Endocrine

Question 1

Diabetes mellitus

Answer 1

chronic disorder of impaired carbohydrate, protein, and lipid metabolism; primarily carbohydrate; deficiency of insulin results in hyperglycemia

Question 2

sub-categories of diabetes

Answer 2

Type 1, Type 2, and metabolic syndrome (pre-diabetes)

Question 3

complications associated with diabetes

Answer 3

microvascular complications, macrovascular complications, reduced healing causing increased risk of infection

Question 4

how does diabetes destroy vasculature

Answer 4

glucose interacts with endothelial vascular wall causing damage, thrombi can form d/t damage of walls, all organs with vascular system experience damage

Question 5

type I diabetes

Answer 5

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

Question 6

type II diabetes

Answer 6

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

Question 7

metabolic syndrome

Answer 7

coexisting risk factors for developing type II diabetes; risk factors include abdominal obesity, hyperglycemia, HTN, high triglyceride levels, low HDL

Question 8

assessment of diabetes

Answer 8

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

Question 9

A1C diagnostic for diabetes

Answer 9

> 6.5

Question 10

dietary reccomendation for diabetes

Answer 10

consistency every day in timing and amount to control blood glucose levels, following american diabetic association diet, carb counting

Question 11

exercise recommendations for diabetes

Answer 11

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

Question 12

oral hypoglycemic medications

Answer 12

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

Question 13

primary intervention for type II diabetes

Answer 13

exercise, diet, and lifestyle; if not working after 6 months than oral hypoglycemics and maybe insulin prescribed

Question 14

only oral hypoglycemic not contraindicated in Type I diabetes

Answer 14

SGLT-2 inhibitors

Question 15

insulin

Answer 15

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

Question 16

dawn phenomenon

Answer 16

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

Question 17

somogyi effect

Answer 17

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

Question 18

common scenarios in Type I diabetes

Answer 18

dawn phenomenon and somogyi effect

Question 19

how much insulin can a pump store?

Answer 19

about 3 days worth

Question 20

hypoglycemia

Answer 20

<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

Question 21

hypoglycemia unawareness

Answer 21

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

Question 22

hypoglycemia s/s

Answer 22

cold, clammy, headache, lethargy, AMS, hungry, tachycardia, jittery, angry

Question 23

hypoglycemia assessment

Answer 23

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

Question 24

hypoglycemia interventions

Answer 24

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

Question 25

if pt found with altered LOC from hypoglycemia

Answer 25

first line is IV dextrose or IM glucagon

Question 26

glucagon

Answer 26

hormone secreted by alpha cells in pancreas that increases blood glucose; increased after 5-20 minutes

Question 27

DKA

Answer 27

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)

Question 28

assessment of DKA

Answer 28

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

Question 29

DKA interventions

Answer 29

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

Question 30

IV insulin for DKA

Answer 30

only use short acting

Question 31

HHS- hyperosmolar hyperglycemic syndrome

Answer 31

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

Question 32

assessment of HHS

Answer 32

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

Question 33

HHS interventions

Answer 33

similar treatment to DKA; fluid and electrolyte repletion; insulin is less critical as there is not ketosis/acidosis

Question 34

diabetic retinopathy

Answer 34

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

Question 35

assessment of diabetic retinopathy

Answer 35

vision changes, blurry vision from macular edema, sudden vision loss d/t retinal detachment (cant fix), cataracts lens opacity

Question 36

interventions for diabetic retinopathy

Answer 36

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

Question 37

diabetic nephropathy

Answer 37

progressive kidney function decline d/t damage of vascular walls causing blood supply issue to kidneys

Question 38

diabetic nephropathy assessment

Answer 38

fatigue, thirst, weight loss, anemia, microalbuminuria, malnutrition, UTIs, neurogenic bladder (incontinence), elevated creatinine

Question 39

interventions for diabetic nephropathy

Answer 39

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

Question 40

diabetic neuropathy

Answer 40

generalized deterioration of nervous system complicated by nonhealing ulcers on feet, gastric paresis, erectile dysfunction

Question 41

diabetic neuropathy assessment

Answer 41

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

Question 42

diabetic neuropathy interventions

Answer 42

early prevention (glucose control), foot care, pain management, bladder training, estrogen containing lubricants, penile injections, surgical decompression

Question 43

diabetes and surgery

Answer 43

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

Question 44

Pituitary gland problems

Answer 44

hypopituitarism, hyperpituitarism (acromegaly), hypophysectomy, Diabetes insipidus, SIADH

Question 45

role of pituitary gland

Answer 45

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)

Question 46

hormones released by anterior pituitary

Answer 46

TSH, ACTH, LH, FSH, GH, prolactin

Question 47

hormones secreted by posterior pituitary

Answer 47

oxytocin and vasopressin

Question 48

hypopituitarism

Answer 48

hyposecretion of one or more pituitary hormones; most often affects GH, gonadotropic hormones, TSH, ACTH (most commonly affected), ADH

Question 49

assessment of hypopituitarism

Answer 49

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)

Question 50

hypopituitarism intervention

Answer 50

hormone replacement, emotional support, pt education on s/s of hypofunction and hyperfunction related to insufficient or excess replacement

Question 51

hyperpituitarism

Answer 51

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

Question 52

assessment of hyperpituitarism

Answer 52

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

Question 53

hyperpituitarism interventions

Answer 53

pharmacological agents to block action of GH, radiation of pituitary gland/stereotactic radiosurgery/hypophysectomy; manage join pain pharmacologically and non-pharmacologically

Question 54

Diabetes insipidus

Answer 54

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)

Question 55

assessment of diabetes insipidus

Answer 55

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

Question 56

diabetes insipidus intervention

Answer 56

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

Question 57

syndrome of inappropriate antidiuretic hormone secretion

Answer 57

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

Question 58

assessment of SIADH

Answer 58

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

Question 59

interventions fo SIADH

Answer 59

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

Question 60

adrenal gland problems

Answer 60

adrenal cortex insufficiency (addisons), addisonian crisis, cushings syndrome, cushings disease, adrenalectomy

Question 61

adrenal gland

Answer 61

cortex synthesizes glucocorticoids, mineralocorticoids and secretes small amounts of sex hormones (androgens); medulla works as part of SNS and produces epi and norepi (catecholamines)

Question 62

zona glomerulosa produces

Answer 62

mineralocorticoids that produce aldosterone to regulate BP, sodium, and potassium

Question 63

addisons disease

Answer 63

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

Question 64

secondary adrenal insufficiency

Answer 64

caused by hyposecretion of ACTH from anterior pituitary gland (mineralocorticoid release is not affected)

Question 65

addisons disease loss of glucocorticoids

Answer 65

leads to decreased vascular tone, decreased vascular response to catecholamines, decreased gluconeogenesis

Question 66

addisons disease loss of mineralocorticoid

Answer 66

leads to dehydration, hypotension, hyponatremia, hyperkalemia

Question 67

diagnoses of addisons disease made by...

Answer 67

clinical assessment and hormone testing

Question 68

adrenal insufficiency assessment

Answer 68

lethargy, fatigue, muscle weakness, GI disturbances, weight loss, menstrual changes, impotence in men, electrolyte imbalance (hyponatremia, hyperkalemia, hypocalcemia), hypoglycemia, hypotension, hyperpigmentation of skin

Question 69

interventions for adrenal insufficiency

Answer 69

monitor VS, weights, IOs; labs- WBCs, glucose, potassium, sodium, calcium; admin prescribed glucocorticoids and/or mineralocorticoids, monitor for s/s of addisonian crisis

Question 70

addisonian crisis

Answer 70

medical emergency caused by acute adrenal insufficiency; caused by stress, infection trauma, surgery, or abrupt withdrawal of supplemental corticosteroids

Question 71

assessment of adddisonian crisis

Answer 71

can result in hyponatremia, hyperkalemia, hypoglycemia, severe headache, abdominal pain, weakness, irritability, confusion, severe hypotension, evidence of shock

Question 72

interventions for addisonian crisis

Answer 72

amin of IV glucocorticoids, fluids, and electrolytes; monitor VS, neuro status, IOs, labs; oral glucocorticoids and mineralocorticoids following resolution

Question 73

pt education fro adrenal insufficiency

Answer 73

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

Question 74

cushings syndrome

Answer 74

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

Question 75

cushings syndrome assessment

Answer 75

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

Question 76

cushing syndrome intervention

Answer 76

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

Question 77

adrenalectomy

Answer 77

surgical removal of adrenal gland; glucocorticoid therapy is lifelong if both glands removed but temporary if one removed; surgery results in drop of catecholamine

Question 78

thyroid gland problem

Answer 78

hypothyroidism, hyperthyroidism, myxedema coma, thyroid storm, thyroidectomy

Question 79

thyroid gland

Answer 79

controls rate of body metabolism and growth, produces thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin

Question 80

thyroxine T4

Answer 80

primary hormone made by thyroid and is converted to T3 in blood stream

Question 81

Triiodothyronine T3

Answer 81

lower amounts produced in thyroid gland but has larger effect on metabolism

Question 82

thyrocalcitonin

Answer 82

limits the amount of calcium; is not affected by hypo/hyperthyroidism

Question 83

hypothyroidism

Answer 83

hyposecretion of thyroid hormones; decreased rate of body metabolism; T4 is low and TSH is high

Question 84

primary hypothyroidism

Answer 84

source of dysfunction is the thyroid gland which cannot produce the necessary amount of hormones

Question 85

secondary hypothyroidism

Answer 85

thyroid is not being stimulated by the pituitary to produce the hormones; anterior pituitary is not releasing TSH

Question 86

assessment of hypothyroidism

Answer 86

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

Question 86

hypothyroidism interventions

Answer 86

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)

Question 87

myxedema coma

Answer 87

rare but serious disorder caused by low thyroid hormone production; can be precipitated by illness, withdrawal of thyroid meds, anesthesia.surgeru, hypothermia, sedatives

Question 88

myxedema assessment

Answer 88

hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, gen edema, resp fail, coma

Question 89

myxedema interventions

Answer 89

maintain patent airway, asp. precautions, IV fluids, levothyroxine IV, glucose IV, corticosteroids, assess temp/blood pressure/mental status/ electrolytes/glucose, keep pt warm

Question 90

hyperthyroidism

Answer 90

hypersecretion of thyroid hormones T3 and T4; increased body metabolism; commonly caused by graves disease; T3 and T4 elevated with TSH low

Question 91

hyperthyroidism assessment

Answer 91

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

Question 92

hyperthyroidsim interventions

Answer 92

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

Question 93

thyroid storm

Answer 93

manifests as fever, tachycardia, systolic HTN, N/V/D, agitation, tremors, confusion, can progress to seizures delirium and coma

Question 94

treatment of thyroid storm

Answer 94

patent airway and adequate ventilation, administration of antithyroid meds, monitor VS, watch for dysrhythmias, non-salicylate antipyretics, cooling blanket for increased temp

Question 95

thyroidectomy

Answer 95

removal of the thyroid gland; done for persistent or uncontrolled hyperthyroidism; subtotal is preferred; monitor for thyroid storm

Question 96

parathyroid gland problems

Answer 96

hypoparathyroidism, hyperparathyroidism, parathyroidectomy

Question 97

parathyroid gland

Answer 97

4 of them and they control calcium and phosphorus metabolism; production of PTH

Question 98

PTH

Answer 98

activates osteoclasts and increased serum calcium, increases absorption of calcium from food, kidney increases calcium reabsorption

Question 99

hypoparathyroidism

Answer 99

hyposecretion of parathyroid hormone by parathyroid gland; can occur following thyroidectomy that removes parathyroid tissue

Question 100

hypoparathyroidism assessment

Answer 100

hypocalcemia, hyperphosphatemia, numbness/tingling in face, muscle cramps in extrem., abdominal cramping, + trosseaus or + chvosteks, signs of overt tetany, hypotension, anxiety, irritability, depression

Question 101

hypocalcemia CATS

Answer 101

convulsions, arrhythmias, tetany, stridor and spasms

Question 102

calcitonin

Answer 102

decreases calcium

Question 103

hypoparathyroidism interventions

Answer 103

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

Question 104

hyperparathyroidism

Answer 104

over secretion of PTH by parathyroid gland

Question 105

hyperparathyroidism assessment

Answer 105

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

Question 106

hyperparathyroidism interventions

Answer 106

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

Question 107

parathyroidectomy

Answer 107

removal of parathyroid gland (one or more); endoscopic radio guided; complications can cause hypocalcemic crisis, change in voice, laryngeal nerve damage