Final Exam - Endocrine Disorders

endocrine system - closely linked with which 2 systems?

• neurologic

• immune

hypothalamus and pituitary gland relationship

• hypothalamus monitors ALL hormones in the body, and if it detects a deficiency or excess of a specific hormone, it stimulates the pituitary to stimulate the specific gland to either stop production or increase production of the hormone

hypo/hyperthyroid - how is the TSH level affected?

• HYPOthyroid - TSH is going to be INCREASED (as it is going to be continuously released to stimulate T3/T4 release, but failing)

• HYPERthyroid - TSH is going to be DECREASED (already too much T3/T4, so releasing more TSH would worsen this)

thyroid - functions

• cell development / growth

• controls cellular metabolic activity

• NECESSARY for normal reproduction

hypothyroidism - what is the autoimmune disease called?

Hashimoto’s disease

hypothyroidism - what is it? what is it characterized by?

a disease where a patient is unable to produce T3 or T4

• characterized by “everything SLOWING DOWN, and is LOW”

hypothyroidism - manifestations

• extreme fatigue

• hair loss

• brittle nails

• dry skin

• constipation

• menstrual disturbances

• low heart rate and BP

• weight GAIN

• cold intolerance

hypothyroidism - management

• synthetic levothyroxine (T4) replacement therapy

  • T4 converts to T3 once in the body

  • need to follow up with blood tests to ensure proper dose (TSH levels)

hypothyroidism - EMERGENCY? what happens?

• myxedema coma (RARE!!!!!!)

  • lethargy progresses to stupor, causes respiratory depression, and can be life threatening

hypothyroidism - how can myxedema coma be precipitated?

• infection

• UNTREATED hypothyroid

hyperthyroidism - another name?

• Grave’s disease

hyperthyroidism - what is it? what is it characterized by?

• TOO MUCH T3/T4, and enlarged thyroid becomes a goiter

  • “everything SPEEDS UP/RUNS you into the grave”

hyperthyroidism - manifestations

• nervousness/tremors

• high HR/systolic BP

• HEAT intolerance

• skin flushed, warm, soft, and moist

• exophthalmos (eyes bulging out of head)

• increased appetite, but weight LOSS

• cardiac dysrhythmias (A-FIB!!!!)

hyperthyroidism - management (meds, surgery)

• meds

  • methimazole (kills the thyroid!!)

    • will be put on levothyroxine for the rest of your life after this; same with thyroidectomy

  • dexamethasone (decreases inflammation)

  • beta-blockers

  • radioactive iodine therapy

• surgery

  • thyroidectomy

hyperthyroidism - EMERGENCY? what precipitates it?

• THYROID STORM (metabolic rate rises RAPIDLY!!)

  • precipitated by uncontrolled hyperthyroid and infection

hyperthyroidism - thyroid storm (4 main s/s)

• HYPERTHERMIA (not a fever response)

• HTN

• delirium

• a-fib

what is the treatment of choice for thyroid cancer?

• THYROIDECTOMY!!

what procedures are done concurrently with the thyroidectomy?

• modified/radical neck dissection

• radioactive iodine therapy to minimize metastasis

thyroidectomy - PREOPERATIVE GOALS

• reduction of stress and anxiety to avoid precipitation of a thyroid storm

thyroidectomy - preoperative education

• dietary guidance to meet patient metabolic needs

  • avoidance of caffeinated beverages and other stimulants

• explanation of tests and procedures

• head and neck support used AFTER surgery

• patient is admitted to the floor after the procedure to ensure that airway is secured!!

thyroidectomy - post-op care

• monitor respirations (potential airway impairment)

• monitor for potential bleeding/hematoma formation

• assess pain and provide pain relief measures

• semi-fowler’s position; support head and neck

• assess voice, discourage talking

• potential hypocalcemia related to injury or removal of parathyroid glands

parathyroid gland - location? function?

• four glands located on the posterior thyroid gland

• parathyroid hormone (PTH) regulates calcium and phosphorus balance

  • INCREASED PTH elevates blood calcium by INCREASING calcium absorption from kidney, intestine, and bone; simultaneously DECREASES phosphorus reabsorption

hyperparathyroidism - manifestations

• HYPERCALCEMIA

• bone decalcification

• renal calculi

• fatigue

• muscle WEAKNESS

• N/V

• constipation

• HTN

• cardiac dysrhythmias

• psychological manifestations

hyperparathyroidism - management

• parathyroidectomy

• hydration therapy

• encouraging mobility

• encourage fluids

• restrict calcium intake

calcium plays a major role in what? what does this mean in HYPERPARATHYROIDISM?

• calcium plays a big role in CLOTTING

  • in hyperparathyroidism, LOTS of clotting can occur, increasing the mortality rate!!

hyperparathyroidism - what is it exclusively caused by?

• tumor/cancer of parathyroid hormone

what is secondary hypothyroidism?

• hypothyroidism that occurs after the patient had hyperthyroid, but either had it killed or taken out

hypoparathyroidism - causes?

• thyroidectomy/parathyroidectomy

• radical neck dissection

hypoparathyroidism - what happens to calcium and phosphorus levels?

• hypocalcemia

• hyperphosphatemia

hypoparathyroidism - manifestations

• tetany (muscle spasms/cramps)

• numbness

• tingling in extremities

• stiffness of hands and feet

• bronchospasm

• laryngeal spasm

• carpopedal spasm

• anxiety/irritability/depression

• delirium

• EKG changes

• Positive Chvostek’s and Trousseau’s sign

hypoparathyroidism - management

• calcium gluconate IV / calcium replacement

• PTH administration

• HIGH calcium/LOW phosphorous diet

• long-term calcium supplementation

adrenals (medulla vs. cortex) - what’s the difference?

• medulla - functions as part of autonomic nervous system (releases epi/norepi)

• cortex - releases glucocorticoids (cortisol), mineralocorticoids (ALDOSTERONE!!), and androgens (male sex hormone)

what hormone causes the adrenal glands to release cortisol?

• ACTH (adrenocorticotropic hormone) released by the pituitary to stimulate the adrenal glands

the human body naturally secretes cortisol, which is equal to how much prednisone each day?

5mg of prednisone / day

adrenal crisis (what is it?)

• adrenal suppression caused by CHRONIC STEROID USE that is abruptly stopped (ACTH is not being released, causing no cortisol release/damage to adrenal gland); this is ACUTE!!!

addison’s disease (what is it?)

• CHRONIC adrenal insufficiency (autoimmune-related, or from tumors)

adrenal crisis/addison’s disease - signs and symptoms

• muscle WEAKNESS

• anorexia

• GI symptoms

• fatigue

• dark pigmentation of skin/mucosa

• HYPOtension

• HYPOnatremia and HYPERkalemia

• emotional instability/apathy

• confusion

adrenal crisis/addison’s disease - how are they treated?

• prednisone (gives the patient the cortisol that is not being released naturally)

adrenal crisis/addison’s disease - nursing considerations

• note ANY ILLNESS OR STRESSORS that may precipitate problems

• F/E status!!

• VS and orthostatic BP!!

• note s/s related to adrenocortical insufficiency (weight loss, muscle weakness, fatigue, etc)

Cushing syndrome - what is it? cause?

• excessive adrenocortical activity!!

  • caused by excessive corticosteroid use (TITRATE THE DOSE OF PREDNISONE TO AVOID GETTING THIS!!)

Cushing syndrome - manifestations

• hyperglycemia

• central-type obesity with “buffalo hump”

• heavy trunk and thin extremities

• fragile/thin skin; ecchymosis; striae

• weakness; osteoporosis (pulls calcium out of bones)

• muscle wasting

• HTN

• “moon face”

• acne

• infection/slow healing

• increased androgens in women →hirsutism (facial hair growth)

• HYPERnatremia

• HYPOkalemia

ACTH - how does it affect sodium and potassium levels?

• ACTH causes renal sodium RETENTION and potassium EXCRETION

Cushing syndrome - same signs and symptoms of what?

s/s are the same as the SIDE EFFECTS of taking prednisone

Cushing syndrome - nursing considerations

• activity level and ability to carry out self-care

• skin assessment!!

• changes in physical appearance and patient responses to these changes

• mental function

• emotional status (especially due to body disturbances)

primary aldosteronism - what is it?

• excess production of aldosterone by the adrenal glands, resulting in low renin levels

primary aldosteronism - (2 most common causes)

1. an aldosterone producing adrenal tumor

2. bilateral adrenal hyperplasia

primary aldosteronism - manifestations

• HTN (especially in young)

• low K+→ALKALOSIS!!

• headache

• vision problems

• fatigue

• muscle cramps/weakness

primary aldosteronism - 2 management techniques

1. surgical removal of gland (permanently resolving high BP and K deficiency, and brings aldosterone levels back to normal)

2. aldosterone-blocking drugs (SPIRONOLACTONE!!) and lifestyle changes (if medications are stopped, high BP and low K will return!!)

primary aldosteronism - surgical removal of gland (when will BP drop?)

• drops gradually after a unilateral adrenalectomy and meds are adjusted

Diabetes - diagnostics

• blood glucose levels!!

  • fasting blood sugar (over 125)

  • hgb A1C (above 6.5% (6-6.4% = PREDIABETES, and will be started on metformin)

  • glucose tolerance test (always done when moms are pregnant)

diabetes (treatment GOALS!!)

• NORMAL blood sugar levels

• prevention of systemic damage

  • hyperglycemia damages EVERY organ system in the body!!

diabetes - hyperglycemia damages EVERY body system/organ, meaning WHAT complications can occur?

• CKD/ESRD

• strokes

• heart attacks

• PAD

• neuropathies

• decreased immune system / healing

diabetes - lifestyle changes

• meal planning (carb control) → DIABETIC DIET!!

• exercise

• medication adherence

insulin types (general)

• rapid acting (sliding scale; given before meals, about 15 min)

• short acting (ONLY on that go in IV!!; can reduce potassium)

• intermediate acting

• long acting

  • BOTH are given 1 time a day to reduce sugars for 24 hours

insulin - EDUCATION!

• uses and action of insulin

• signs and symptoms of hypo/hyperglycemia

  • REQUIRED ACTIONS THAT MUST BE TAKEN!!

• blood glucose monitoring is KEY

• teach patient how to self-inject their insulin

• how to use to insulin pump (usually always for type 1)

Hypoglycemia vs. Hyperglycemia (CHART)

why are oral agents for diabetes not used in TYPE 1 DM?

• type 1 is AUTOIMMUNE, meaning that the pancreas is not working at ALL, meaning this medication would literally do ABSOLUTELY NOTHING!!!!!!

oral diabetic agents - major side effect? metformin?

• MAJOR SIDE EFFECT: hypoglycemia

  • metformin: diarrhea (will eventually go away)

oral diabetic agents - nursing interventions

• MONITOR BLOOD GLUCOSE for hypoglycemia and other potential side effects

2 acute complications of DM? (which complication is associated with which DM type?)

• DKA (Type 1)

• HHS (Type 2 → hyperglycemia WITHOUT the acidosis)

DKA - 2 precipitating factors

• patient does not know that they have diabetes

• INFECTION !!

DKA - general definition

• absence or inadequate amount of insulin, resulting in abnormal metabolism of carbs, proteins, and fats

DKA - 3 clinical features

• hyperglycemia

• dehydration

• acidosis

DKA - diagnostics?

• ABG (GOLD STANDARD) - shows acidosis (metabolic acidosis, with respiratory compensation (KUSSMAUL RESPIRATIONS!!!))

• urinalysis (ketones in blood and urine)

• basic metabolic panel (shows increase in creatinine/BUN, hematocrit, and K (SHOWS DEHYDRATION!!))

DKA - why are patients hyperkalemic? what is given to combat this?

• insulin affects the amount of potassium in the blood (without it, there is nothing pushing potassium back into the cells)

  • that’s why patients are put on an insulin drip, pushing K back into the cells and out of the blood stream 🙂

DKA - ketoacidosis (how do you know?)

• low serum bicarb

• low pH

• low PCO2 reflects respiratory compensation (Kussmaul respirations)

DKA - while on an insulin drip, why is the patient also on dextrose?

• dextrose is given to prevent hypoglycemia while on the insulin drip

DKA - insulin vs. dextrose

• insulin = more focused on helping with the acidosis

• dextrose = more focused on reaching a normal blood glucose level

DKA - what other lab should you look at, indicating metabolic acidosis?

• ANION GAP!! (elevated)

DKA - treatment

• rehydration with IV fluid (leads to increased plasma volume and decreased K)

• IV continuous infusion of regular insulin

  • reverses the acidosis/restores electrolyte balance (TREATING THE ANION GAP, NOT THE BLOOD GLUCOSE VALUE)

  • pushes K from bloodstream into the cells

DKA - when on insulin drip, how often is blood sugar checked?

• EVERY HOUR!!

DKA - when getting treated, what should you monitor?

• blood glucose (EVERY HOUR)

• renal function (Cr/BUN) / urinary output

• anion gap !!!

• EKG (high K is dangerous!!)

  • other electrolyte levels due to dehydration

• VS

• lung assessments for signs of fluid overload (from IV fluids)

HHS - 2 clinical features

• hyperglycemia

• dehydration

  • REMEMBER THERE IS NO KETOACIDOSIS!!!

HHS - what does the hyperglycemia cause?

• osmotic diuresis!!!

• loss of water/electrolytes

• HYPERnatremia

• increased osmolality

HHS - manifestations

• hypotension

• profound dehydration

• tachycardia

• variable neurologic signs, caused by CEREBRAL DEHYDRATION!!

HHS - 2 precipitating factors

• patient does not control their type 2 DM well

• patient does not know they have type 2 DM

HHS - why do patients present sicker?

• the patient’s blood sugar tends to slowly rise overtime, and the body is adjusting to this increase, and the damage is going to be continuously done until it is too late to do anything

HHS - treatment

• rehydration!!

• IV insulin (given to decrease blood sugar, as there is NO ACIDOSIS!!)

• monitor fluid volume and electrolyte status !!!

HHS - prevention

• diagnosis and management of diabetes!!

• assess and promote self-care management skills

DKA vs. HHS (CHART)

hypoglycemia - blood glucose level? causes?

• blood glucose LESS THAN 70

• causes: too much insulin or oral hypoglycemic agents, excessive physical activity, not enough food

hypoglycemia - manifestations

• sweating

• tremors / nervousness

• tachycardia / palpitations

• hunger

• inability to concentrate

• headache

• confusion

• memory lapses

• SLURRED SPEECH (can mimic stroke symptoms)

• drowsiness

SEVERE hypoglycemia - manifestations

• disorientation

• seizures

• loss of consciousness (usually at around 40 years old)

• DEATH!!

hypoglycemia management (CONSCIOUS patient)

• give 15 g of fast-acting, concentrated carbohydrates

  • 3-4 glucose tablets

  • 4-6 oz of juice or regular soda (NOT DIET)

• retest blood glucose in 15 minutes (retreat if STILL below 70 or if symptoms persist more than 10-15 min/testing is not possible)

• provide a snack with protein and carbs (unless patient plans to eat a MEAL within 30-60 min)

hypoglycemia - why is simply giving a patient juice/soda NOT enough for blood sugar fluctuation?

• this is only going to TEMPORARILY raise their blood sugar back to a normal level, and it will not sustain it

  • this is why we give the patient a MEAL with complex carbs to sustain a normal blood sugar

hypoglycemia management (UNCONSCIOUS PATIENT)

• subq or IM glucagon (1 mg)!!!

  • serves sort of like an “epipen” in DM type 1

• 25-50 mL of 50% dextrose solution IV