NURS 5315 Endocrine Midterm Test Latest Upload 2026

NURS 5315 Endocrine Midterm Test Latest Upload 2026 Thyroid hormones - -T3, T4 and calcitonin Pancreas hormones - -Insulin and glucagon 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 Primary thyroid disorders - -result in alterations of thyroid hormone (TH) levels with secondary feedback effects on pituitary thyroid stimulating hormone (TSH) EX: primary elevation in TH à TSH level secondarily decreases d/t negative feedback and vice versa Subclinical Thyroid disease - -Thyroid disease that presents with minimal to no symptoms but with abnormal lab values Secondary Thyroid disorders - -conditions that results d/t dysfunction of the pituitary gland TSH production Ex: Excess TSH production - TH level is elevated secondary to primary elevation of TSH Inadequate TSH production -TH level is decreased secondary to primary decrease of TSH Thyrotoxicosis (hyperthyroidism) - -a condition that results over secretion of TH; d/t thyroid cancer, thyroid nodules or Grave's Disease; Will have low TSH levels and high T4 level. S&S: increased metabolic rate, heat intolerance, goiter, menstrual irregularities, weight loss, diaphoresis, fine tremor, tachycardia, frequent bowel movements, restlessness, short attention span, hair loss, anorexia, exophthalmos, pretibial edema, and heart failure. Thyrotoxic Crisis(thyroid storm) - -SUDDEN release of TH to a dangerous level of 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. NURS 5315 NURS 5315 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 Hyperthyroidism from nodular thyroid disease - -Disease that results from follicular hypertrophy of the thyroid cells causing 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. S&S develop SLOWLY and will NOT display exophthalmos or pretibial myxedema 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 Secondary hypothyroidism - -Malfunction in the pituitary or hypothalamus glands causing insufficient amounts of TH which leads to a lack of TSH. Most common cause is pituitary tumors. Other causes include TBI, subarachnoid hemorrhage, or pituitary infarction Subclinical hypothyroidism - -mild thyroid failure. defined by elevated TSH level with normal T3 and T4 level. 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 HIGH TSH and LOW T3/T4 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. common in elderly with UTI or HF/stroke; other S&S hypotension, hypoventilation, shivering, hypothermia, lactic acidosis, coma, and hypoglycemia. 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. Diagnosed before age 30, typically between 9 months and 12 years NURS 5315 NURS 5315 Type 1 clinical manifestations - -polydipsia, polyuria, polyphagia, weight loss and fatigue. Typer 2 DM - -pathological defect is insulin resistance. A decrease in number of insulin cell receptors or insufficient amounts of insulin secretion to meet metabolic needs d/t pancreatic disease, steroid use, Cushing Syndrome, acromegaly, excess glucagon secretion More common in Native Americans, Hispanics, African Americans Risk factors: HTN, physical inactivity, fam hx of DM Type 2 DM clinical manifestations - -recurrent infections, genital pruritus, visual changes, paresthesias, fatigue, and acanthosis nigricans(brown to black pigmentation in body folds) 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. Often have NO S&S Hemoglobin A1c - -test that measures permanent attachment of glucose to hemoglobin molecules; reflects average plasma glucose exposure over the life of a RBC (aprox 120 days); provides measurement of long-term control of blood glucose for the preceding two to three months. Fasting plasma glucose - -DM diagnostic level: greater or equal to 126. At risk for DM level: 100-125 Oral Glucose Tolerance Test (OGTT) - -DM diagnostic level: 2 hr plasma glucose greater than or equal to 200. At risk for DM level: 2 hr PG: 140-199 Random plasma glucose diagnostic level - -greater or equal to 200 with symptoms of diabetes 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. NURS 5315 NURS 5315 Diabetic Ketoacidosis (DKA) - -Complication of DM that is a SLOW onset, that results from insulin deficiency leading to the release of counter regulatory hormones (catecholamines, glucagon, cortisol), increase in hepatic glucose production, decrease in peripheral glucose utilization, initiation of glucogenesis. Most common predisposing factors are illness, infection, trauma, surgery, MI and lack of medication compliance. More common in Type 1 DKA diagnostic criteria - -Glucose 250. Serum bicarb18. Serum pH7.3. Elevated anion gap. presence of urine and serum KETONES. fluid volume deficit. electrolyte imbalance S&S: Kussmaul respirations (hyperventilation) Fruity or Acetone odor on breath Postural dizziness CNS depression Ketonuria NV, abd. Pain Polyuria, polydipsia Coma DKA treatment - -IV fluids, IV insulin, treatment of electrolyte imbalances and treatment of precipitating event Hyperosmolar Hyperglycemic state (HHS) - -uncommon, but occurs with type 2. Usually triggered by an infection, cardiovascular or renal disease. SLOWEST ONSET complication of DM; 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, WITHOUT ketone production HHS diagnostic criteria - -Glucose600. NORMAL serum bicarb. Serum osmolality320. Absent or low levels of ketones S&S: Polyuria, polydipsia, Hypovolemia, dehydration (poor skin turgor, parched lips), hypotension, tachycardia, weight loss, NV, abd. pain, Stupor/coma 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) NURS 5315 NURS 5315 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. Microvascular disease - -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 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 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 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 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. 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. 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 NURS 5315 NURS 5315 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 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 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 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. Cushing disease - -Characterized by a chronic over secretion of cortisol. More common in elderly and women; D/t exogenous steroid use, over-secretion of ACTH 2nd to pituitary tumor, ectopically produced ACTH from a non-pituitary carcinoma or adrenal adenoma Cushing disease S&S - -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 - -Disease of the adrenal cortex that results in decreased cortisol and aldosterone secretion. d/t AUTOIMMUNE reaction which targets the adrenal cortex and causes adrenal atrophy and hypofunction. NURS 5315 NURS 5315 May be caused by TB, metastatic tumors, infection, HIV, fungal infections, amyloidosis or cessation of steroid therapy. 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 Addisonian 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 - -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: is idiopathic in nature Secondary: caused by another condition like 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 because progresses SLOWLY 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. Bone density classifications - -normal bone mass833. Osteopenia: 648-833. Osteoporosis648 Osteoarthritis (OA) - -joint disease that results in the loss of articular cartilage and destruction of the joint capsule. May occur 2ndary 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, leads to increased remodeling of the cartilage and loss of smooth frictionless joint. This is progressive which will eventually require joint replacement surgery