 1: is caused by deficient insulin resulting from T–cell-mediated
autoimmune destruction of the pancreas' insulin-secreting beta cells. The individual
has circulating autoantibodies to islet cells, insulin, and enzymes involved in insulin
production. This form of the disease has a strong genetic influence based on multiple
genetic variants. The beta-cell damage rate is variable among affected individuals,
being rapid mainly in infants and children and slow mostly in adults. The presenting
sign of T1DM is often ketoacidosis, particularly in children. Many affected adults retain
some beta-cell function that prevents ketoacidosis for many years, but they
eventually become dependent on exogenous insulin for survival. DX: The gold
standard laboratory test used to diagnose diabetes is a fasting plasma glucose level.
A fasting plasma glucose level greater than 126 mg/dL on two separate days confirms
the diagnosis. Random plasma glucose greater than 200 mg/dL repeated on more
than one occasion is also a diagnostic of the disorder.
Type I diabetes is a fairly common condition autoimmune condition typically seen in
the younger population. Often one of the first signs of Type I Diabetes is DKA.
Ketones are acidic and give rise to ketoacidosis when in excess.
The pancreas has a number of endocrine responsibilities including the release of
insulin when glucose levels are high to help recruit glucose transporters to the
cells.
The relationship between insulin and obesity is best described by the phase – insulin
resistance leads to excess blood glucose levels that are converted into fat by the
liver.
Hormones released from the gastrointestinal (GI) tract play a role in insulin resistance,
beta-cell function, and diabetes. Ghrelin stimulates GH secretion, controls appetite,
and plays a role in obesity and insulin sensitivity regulation. Ghrelin is a peptide
produced in the stomach and pancreatic islets that regulate food intake, energy
balance, and hormonal secretion. Decreased levels of circulating ghrelin have been
associated with insulin resistance and increased fasting insulin levels. The incretins
are a class of peptides released from the GI tract in response to food intake and
function to increase the secretion of insulin and have many other positive effects on
metabolism. The most studied incretin is called glucagon-like peptide 1 (GLP-1), and
studies have demonstrated that beta-cell responsiveness to GLP-1 is reduced both in
prediabetes and in type 2 diabetes. Incretin therapies include GLP-1 receptor agonists
(GLP-1 RAs) and dipeptidyl peptidase IV (DPP-IV) inhibitors, which can help control
postprandial glucose levels by promoting glucose- dependent insulin secretion.
DIABETES TYPE 2:Type 2 DM is a resistance to insulin by insulin sensitive tissues. It is
a chronic condition affecting how the body metabolizes glucose. There have been
studies done that show Ghrelin may be reduced in people with Type II DM. These
patients do not usually have an absolute insulin deficiency so they are less likely to
develop ketoacidosis.
The cause of microvascular complications in diabetics is that the capillary basement
membranes thicken and there is endothelial cell hyperplasia.Hyperosmolar
hyperglycemic nonketotic state in type 2 diabetes is characterized by striking
dehydration, severe hyperglycemia, no or slight ketosis, and a mortality rate of
11%. Nonketotic hyperglycemic hyperosmolar coma is more likely to occur in
,institutionalized patients, especially patients unable to recognize or respond
appropriately to thirst.Obesity is present in approximately 80% of patients with type
2 DM, and when weight is lost, insulin responsiveness improves.
The relationship between insulin and obesity is best described by the phrase:
Insulin resistance leads to excess blood glucose levels that are converted into fat
by the liver.
,Some information I would like to highlight about DM Type I and Type II
Insulin is produced by the pancreatic beta cell in the Islet of Langerhans. Alpha
cells secrete glucagon.
It is important to understand the diagnostic criteria that patients must meet before
being diagnosed with type 2 diabetes. Often some of the first signs of DM are
polyuria, polydipsia, and polyphagia. Excess thirst results from the intracellular
dehydration that occurs as blood - glucose lever rises and water is pulled out of the
body cells.
Excess hunger polyphagia (usually seen in type 1) happens due to cellular
starvation and depletion of cellular stores of carbs, fats and proteins.
Excess urine (polyuria) happens when the osmotic shift that occurs as excess blood
glucose is retained in the filtrate causing water to be retained
In both type 1 DM and type 2 DM complications can occur overtime if left untreated
or poorly managed. In many people with type 2 diabetes macrovascular disease
may be present at diagnosis. The changes can be both microvascular (retinopathies,
neuropathies, nephropathies) or macrovascular (coronary artery, cerebral vascular,
peripheral vascular disease).
In microvascular complications there is a thickening of the capillary basement
membrane and hyperplasia of endothelial cells.
Macrovascular complications occur due to numerous risk factors: obesity,
hypertension, hyperglycemia, hyperinsulinemia, hyperlipidemia, altered platelet
function, endothelial dysfunction, elevated fibrinogen levels and systemic
inflammation.
Another condition that can occur due to obesity, metabolic syndrome is NAFLD (non
alcoholic fatty liver disease). This happens due to a few different factors.
Hyperinsulinemia (causes insulin resistance over time). Insulin pushes glucose into
the hepatocytes and it converts this glucose to fat and the body stores it as energy.
When there is too much glucose and too much insulin, it can lead to fatty liver over
time. The liver uptakes free fatty acids and triglycerides resulting in a “fatty” liver.
Diabetes can cause poor wound healing so we must check our patients skin often for
wounds, especially their feet.
ENDOMETRIOSIS: Pathogenesis of endometriosis is believed to involve some
combination of hereditary factors, exposure to environmental toxins, and
compromise to the immune system
Endometriosis is the presence of endometrial tissue outside the lining of the uterine
cavity. The only normal location for endometrial tissue is the endometrial lining of
the uterus, but with endometriosis, the tissue is found outside the uterine cavity.
Diagnosis is made by a physician based on symptoms. The most prominent symptom
of endometriosis is dysmenorrheal.
Endometriosis is a chronic disease causing damage to the ovarian tissue, impair
ovulation, and can cause infertility (Dlugasch & Story, 2021).
, Just to summarize a few things:
Endometriosis is a condition in which the endometrial tissue that normally lines the
uterus, grows outside the uterus and sometimes even outside of the pelvic cavity.
Typically this occurs in the ovaries, fallopian tubes and peritoneum. Typical
symptoms are pelvic pain and infertility.
When typical functioning endometrial tissue breaks down, it thickens and bleeds with
a normal menstrual cycle. In endometriosis, the endometrial tissue has no way to
leave the body and becomes trapped and irritates surrounding tissue. Pain, cysts,
scarring and adhesion develop because of the inflammation. Cysts in the ovaries are
called endometriomas. The scarring and adhesions result in altered ovarian function,
impaired fertilization and implantation. Adhesions can damage and block the
Fallopian tubes. Sometimes patients may have no other symptoms and they present
only with infertility.
Etiology: pathogenesis is not entirely clear; increase in Western countries, genetic
factors, inappropriate immune response, environmental triggers, retrograde
menstruation, early menarche
Typically diagnosed between the ages of 25 – 35 years old
Symptoms: Dysmenorrhea, pelvic pain, infertility, dyspareunia, bladder pain,
irregular vaginal bleeding, low back pain, partial bowel obstruction, bowel
dysfunction, pain during vaginal exam, some patients may have no symptoms
Diagnosis: History, physical exam and pelvic ultrasound. Laparoscopy confirms
diagnosis
Treatment: Hormone therapy (oral contraceptives), surgical repair, analgesics (NSAIDS)
There is no cure for endometriosis but it requires life-long management. “With
endometriosis, the endometrium tissue begins growing and forming lesions in areas
outside the uterus. Although such ectopic endometrial tissue most commonly occurs in
the fallopian tubes, ovaries, and peritoneum, it can be found anywhere in the body”
(2021, P. 357). Endometriosis can be extremely painful and the patient at times feels
as though no one really believes how bad the pain is. This can lead to anxiety,
depression and other mental health problems. endometriosis, according to
Grundstrom (2020), is an estrogen-dependent, chronic and inflammatory disease
every one in ten female individuals of childbearing age have in their uterus at birth
congruent with your submission.
Characteristically, some cells appear like the endometrium outside the uterus, whose
implantation and growth trigger inflammation, pain, and excessive bleeding that could
lead to cysts, adhesions, and lesions (Grundstrom). As pointed out in your
presentation, the symptoms that go with endometriosis include persistent pelvic pain,
weariness, pain during menstruation, dyspareunia, reduced infertility, intestinal and
urinary complaints. Unfortunately, many individuals diagnosed with endometriosis
report that they are not treated professionally by healthcare workers when seeking
care. “They often report experiences of normalization, trivialization and a lack of
knowledge from healthcare professionals.” (Grundstrom). p 20. This trivialization and
normalization of the victim’s menstruation pain by friends, family members, and the
general public, including the healthcare personnel, have been identified as one of the
reasons for the delays in the diagnosis of the disease (Grundstrom). Treatment is
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