NURS 5315 Endocrine

Aging in the adrenal gland

After age 50, the adrenal cortex develops fibrous tissue. As we age we cannot clear glucocorticoids that our bodies produce very well. Less cortisol is used as we age as well. With decreased clearance and use of cortisol the circulating levels of cortisol are elevated

Diabetic Ketoacidosis (DKA)

Complication which results from insulin deficiency and the release of counter regulatory hormones(catecholamines, glucagon, cortisol). Most common predisposing factors are illness, infection, trauma, surgery, MI and lack of medication compliance. The lack of insulin causes an increase in hepatic glucose production, a decrease in peripheral glucose utilization, initiation of gluconeogenesis and formation of ketone bodies and metabolic acidosis.

Fasting plasma glucose

DM diagnostic criteria is greater or equal to 126. Risk for DM level at 100-125

Oral Glucose Tolerance Test (OGTT)

DM level: 2 hr plasma glucose greater than or equal to 200. Risk for DM level: 2 hr PG 140-199

Random plasma glucose

DM: greater or equal to 200

Pancreas hormones

Insulin and glucagon

Myxedema coma

thyroid emergency which has the opposite effect of thyroid storm. Results in decreased LOC and is usually precipitated by an event such as infection, discontinuation of thyroid medications, narcotic or sedative use. other S&S hypotension, hypoventilation, shivering, hypothermia, lactic acidosis, coma, and hypoglycemia.

Stroke

twice as common in diabetics. Ischemic and lacunar strokes are more common. Aggressive management of hypertension, hyperlipidemia, hyperglycemia have shown to decrease incidence of stroke

Hyperosmolar Hyperglycemic state (HHS)

uncommon in type 2. Usually triggered by an infection, cardiovascular or renal disease. Patho for HHS is same as DKA except for the production of ketone bodies. Poor glucose controls leads to elevated glucose which causes high serum osmotic pressure, and osmotic diuresis leads to severe dehydration, low blood volume and poor perfusion

Thyrotoxic Crisis(thyroid storm)

worsening hyperthyroid state triggered by an igniting even such as infection, trauma, cardiopulmonary disorder, burns, seizures surgery, or spontaneously. S&S: extreme restlessness and agitation, delirium, seizures, coma, severe tachycardia, heart failure, hyperthermia, delirium, volume depletion, NVD and death if not treated.

Duchenne Muscular Dystrophy (DMD)

x-linked genetic disorder that mainly affects boys. Caused by the deletion of one or more exons on the DMD gene. Normally, the DMD gene makes a membrane stabilizing protein called dystrophin which anchors the actin cytoskeleton of the skeletal muscle to the basement membrane. This is absent in DMD. The lack of dystrophin allows for muscle fibers to be torn apart during contraction. Free calcium then enters the muscle cells and causes cell death and necrosis.This decstruction leads to increased levels of CK.

Cushing disease

Characterized by a chronic over secretion of cortisol. Etiologies include exogenous steroid use, over-secretion of ACTH 2nd to pituitary tumor, ectopically produced ACTH from a non-pituitary carcinoma or adrenal adenoma

Hyperthyroidism from nodular thyroid disease

Follicular hypertrophy of the thyroid cells is responsible for the formation of the thyroid nodules which secrete extra hormones. Nodules develop bc of normal changes during pregnancy or puberty or as a result of an autoimmune issue, viral infection or genetic influence. Symptoms develop slowly and will not display exophthalmos or pretibial myxedema

DKA diagnostic criteria

Glucose >250. Serum bicarb<18. Serum pH<7.3. Elevated anion gap. presence of urine serum ketones. fluid volume deficit. electrolyte imbalance

HHS diagnostic criteria

Glucose>600. Normal serum bicarb. Serum osmolality>320. Absent or low levels of ketones

Diabetic Nephropathy

Hyperglycemia leads to activation of the polyol pathway, hexosamine pathway, protein kinase C and inflammation and the production of advanced glycation end products which all cause kidney tissue injury yet exact process is not known. The glomeruli are also injured.

DKA treatment

IV fluids, IV insulin, treatment of electrolyte imbalances and treatment of precipitating event

Typer 2 DM

pathlogical defect is insulin resistance. A decrease in number of insulin cell receptors or insufficient amounts of insulin secretion to meet metabolic needs are characteristic of DM 2.

Type 1 clinical manifestations

polydipsia, polyuria, polyphagia, weight loss and fatigue.

Thyrotoxicosis

(hyperthyroidism) a condition that results from any cause of increased TH levels. Will how low TSH levels and high T4 level. S&S: increased metabolic rate, heat intolerance, goiter, menstrual irrregularities, weight loss, diaphoresis, fine tremor, tachycardia, frequent bowel movements, restlessness, short attention span, hair loss, anorexia, exophthalmos, pretibial edema, and heart failure.

Secondary Thyroid disorders

conditions that results from the dysfunction of the pituitary gland TSH production

Osteoarthritis (OA)

joint disease that results in the loss of articular cartilage and destruction of the joint capsule. May occur 2nd to aging or as a result of long term mechanical stress caused by sports, obesity or chronic diseases. Patho is the degeneration of the articulating cartilage. This leads to increased remodeling of the cartilage and loss of smooth frictionless joint. This is progressive which will eventually require joint replacement surgery

Anorexia or aging consequences

malnutrition, physical frailty, mitochondrial dysfunction, reduced regenerative capacity, increased oxidative stress and imbalanced hormonal levels. Death rates are higher when this is present

Primary thyroid disorders

result in alterations of thyroid hormone (TH) levels with secondary feedback effects on pituitary thyroid stimulating hormone (TSH)

Peripheral arterial disease

DM increases the incidence of this with claudication, ulcers, gangrene, and amputation. Occlusions of the small arteries and arterioles particularly below the knee, cause most of the gangrenous changes of the lower extremities. The lesions begin as ulcers and progress to osteomyelitis or gangrene requiring amputation. Peripheral neuropathies and risk for infection advance the disease

Infection

DM people are at an increased risk for infection d/t decreased visual and tactile sensations, hypoxia, pathogens d/t the increased amount of glucose in the blood which provides energy for the pathogen, decreased blood supply which decreases WBC count to the affected area, suppressed immune response, and delayed wound healing.

Aging in the pancreas

Decline in beta cell function which leads to glucose intolerance or diabetes. Pancreatic cell regeneration declines. Growth hormone secretion decreases with age which causes a decrease in muscle size and function. Elevated levels of PTH are associated with increased mortality. Decreased vit. D levels has been associated with osteoporosis, cancer, autoimmune disorders, diabetes, cardiovascular disease and mental health disorders.

Anorexia or aging

Decrease in appetite or food intake. Results from reduced energy needs, waning hunger, diminished senses of smell and taste, decreased production of saliva, altered GI satiety control mechanisms and presence of comorbidities.

Primary hypothyroidism

Defect is in the thyroid gland itself which causes insufficient amounts of thyroid hormone. Causes include congenital defects, thyroidectomy, thyroid radiation, iodine deficiency, anti-thyroid medications, or impairment in thyroid hormone synthesis

OA S&S

Dependent on the affected joint. Pain and stiffness are the predominant symptoms. Joint swelling, tenderness and deformity are common. Symptoms are worsened with weight bearing or joint use and relieved with rest

Addison's Disease

Disease of the adrenal cortex that results in decreased cortisol and aldosterone secretion. Patho is d/t autoimmune reaction which targets the adrenal cortex and causes adrenal atrophy and hypofunction. May be caused by TB, metastatic tumors, infection, HIV, fungal infections, amyloidosis or cessation of steroid therapy.

Dawn phenomenon

Early morning rise in blood glucose concentration caused by nocturnal elevations of GH which decreases metabolism of glucose by muscle and fat. Increasing the dose of evening insulin manages the problem.

Diabetic Retinopathy

Leading cause of blindness. Results from damage to retinal blood vessels and RBCs, platelet aggregation, relative hypoxemia and hypertension. S&S: blurring or loss of vision, reduced visual acuity, cataracts, and defects in the eye muscle

Sarcopenia

Loss of muscle mass 2nd to aging and is cause of age related loss of strength. We lsoe 10% of muscle mass by age 50. Muscle mass declines 15% per decade and 30% after age 80. Muscle strength declines faster than muscle mass. In sarcopenia there is a loss of type 2 fiber and a loss of satellite cells. Reduced RNA synthesis, loss of mitochondrial volume and shortening telomeres and reduction in size of motor units contribute to sarcopenia.

Adrenal Glands hormones

Made up of the cortex which secretes steroids such as cortisone and aldosterone and the medulla which secretes catecholamines such as epi and norepi

Secondary hypothyroidism

Malfunction in the pituitary or hypothalamus glands which leads to a lack of TSH. Most common cause is pituitary tumors. Other causes include TBI, subarachnoid hemorrhage, or pituitary infarction

Diabetic Nephropathy S&S

Microalbuminuria is the first manifestation and develops within 5-10 years. Later, hypoproteinemia, reduction in plasma oncotic pressure, fluid overload, anasarca and hypertension may occur. As it continues, people with type 1 may have problems with hypoglycemia. Glomerular filtration rate drops, and nausea, lethargy, acidosis, anemia and uncontrolled hypertension may occur.

Microvascular disease

Microangiopathy is what occurs when the small vessels have been damaged from glucose and is directly related to the duration of the disease. Issues of this will manifest 10 years after diagnosis. The damages includes thickening of the capillary membrane, endothelial cell hyperplasia and thrombosis which all decrease perfusion. Can cause retinopathy, blindness, and CKD

Grave's disease

Most common cause of hyperthyroidism and is an autoimmune disorder. Antibodies attach to the thyroid cells and mimic the function of TSH which results in an increased secretion of T3 and T4 and overrides the negative feedback mechanisms which regulate TSH secretion. The stimulation of the receptors by the antibodies results in the development of goiter. May also experience exophthalmos, periorbital edema, and extraocular muscle weakness leading to strabismus and diplopia

Coronary artery disease

Most common cause of morbidity and mortality in DM. Prevalence increases with duration but not severity of DM. MI's lead to death in 75% of diabetics bc they are often asymptomatic d/t peripheral and autonomic neuropathies

Diabetic neuropathies

Most common complication of diabetes Affects all types of nerves > peripheral (sensorimotor) nerves > autonomic (somatic) nerves > spinal nerves Prevalence increases with age of person & duration of DM May be the first symptom of diabetes May appear during periods of "good" glucose control If blood glucose controlled, neuropathies decreased by 60% Capillary basement membrane thickening & capillary closure may be present Demyelinization of the nerves related to hyperglycemia > delayed conduction > nerve degeneration > sensory deficits/symptoms more common than motor Cognitive dysfunction can occur with chronic hyperglycemia Some neuropathies are progressive & some may improve spontaneously

Diabetic Retinopathy patho

Stage 1 nonproliferative: characterized by thickening of the retinal capillary basement membrane and an increase in retinal capillary permeability, vein dilation, microaneurysm formation and hemorrhages. Stage 2 preproliferative: progression of retinal ischemia with areas of poor perfusion that culminate in infarcts. stage 3 proliferative: the result of neovascularization and fibrous tissue formation within the retina or optic disc

Hypothyroid S&S

confusion, syncope, slow speech and thinking, anemia, bradycardia, reduced stroke volume and cardiac output, dyspnea, hypoventilation, decreased appetite, weight gain, dry hair, cold intolerant, constipation, hyperlipidemia, periorbital edema, peripheral edema, myxedema(puffy face), increased total body water, hyponatremia, reduced renal blood flow

Gestational DM

develops when hyperglycemia appears during pregnancy and usually resolves after birth. All women should be screened during their first prenatal visit and again between 24-28 weeks. Risk factors include obesity, family history, and high maternal age. upon birth the child may have hyperplasia of the pancreatic islet cells and hypoglycemia. 3w2

Obesity patho

directly related to the white adipose tissue (WAT). WAT increase in the size and number, they store triglycerides and secrete adipokines. Adipokines and other hormones regulate food intake and metabolism. They increase or decrease fat mass, provide signals to the hypothalamus, brainstem, ANS and the hunger center to regulate satiety and energy balance. Visceral WAT causes a dysfunction in this regulatory signaling center and leads to the complications associated with obesity. The hypothalamus regulates food intake and energy balance by regulating neurons which increase appetite and decrease appetite.

DMD S&S

noticed around ages 3-4 when the gait abnormalities first appear. The child will toe walk, have difficulty getting up from the ground and fall frequently. Muscle weakness which starts in the pelvic area and have calf muscle hypertrophy. They display Gower sign, have progressive weakness, unable to ambulate by age 12-15. Slow progression occurs which leads to resp. insufficiency, cardiomyopathy, scoliosis and other orthopedic and cognitive deficits. Most live into their mid-20s

Somogyi effect

occurrence of hypoglycemia around 3am caused by too much intermediate-acting insulin given at dinner time followed by rebound hyperglycemia caused by normal early secretion of counter regulatory hormones (epi, GH, and corticosteroids)

Type 2 DM clinical manifestations

recurrent infections, genital pruritus, visual changes, paresthesias, fatigue, and acanthosis nigricans(brown to black pigmentation in body folds)

Thyroid hormones

T3, T4 and calcitonin

Hypoglycemia

Blood glucose level <47 in newborns and <70 in children and adults. S&S: pallor, tremor, anxiety, tachycardia, palpitations, diaphoresis, headache, dizziness, irritability, fatigue...symptoms d/t release of epi and cortisol. beta blockers can mask the symptoms.

Hemoglobin A1c

A test that measures the level of hemoglobin A1c in the blood as a means of determining the average blood sugar concentrations for the preceding two to three months. DM diagnostic is greater than or equal to 6.5. Increased risk for DM level 5.7-6.4%

Type 1 DM

3 types: 1A is autoimmune, 1B is idiopathic and 3c is associated with chronic pancreatitis. in 1A: autoimmune response destroys the beta cells in the pancreas which leads to apoptosis. Beta cell destruction is what causes a lack of insulin to be produced.

Cushing disease results

>increased glycogenolysis which results in hyperglycemia and type 2 DM >abnormal redistribution of fat and elevated blood lipid products. Body changes include truncal obesity, moon face and formation of a buffalo hump. "cushingoid" appearance>weakened collagen fibers leads to skin fragility, bruising and skin tears. They will have purple striae over areas of increased fat deposits>Increased ACTH will cause hirsutism(increased hair growth) and acne>people will bleed more easily and are more susceptible to infection

Addison's disease S&S

Before S&S appear 90% of gland has been destroyed. S&S: hypoglycemia, weakness, fatigue, apathy, mental confusion, avorexia, nvd, abdominal pain and addisonia triad-hyperkalemia(not enough aldosterone to rid of potassium), hyponatremia(not enough aldosterone to retain sodium), and hypotension(not enough cortisol to maintain vascular tone)

Osteoporosis patho

Bone homeostasis is dependent upon the balance between the cytokine receptor activator of nuclear factor κβ ligand (RANKL), its receptor RANK and its decoy receptor osteoprotegerin (OPG). Osteoblasts express RANKL which is necessary for osteoclast development. RANKL activates the RANK receptor which is expressed on osteoclasts. This prolongs the life of the osteoclasts. The effects of RANKL are mitigated by OPG, which acts as a decoy receptor for RANKL and prevents it from binding to RANK. This process is regulated by cytokines and hormones. An alteration in this system leads to osteoporosis, immune mediated bone diseases, malignant bone disorders and inherited skeletal diseases.

Subclinical Thyroid disease

Thyroid disease that presents with minimal to no symptoms but with abnormal lab values

Aging in the thyroid

Undergoes some atrophy and fibrosis. Inflammation and nodularity also occurs. Signs of thyroid disease are more occult in the elderly. TSH secretion is thought to be increased.

Bone density classifications

normal bone mass>833. Osteopenia: 648-833. Osteoporosis<648

Macrovascular disease

elevated glucose leads to the development of atherosclerosis of the large and medium size vessels of the brain, heart,aorta, and femoral arteries. Disease which results include PVD, cerebral atherosclerosis which may cause TIA or stroke, and coronary artery disease which may lead to an MI

Anorexia of aging risk factors

functional impairments and deficiencies, medical and psychiaric conditions, loneliness and grief, medications, social isolation, and abuse or neglect

Subclinical hypothyroidism

mild thyroid failure. defined by elevated TSH level with normal TH level.

Osteoporosis

most common bone disease in humans and is marked by low bone mineral density, impaired structural integrity, and decreased bone strength. Increased risk of fractures. Primary osteoporosis is idiopathic in nature and 2nd is caused by another condition. 2nd conditions include hormone imbalances, DM, hyperparathyroidism, hyperthyroidism, heparin, corticosteroids, phenytoin, barbiturate, lithium, tobacco, ethanol, HIV, rheumatoid disease, CKD, liver disease, and malabsorption syndromes. Old bone breaks down faster than it is being made and the bone become porous and thin. Commonly diagnosed after someone has sustained a fracture.