endocrine Flashcards
hormones produced by the thyroid gland x3
T3
T4
calcitonin
calcitonin action
decreases serum Ca by taking Ca out of blood and returning it to bone
iodine purpose
hormone creation
thyroid hormone purpose
energy
hyperthyroidism
aka Graves Disease
too much energy!
hyperthyroidism: s/s
nervous, irritable
sweaty, hot
exophthalmos
thyroid hypertrophy
decreased
- attention span
- weight
increased
- appetite, gi motility
- bp (workload of heart)
hyperthyroidism: dx
increased serum T4
thyroid scan
antiarrhythmic drug containing high levels of iodine
amiodarone (Cordarone) - may affect thyroid function
prior to thyroid scan…?
discontinue iodine-containing medications 1 week prior
hyperthyroidism: tx
anti-thyroid medications iodine compounds beta blockers radioactive iodine surgery
anti-thyroid medications: action
- stops thyroid from making thyroid hormone
- for hyperthyroidism
used prepoperatively to stun thyroid
anti-thyroid med
iodine compounds: action
- decreases the size and vascularity of thyroid gland
- for hyperthyroidism
beta blockers for hyperthyroidism: action
decreases myocardial contractility
- decreases HR, BP, anxiety
- could decrease cardiac output
radioactive iodine: administration
- for hyperthyroidism
- 1 dose PO (liquid or tablet form)
- RULE OUT PREGNANCY FIRST
important nursing consideration for radioactive iodine
rule out pregnancy before admin!
radioactive iodine: action
destroys thyroid cells resulting in hypothyroidism (not ae - expected)
possible rebound effect post-radioactive iodine
thyroid storm
thyroid storm
thyrotoxicosis, thyrotoxic crisis
- uncontrollable hyperthyroidism
- can be caused by thyroid manipulation, severe infection, stress
MEDICAL EMERGENCY
do not give beta blockers to… x2
asthmatics or diabetics
- block catecholamine sites (epi, NE)
thyroid gland regulates
body metabolism and growth
use straw with iodine compounds because…?
stains teeth
radioactive precautions
no babies or kisses for 24 hours
thyroidectomy: positioning
HOB up to decrease risk of edema
sign of recurrent laryngeal nerve damage post-thyroidectomy
hoarseness
why keep a trach set at the bedside post-thyroidectomy?
- swelling
- recurrent laryngeal nerve damage (vocal cord paralysis)
- hypocalcemia
why is hypocalcemia a consideration post-thyroidectomy?
possible parathyroid removal
s/s hypocalcemia: tight, rigid muscles, seizure possiblity
hyperthyroidism and eyes
dry eyes, photosensitivity
hypothyroidism aka
myxedema
hypothyroidism: s/s
no energy!!, fatigue increased weight cold decreased gi motility, speech no expression
cretinism
hypothyroidism present at birth, can lead to slowed mental and physical development if undetected
hypothyroidism: tx
meds (levothyroxine, thyroglobulin, liothyronine): take FOREVER
common hypothyroidism co-morbidity
CAD - every aspect of metabolism slows down; basement membranes not proliferating = narrower artery walls = CAD
possible to throw clots!
hyperthyroidism + hypoglycemia
do not give beta blockers to diabetics because they block signs of hypoglycemia
beta blockers: decrease HR, BP, clammy (sweaty), nervous/anxious
hypothyroidism + depression
tired, weight gain, immobility (in bed)
parathyroid problem think
calcium!
parathyroid hormone: action
pull Ca from bone and into serum - serum Ca goes up
hyperparathyroidism =
hypercalcemia = hypophosphatemia
hypoparathyroidism =
hypocalcemia = hyperphosphatemia
hyperparathyroidism: s/s
too much PTH
serum Ca up
serum P down
SEDATED!
hyperparathyroidism: tx
partial parathyroidectomy
partial parathyroidectomy
take out 2 parathyroid glands
PTH secretion goes down, serum Ca goes down
monitor for what post-parathyroidectomy?
hypocalcemia: tight, rigid muscles, seizures
hypoparathyroidism: s/s
not enough PTH
serum Ca down
serum P up
hypocalcemia s/s
hypoparathyroidism: tx
IV calcium - give SLOWLY
phosphorous binding drugs
ESRD patients tend to retain…
phosphorous therefore serum Ca is down
adrenal glands for
stress
adrenal medulla hormones
epinephrine
norepinephrine
pheochromocytoma
benign tumors on adrenal medulla that secrete epi and NE in boluses
pheochromocytoma: s/s
increased BP, HR
flushing, diaphoretic
vanillylmandelic acid test
24 hour urine specimen checking for increased levels of catecholamines (epi, NE) - used for dx of pheochromocytoma
pheochromocytoma: tx
surgery to remove tumors
adrenal cortex hormones
glucocorticoids
mineralocorticoids
sex hormones
glucocorticoids: actions x4
- mood
- immunosuppression (decrease inflammation)
- inhibit insulin = hyperglycemic…
- fat, protein metabolism
accuchecks + steroids
steroids (glucocorticoids) inhibit insulin
major mineralocorticoid
aldosterone
aldosterone: retain & lose what?
retain: Na, H2O
lose: K+ (dilutional hypokalemia + urinary excretion)
too much aldosterone
fluid volume excess
hypokalemia
not enough aldosterone
fluid volume deficit
hyperkalemia
major glucocorticoid
cortisol
pituitary + cortisol
pituitary secretes adrenocorticotropin hormones (ACTH)
ACTH stimulate adrenal cortex to produce cortisol
ACTH = cortisol
adrenocorticotropin hormones (ACTH)
stimulate adrenal cortex to produce cortisol
secreted by pituitary
addison’s disease
adrenocortical insufficiency: not enough steroids (gluco, mineralo, sex)
ADRENAL CORTEX PROBLEM
addison’s disease: s/s
majority result from hyperkalemia
- progression: muscle twitching - weakness - flaccid paralysis
other:
gi: gut slows down - anorexia, nausea, decreased bowel sounds, gi upset
hyperpigmentation, vitiligo
hypotension
decreased Na, increased K, hypoglycemia
hyperpigmentation
bronzing color of skin and mucus membranes
sign of addison’s
vitiligo
white patchy area of depigmented skin
sign of addison’s
addison’s + hypoglycemia
addison’s = not enough steroids = decreased glucocorticoids
not enough glucocorticoid = not enough glucose
also inhibits insulin
addison’s + aldosterone
addison’s = not enough steroids = decreased mineralocorticoids (aldosterone)
insufficient aldosterone = lose Na = retain K = hyperkalemia
addison’s + hyperkalemia
addison’s = not enough steroids = decreased mineralocorticoids (aldosterone)
insufficient aldosterone = lose Na = retain K = hyperkalemia
addison’s + shock
addison’s = insufficient steroids = insufficient mineralocorticoids (aldosterone)
decreased aldosterone = lose Na and H2O = lose blood volume = SHOCK
addison’s tx
- combat shock
- increase dietary Na
- i/o + daily weight
addison’s + hypotension
decreased BP due to loss of Na
fludrocortisone (Florinef)
mineralocorticoid replacement - aldosterone
- daily weights very important
- given for addison’s disease
daily weights + florinef
crucial for adjustment of florinef dose, similar to insulin for diabetics
addisonian crisis
severe hypotension and vascular collapse
could result from abrupt d/c of steroids
consideration for discontinuation of steroids
taper! never stop abruptly - could result in addisonian crisis
cushing’s syndrome
too many steroids! glucocorticoids, mineralocorticoids, sex hormones
cushing’s: s/s due to too many glucocorticoids
growth arrest thin extremities, lypolysis increased risk of infection hyperglycemia, hypoinsulinemia psychosis to depression moon face truncal obesity/lipogenesis buffalo hump (fat redistribution)
buffalo hump due to
glucocorticoid excess
fat redistribution
moon face due to
glucocorticoid excess
fat redistribution or fluid retention
cushing’s: s/s due to too many sex hormones
oily skin/acne
women with male traits
poor libido
cushing’s: s/s due to too many mineralocorticoids
high BP CHF weight gain fluid volume excess decreased serum K
cushing’s: tx
adrenalectomy
quiet environment
avoid infection
pre-treatment diet:
increased K, protein, Ca
decreased Na
cushing’s: pre-treatment diet
increased K (cushing’s = decreased serum K)
increased protein (too many glucocorticoids = breakdown of fat and protein)
increased Ca (steroids decrease serum Ca through GI excretion)
decreased Na (retaining already(
how do steroids decrease serum Ca?
via GI excretion
cushing’s: may appear in urine
glucose and ketones
protein can’t come out of glomerulus unless it is damaged!
diabetes: type 1
little or no insulin; appears abruptly despite years of beta cell destruction
usually diagnosed in childhood (by age 30)
type 1 DM causes
auto-immune response (type 1A)
idiopathic (type 1B)
first sign of type 1 DM typically
DKA
type 1 diabetes: pathophys
little to no insulin = glucose builds up in vascular space
blood = hypertonic, pulls fluid in
kidneys filter excess glucose and fluids
cells starving and start breaking down protein and fat for energy
breakdown of fat results in ketones
leads to metabolic acidosis (DKA)
type 1 diabetes: s/s
polyphagia
polyuria
polydipsia
do oral hypoglycemics work for type 1 dm clients?
NOPE - need insulin
type 2 diabetes: pathophys
insufficient insulin or bad insulin (usually just enough to prevent fat breakdown, therefore typically overweight)
can’t keep up with the glucose load being taken in
not as abrupt as type 1, usually found by accident or client presents with other problems (ulcers, infections, etc)
evaluate for metabolic syndrome!
metabolic syndrome featuers
- insulin resistance
- waist circumference 40+ m, 35+ f
- increased triglycerides + decreased HDL
- increased BP
- CAD
type 2 diabetes: treatment
start with diet and exercise
then add oral agents
then insulin (especially in presence of non-compliance)
gestational diabetes
resembles type 2; mom needs 2-3x more insulin than normal during pregnancy
screen all moms when for gestational diabetes?
24 - 28 weeks gestation
1st prenatal visit, if risk factors present
gestational diabetes: complications for baby
increased birth weight
hypoglycemia after birth
diabetes diet: majority of calories should come from x3
complex carbs
fats
protein (limit 10-20%)
why are diabetics prone to CAD?
sugar destroys vessels just like fat
diabetics + kidney
tend to have kidney disease
diabetes + high fiber
- keeps blood sugar steady (may have to decrease insulin)
- slows down glucose absorption in intestines, which eliminates sharp rise/fall in blood sugar
- sharp rise/fall of blood sugar = vascular damage
how do oral hypoglycemics work?
only for type 2. they stimulate the pancreas to make insulin (at least, for the NCLEX)
bottomline: all oral hypoglycemics work to decrease the amount of circulating glucose
average adult dose of insulin
0.4 - 1.0 units / kg / day
need more insulin if what are present in urine?
glucose, ketones
cloudy insulin
NPH
clear insulin
regular
also, Lantus (long-acting)
long-acting insulin
Lantus
what is the only type of insulin you can give IV?
regular
long-acting insulin peak
none!
rapid acting insulin peak
meal time
when insulin is at its peak, blood glucose…
is at its lowest
client should eat when insulin is at its
peak
how do you draw up regular and NPH insulin together
clear to cloudy
regular then NPH
glycosylated hemoglobin HbA1c blood test
gives an average of what your blood sugar has been over the past 3 months
HbA1c goal for diabetics
4-6% or less
HbA1c level that is diagnostic for diabetes
6.5 - 7%
sq infusion pumps are only used for which type of insulin?
rapid acting insulin
coverage provided by sq insulin infusion pump
basal (continuous)
and
bolus (on-demand)
rapid-acting insulin!
diabetics: illness =
dka
s/s hypoglycemia
cold clammy headache nervous confusion nause increased HR glucose less than 70mg/dL
hypoglycemic should eat what?
4-6 oz of simple sugar
followed by complex carb + protein once BG is up
hypoglycemia prevention x4
- eat
- take insulin regularly
- know s/s
- check BG regularly
glucose absorption delayed in foods with lots of
FATS!
D50 W
for unconscious diabetic in hospital
requires large bore IV
injectable glucagon (GlucaGen)
for unconscious diabetic in hospital with no IV access
given IM
diabetic ketoacidosis pathophys
absent or inadequate insulin = BG sky high = poly(uria, dipsia, phagia) = fat breakdown (acidosis) = kussmaul respirations + more acidotic = LOC decreases
kussmaul respirations
diabetic client in dka trying to blow off CO2 to compensate for metabolic acidosis
diabetic client + polyuria =
think shock
IV insulin action
decreases glucose and K by driving them out of vascular space and into cell
dka tx
- find cause
- IV insulin
- hourly BG, K levels (d/t insulin), UOP
- EKG
IVF progression for DKA
NS (2 a/c IV if possible)
when BG ~300, switch to D5W
- prevents throwing client into hypoglycemia
hyperosmolar hyperglycemic nonketosis (HHNK)
aka
hyperglycemic hyperosmolar state (HHS)
looks like DKA but no acidosis
making just enough insulin so not breaking down fat
no fat breakdown = no ketones = no acidosis = no kussmaul respirations
type 1 diabetes can lead to
type 2 diabetes can lead to
dka & HHNK (HHS)
diabetic neuropathy issues x4
sexual problems (irreversible so SCREEN)
foot/leg problems: pain, paresthesia, numbness
neurogenic bladder
gastroparesis
gastroparesis
stomach emptying is delayed due to decreased mesenteric perfusion s/t diabetes meaning increased risk for aspiration
neurogenic bladder
bladder does not empty properly
- may empty spontaneously (incontinence)
- may not empty at all (retention)
complications of diabetes x5
dka HHNK (HHS) vascular problems neuropathy infection
vascular problems in diabetes x2
macrovascular (ex: coronary arteries)
microvascular (ex: kidneys)
