Endocrine Flashcards
Diabetes mellitus
chronic disorder of impaired carbohydrate, protein, and lipid metabolism; primarily carbohydrate; deficiency of insulin results in hyperglycemia
sub-categories of diabetes
Type 1, Type 2, and metabolic syndrome (pre-diabetes)
complications associated with diabetes
microvascular complications, macrovascular complications, reduced healing causing increased risk of infection
how does diabetes destroy vasculature
glucose interacts with endothelial vascular wall causing damage, thrombi can form d/t damage of walls, all organs with vascular system experience damage
type I diabetes
nearly absolute deficiency of insulin due to autoimmune primary beta cell destruction (negligible insulin); if insulin is not given then fat is metabolized for energy causing DKA; genetic
type II diabetes
relative lack of insulin or resistance t the action of insulin; insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate; develops over time
metabolic syndrome
coexisting risk factors for developing type II diabetes; risk factors include abdominal obesity, hyperglycemia, HTN, high triglyceride levels, low HDL
assessment of diabetes
polyuria, polydipsia, polyphagia, hyperglycemia, weight loss, blurred vision, slow wound healing, vaginal infections, weakness/parasthesias, signs of inadequate circulation of feet, signs of accelerated atherosclerosis
A1C diagnostic for diabetes
> 6.5
dietary reccomendation for diabetes
consistency every day in timing and amount to control blood glucose levels, following american diabetic association diet, carb counting
exercise recommendations for diabetes
exercise at same time each day when glucose is peaking from meal; monitor levels before during and after; do not exercis if >250 mg/dL and urinary ketones present
oral hypoglycemic medications
sulfonyureas- increase insulin secretion; thiazolidinediones- improve insulin sensitivity; biguanides- decrease liver glucose output; alpha-glucosidase inhibitors- delay intestinal glucose absorption; GLP-1 receptor agonists-enhance incretin activity; SGLT-2 inhibitors- promote renal glucose excretion
primary intervention for type II diabetes
exercise, diet, and lifestyle; if not working after 6 months than oral hypoglycemics and maybe insulin prescribed
only oral hypoglycemic not contraindicated in Type I diabetes
SGLT-2 inhibitors
insulin
increases glucose transport into cells and promotes conversion of glucose to glycogen causing decrease in serum glucose levels; primarily acts in the liver, muscle, and adipose tissue
dawn phenomenon
hyperglycemia on morning awakening resulting from excessive release of GH and cortisol early in morning; treatment is increase in insulin dose or change in administration timing
somogyi effect
normal/elevated glucose at bedtime, hypoglycemia around 2am causing increase in production of counterregulatory hormones; blood glucose rebounds by 7am in response to counterregulatory hormones and pt is hyperglycemic; treat with decreased insulin and or having large bedtime snack
common scenarios in Type I diabetes
dawn phenomenon and somogyi effect
how much insulin can a pump store?
about 3 days worth
hypoglycemia
<70 mg/dL or rapid drop from elevated level; caused by too much insulin, too much oral hypoglycemic, too little food, or too much exercise
hypoglycemia unawareness
warning signs of hypoglycemia are not evident until blood glucose is dangerously low; commonly seen in those with frequent hypoglycemia episodes, older patients, or those taking beta-adrenergic blockers
hypoglycemia s/s
cold, clammy, headache, lethargy, AMS, hungry, tachycardia, jittery, angry
hypoglycemia assessment
mild is 40-70: fully awake with neurogenic symptoms like tremors, palpitations, sweating, hunger; moderate is 20-39: s/s of worsening hypoglycemia like dizziness, drowsiness, and weakness; severe is <20: severe neuroglycopenic symptoms like delirium, seizure, coma, and death
hypoglycemia interventions
check BGL, 15/15 rule- if symptomatic or below 70mg/dL give 15 gram of simple carbs (4oz juice), recheck BGL in 15 min and administer another 15g, if still below 70 after 45 g sugar admin 15-50 ml of 50% dextrose or 1mg glucagon; pt should then eat snack
if pt found with altered LOC from hypoglycemia
first line is IV dextrose or IM glucagon
glucagon
hormone secreted by alpha cells in pancreas that increases blood glucose; increased after 5-20 minutes
DKA
life threatening complication of type I that can occur with severe insulin deficiency; too much breaking down of fats producing ketones which are acidic; hyperkalemia can be seen (H into cell and K out into blood stream)
assessment of DKA
precipitated by infection, stress, inadequate insulin, or can be sudden; glucose >300 Cr > 1.5, urine has ketones, K elevated with acidosis, ABG show acidotic, dehydrated, polydipsia, polyuria, weight loss, dry skin, sunken eyes, lethargy, coma
DKA interventions
restore blood volume, IV insulin with infusion of NS or 1/2 NS with dextrose added; monitor K and correct imbalances in electrolyte; cardiac monitoring if needed
IV insulin for DKA
only use short acting
HHS- hyperosmolar hyperglycemic syndrome
extreme hyperglycemia without ketosis/acidosis; more often inn Type II diabetes; enough insulin is present to prevent breakdown of fts for energy (no ketosis); need to have neurological side effects present
assessment of HHS
gradual onset precipitated by infection, stressors, poor fluid intake; neurological symptoms from altered CNS function; dehydration and electrolyte imbalance from high glucose displacing electrolytes; polyuria, polydipsia, weight loss, sunken eyes, dry skin, lethargy, coma; glucose >800, hypokalemia, hyponatremia, elevated creatinine, negative urine ketones; ABD does not show acidosis
HHS interventions
similar treatment to DKA; fluid and electrolyte repletion; insulin is less critical as there is not ketosis/acidosis
diabetic retinopathy
chronic progressive impairment of retinal circulation leading to eventual rupture of small microaneurysms in retinal blood vessels; vision changes can be permanent and can result in loss
assessment of diabetic retinopathy
vision changes, blurry vision from macular edema, sudden vision loss d/t retinal detachment (cant fix), cataracts lens opacity
interventions for diabetic retinopathy
ensure safety/promote early prevention with HTN management and glucose control, laser therapy to remove hemorrhagic tissue, vitrectomy to remove vitreous hemorrhages, cataract removal with lens implant
diabetic nephropathy
progressive kidney function decline d/t damage of vascular walls causing blood supply issue to kidneys
diabetic nephropathy assessment
fatigue, thirst, weight loss, anemia, microalbuminuria, malnutrition, UTIs, neurogenic bladder (incontinence), elevated creatinine
interventions for diabetic nephropathy
early prevention with HTN control and glucose management, monitor VS/IOs, monitor BUN creatinine and urine albumin, restrict dietary potassium sodium and protein, avoid nephrotoxic medications, prep fir dialysis kidney transplant or pancreas transplant
diabetic neuropathy
generalized deterioration of nervous system complicated by nonhealing ulcers on feet, gastric paresis, erectile dysfunction
diabetic neuropathy assessment
parasthesias, decreased/absent reflexes, decreased sensation, pain/aching in lower extrem., diminished peripheral pulses, skin breakdown with infection, weakened sensation to cranial nerves III/IV/V/VI, diarrhea/constipation, impotence, hypoglycemia unawareness, incontinence
diabetic neuropathy interventions
early prevention (glucose control), foot care, pain management, bladder training, estrogen containing lubricants, penile injections, surgical decompression
diabetes and surgery
prior- may need to hold oral hypoglycemics, may need to hold long acting insulin, monitor BGL levels; post- admin glucose/insulin as needed until oral intake resumes, admin short acting insulin as needed, risk for impaired wound healing
Pituitary gland problems
hypopituitarism, hyperpituitarism (acromegaly), hypophysectomy, Diabetes insipidus, SIADH
role of pituitary gland
promotes tissue growth, influences water absorption by kidney, controls sexual development and function; attached to hypothalamus; consists of anterior (more vascular) and posterior (more nerves)
hormones released by anterior pituitary
TSH, ACTH, LH, FSH, GH, prolactin
hormones secreted by posterior pituitary
oxytocin and vasopressin
hypopituitarism
hyposecretion of one or more pituitary hormones; most often affects GH, gonadotropic hormones, TSH, ACTH (most commonly affected), ADH
assessment of hypopituitarism
mild-moderate obesity (GH and TSH), reduced cardiac output (GH and ADH), infertility/sexual dysfunction (gonadotropins and ACTH), fatigue and hypotension (TSH, ADH, ACTH, GH)
hypopituitarism intervention
hormone replacement, emotional support, pt education on s/s of hypofunction and hyperfunction related to insufficient or excess replacement
hyperpituitarism
hypersecretion of growth hormone by anterior pituitary gland; if growth plates open like in children then results in long bone growth; if growth plates closed like in adults then results in growth in end plates like jaw and hands
assessment of hyperpituitarism
large hands/feet, thickening/protrusion of jaw, arthritic changes, visual disturbances, diaphoresis, organomegaly, HTN/cardiomegaly/HF, dysphagia, deepening of voice, thickening of tongue/narrowing of airway/sleep apnea, hyperglycemia, colon polyps
hyperpituitarism interventions
pharmacological agents to block action of GH, radiation of pituitary gland/stereotactic radiosurgery/hypophysectomy; manage join pain pharmacologically and non-pharmacologically
Diabetes insipidus
hyposecretion of ADH by posterior pituitary (too little ADH so too little water is reabsorbed); kidney fails to reabsorb water; Central Di is decreased ADH production; Nephrogenic DI is adequate ADH production but kidneys do not respond appropriately (very rare)
assessment of diabetes insipidus
large amount of dilute urine; polydipsia, dehydration, inability to concentrate urine, low urine specific gravity; fatigue and muscle weakness; headache; postural hypotension that may cause vascular collapse; tachycardia
diabetes insipidus intervention
monitor VS, neuro status, cardio status, fluids, electrolytes, IOs, weight; maintain adequate fluid intake with IV hypotonic saline to replace urinary loss; avoid diuresing foods and liquids; vasopressin if indicated; ensure safe environment; pt education on prescribed meds
syndrome of inappropriate antidiuretic hormone secretion
hyperfunctioning of posterior pituitary causing excess ADH release; caused by trauma, stroke, malignancies, meds, stress; resulting in increased intravascular volume, water intox., dilutional hyponatremia; may cause cerebral edema or seizures
assessment of SIADH
s/s of fluid overload, mental status changes (change in LOC), wieght gain without edema, HTN, tachycardia, anorexia, N/V, hyponatremia, low urine output, concentrated urine
interventions fo SIADH
monitor VS, cardio status, neuro status, signs of ICP, wight, fluid/electrolytes, implement seizure precautions/safe environment, elevate HOB max of 10 degrees, restrict fluid intake, NS/hypertonic saline to offset hypotonic fluid in vasculature, loop diuretics, vasopressin antagonists
adrenal gland problems
adrenal cortex insufficiency (addisons), addisonian crisis, cushings syndrome, cushings disease, adrenalectomy
adrenal gland
cortex synthesizes glucocorticoids, mineralocorticoids and secretes small amounts of sex hormones (androgens); medulla works as part of SNS and produces epi and norepi (catecholamines)
zona glomerulosa produces
mineralocorticoids that produce aldosterone to regulate BP, sodium, and potassium
addisons disease
aka primary adrenal insufficiency; causes hyposecretion of adrenal cortex hormones like glucocorticoids(cortisol), mineralocorticoids (aldosterone), and androgens; commonly caused by autoimmune destruction; requires lifelong replacement of glucocorticoids; fatal if left untreated
secondary adrenal insufficiency
caused by hyposecretion of ACTH from anterior pituitary gland (mineralocorticoid release is not affected)
addisons disease loss of glucocorticoids
leads to decreased vascular tone, decreased vascular response to catecholamines, decreased gluconeogenesis
addisons disease loss of mineralocorticoid
leads to dehydration, hypotension, hyponatremia, hyperkalemia
diagnoses of addisons disease made by…
clinical assessment and hormone testing
adrenal insufficiency assessment
lethargy, fatigue, muscle weakness, GI disturbances, weight loss, menstrual changes, impotence in men, electrolyte imbalance (hyponatremia, hyperkalemia, hypocalcemia), hypoglycemia, hypotension, hyperpigmentation of skin
interventions for adrenal insufficiency
monitor VS, weights, IOs; labs- WBCs, glucose, potassium, sodium, calcium; admin prescribed glucocorticoids and/or mineralocorticoids, monitor for s/s of addisonian crisis
addisonian crisis
medical emergency caused by acute adrenal insufficiency; caused by stress, infection trauma, surgery, or abrupt withdrawal of supplemental corticosteroids
assessment of adddisonian crisis
can result in hyponatremia, hyperkalemia, hypoglycemia, severe headache, abdominal pain, weakness, irritability, confusion, severe hypotension, evidence of shock
interventions for addisonian crisis
amin of IV glucocorticoids, fluids, and electrolytes; monitor VS, neuro status, IOs, labs; oral glucocorticoids and mineralocorticoids following resolution
pt education fro adrenal insufficiency
educate on lifelong therapy (increase corticosteroids during stress), avoid risk of infection, avoid strenuous activity, avoid stress, high protein carb calcium and vitamin D, wear medicalert bracelet, understanding of when to call for under or over replacement therapy
cushings syndrome
metabolic disorder causing chronic excessive production of cortisol d/t increased ACTH from pituitary; iatrogenic- cortisol coming from adrenal cortex resulting from prolonged admin of high dose glucocorticoids; can be caused by ACTH secreting tumors
cushings syndrome assessment
generalized muscle weakness and wasting, moon face, buffalo hump, truncal obesity with thin extrem., weight gain, hirsutism (masculinity in women), electrolyte imbalance (hypernatremia, hypokalemia, hypocalcemia), hyperglycemia, HTN, fragile skin, easy bruising, red/purple striation on abdomen and thighs
cushing syndrome intervention
monitor VS, weight, IOs; monitor labs- WBC, glucose, sodium, potassium; chemotherapeutic agents for inoperable adrenal tumors, removal of pituitary, adrenalectomy d/t adrenal adenoma; increased glucocorticoid during stress for those with lifelong therapy; assess for post op thrombus formation, medic alert bracelet
adrenalectomy
surgical removal of adrenal gland; glucocorticoid therapy is lifelong if both glands removed but temporary if one removed; surgery results in drop of catecholamine
thyroid gland problem
hypothyroidism, hyperthyroidism, myxedema coma, thyroid storm, thyroidectomy
thyroid gland
controls rate of body metabolism and growth, produces thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin
thyroxine T4
primary hormone made by thyroid and is converted to T3 in blood stream
Triiodothyronine T3
lower amounts produced in thyroid gland but has larger effect on metabolism
thyrocalcitonin
limits the amount of calcium; is not affected by hypo/hyperthyroidism
hypothyroidism
hyposecretion of thyroid hormones; decreased rate of body metabolism; T4 is low and TSH is high
primary hypothyroidism
source of dysfunction is the thyroid gland which cannot produce the necessary amount of hormones
secondary hypothyroidism
thyroid is not being stimulated by the pituitary to produce the hormones; anterior pituitary is not releasing TSH
assessment of hypothyroidism
lethargy, fatigue, weakness, muscle aches, parasthesias, cold intolerance, weight gain, dry skin/hair, hair loss, bradycardia, constipation, myxedema (edema around eyes and face), forgetfulness, menstrual disturbances, goiter, cardiac enlargement
hypothyroidism interventions
monitor VS, admin thyroid replacement as prescribed, assess for constipation, educate pt on therapy compliance, monitor for signs of hypo/hyperthyroidism, encourage low cal low cholesterol low sat fat die, include fiber, plenty of fluids for constipation, provide warm environment, avoid sedating meds d/t increases sensitivity and increased sedation effects (may cause myxedema coma)
myxedema coma
rare but serious disorder caused by low thyroid hormone production; can be precipitated by illness, withdrawal of thyroid meds, anesthesia.surgeru, hypothermia, sedatives
myxedema assessment
hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, gen edema, resp fail, coma
myxedema interventions
maintain patent airway, asp. precautions, IV fluids, levothyroxine IV, glucose IV, corticosteroids, assess temp/blood pressure/mental status/ electrolytes/glucose, keep pt warm
hyperthyroidism
hypersecretion of thyroid hormones T3 and T4; increased body metabolism; commonly caused by graves disease; T3 and T4 elevated with TSH low
hyperthyroidism assessment
irritability, agitation, mood swings, nervousness, fine tremors, weakness, muscle aches, parasthesias, heat intolerance, weight loss, smooth soft skin/hair, palpitations/dysrhythmias, diarrhea, exophthalmos, diaphoresis, HTN, goiter
hyperthyroidsim interventions
cool quiet environment for adequate rest; daily weights; high cal diet; admin sedatives; avoid stimulants, pharmacological meds such as antithyroid;, iodine preps; propanolol; radiocative iodine therapy; subtotal thyroidectomy; if exophthalmos then elevate HOB, artificial tears, dark sunglasses, tape eyelids closed
thyroid storm
manifests as fever, tachycardia, systolic HTN, N/V/D, agitation, tremors, confusion, can progress to seizures delirium and coma
treatment of thyroid storm
patent airway and adequate ventilation, administration of antithyroid meds, monitor VS, watch for dysrhythmias, non-salicylate antipyretics, cooling blanket for increased temp
thyroidectomy
removal of the thyroid gland; done for persistent or uncontrolled hyperthyroidism; subtotal is preferred; monitor for thyroid storm
parathyroid gland problems
hypoparathyroidism, hyperparathyroidism, parathyroidectomy
parathyroid gland
4 of them and they control calcium and phosphorus metabolism; production of PTH
PTH
activates osteoclasts and increased serum calcium, increases absorption of calcium from food, kidney increases calcium reabsorption
hypoparathyroidism
hyposecretion of parathyroid hormone by parathyroid gland; can occur following thyroidectomy that removes parathyroid tissue
hypoparathyroidism assessment
hypocalcemia, hyperphosphatemia, numbness/tingling in face, muscle cramps in extrem., abdominal cramping, + trosseaus or + chvosteks, signs of overt tetany, hypotension, anxiety, irritability, depression
hypocalcemia CATS
convulsions, arrhythmias, tetany, stridor and spasms
calcitonin
decreases calcium
hypoparathyroidism interventions
monitor VS, monitor for hypocalcemia and tetany, seizure precautions, emergency trach set O2 and suction at bed, increase calcium intake (calcium gluconate IV, high calcium low phos diet, vit d supps), admin phosphate binding agents to excrete via GI, encourage medic alert bracelet
hyperparathyroidism
over secretion of PTH by parathyroid gland
hyperparathyroidism assessment
hypercalcemia, hypophosphatemia, fatigue, muscle weakness, skeletal pain/tenderness, bone deformities resulting in pathological FX, anorexia, N/V, epigastric pain, weight loss, constipation, HTN, dysrhythmias, renal stones
hyperparathyroidism interventions
monitor VS, watch for dysrhythmias, IOs, skeletal pain, calcium and phos levels, encourage fluid, admin IV fluids, meds to lower calcium (furosemide, phosphates, calcitonin, bisphosphonates), prep for parathyroidectomy, importance of exercise program and avoid prolonged activity
parathyroidectomy
removal of parathyroid gland (one or more); endoscopic radio guided; complications can cause hypocalcemic crisis, change in voice, laryngeal nerve damage
