Endocrine/Diabetes Flashcards
glands and hormones excreted- pancreas, thyroid, parathyroid, pituitary, adrenal
pancreas- insulin, Glucagon
thyroid gland- T3 and T4
parathyroid- PTH
Pituitary- ADH, oxytocin
Adrenal cortex- cortisol, aldosterone, glucacorticoids (steroids)
adrenal medulla- norepinephrine, epinephrine
T3-t4
thyroid- regulates metab activity
t3- rapid metab changes
t4- steady metab (ex. thyroid horm replacement)
metabolic activity controllers
t3- triiodothyronine
t4- thyroxine- main source table salt
range 0.4-4
TSH
thyroid-stimulating hormone
inc if t3/t4 low (hypothyroidism)
dec if t3/t4 high (hyperthyroidism)
hypothyroidism- def and types
common type- Hashimoto's thyroiditis caused by disord affecting anter pit or hypothal primary hypothyroidism- thyroid secondary- ant pit tertiary- hypothal
hypothyroidism s/s
tired, dry skin, extreme fatigue, constipation, impaired physical mobility, dec rr
hypothyroidism acute illness s/s- myxedmea
myxedmea- slows all metab processes low temp, hr, rr, dec LOC, dec Na inc TSH low t3/t4
hypothyroidism acute illness- myxedema considerations
cardiac complications
dec respir r bc inc cdo2 accum, secondary to hypoventilation (requires lower dose meds)
hypothyroidism acute illness- myxedema treatment
passive rewarming (if inc too fast have circ collapse due to excessive vasodil)
oral thyroid horm replacement (levothyroxine)(TITRATE, inc dose too fast inc O2 demand)
can inc o2 demand (report SOB and chest pain)
take 30/60 min before eating
hypothyroidism acute illness-management
diagnosis confirmed through lab (t3-t4, TSH)
oral replacement meds
montior abg’s (hypoxia, metabolic acidosis)
assess all vitals- dis affects entire body
hyperthyroidism- def
inc metab, autoimmune
inc t3/4, dec TSH
“Graves disease”
hyperthyroidism- diagnosed
radioactive iodine uptake test- inc amnt iodine uptake show in imagery= hyperthyroidism
* check for shellfish allergy- (contained in iodine)
labs- inc t3-4, dec TSH
hyperthyroidism- s/s
inc hr, rr, bp, temp, hair loss, diff sleeping, anxiety, exophthalmos (BULGING EYES), inc appetite
complications- dec cardiac output
hyperthyroidism- treatment
thyroid suppressing meds (inhib horm production)
subtotal/total thyroidectomy
if too aggressive- risk for hypothyroidism
during surgery can damage parathyroid gland (leads to dec Ca lvls)
hypocalcemia and hyperthyroidism
from damage to parathyroid during thyroidectomy
s/s numbness, tingling, twitching, tetany
diagnosed w/ serum lvls, facial twitching (chvosteks)or rigid hand curling w/ inflated bp cuff (trousseau’s)
hyperthyroidism- treatment
cool environment, O2 therapy, iv fluid w/ dextrose, high protein nutrition
hyperthyroidism- complications
thyroid storm
thyrotoxicosis
life threatening
risks- stress, trauma, infection (common in elderly)
s/s- alt CNS (inc anxiety/delerium), cardiac dysrhyth
thyroid storm-treatment (meds)
beta blockers (dec o2 demands cardiac tissue, dec bp/hr)
hypoparathyroidsim- cause
cause- removal parathyroid glands (total thyroidectomy/ neck Ca surgery)
lack PTH
PTH and Ca
direct relationship
pth dec = Ca dec
hypoparathyroidism=hypocalcemia
Ph inverse relations Ca
inc Ca= Low phosphorushypoparathyroidism- manifestations
dec Ca, numbness, tingling, musc cramps, spasms, tetany
hypoparathyroidism-management
raise Ca lvls
Iv Ca gluconate- stabalize airway spams
inc foods high Ca, and low in Ph (meat/eggs)
SIDAH- cause
inc ADH(pit gland)= fluid vol excess brain/lung tumor, meds (anti-dep, NSAIDs)
SIDAH- s/s
syndrome of inappropriate antidiuretic hormone
hyponatremia-altered mental status, headache, dizzy, fatigue, nausea, thirst
SIDAH- management
monitor urine specific grav, serum/urine osmolality
diuretics
fluid restriction (1L/24hr)
Mental status
hypertonic sol (caution)(pulls fluid out of cells)
adrenal cortical insuff (addisons)
dec secretion corticotropin-releasing horm and ACTH from anterior pit
dec secretion glucocorticoids/mineralocorticoids frm adrenal cortex
adrenal cortical insuff (Addisons)- manifestations
low bp, sings potential circ collapse (tired, weak), hypovolemic
fatigue, low Na, hypotensive, High K, dec glucose, dec aldosterone
adrenal cortical insuff (Addisons)- cause
after 90% adrenal cortex gone or nonfunctioning frm extended use steroids or withdrawl
adrenal cortical insuff (Addisons)- management
monitor vs, fluid status, signs of shock
hydrocortisone, iv (cortisol replacement), iv replacement fluids (D5NS)- dec glucose and Na
orthostatic vitals (bp especially, drop 15-20), body unable to compensate - inefficient tissue perfusion *if low bp when laying, put in recumbent position w/ legs elevated promote blood return cardiac tissues inc steroid dosage
adrenal cortical insuff (Addisons)-diagnosis
cortisol lvl in morning, ACTH
adrenal cortex hyperfunction (cushings)
excess glucocorticoids, and aldosterone
adrenal cortex hyperfunction (cushings)- manifestations
inc glucose, fluid retention, dec K, abnormal fat distribution, dec musc mass, inc Na, high bp
adrenal cortex hyperfunction (cushings)- cause
excess horm production from ant pit, excess ACTH, tumors, exogenous steroids
adrenal cortex hyperfunction (cushings)- complications
inc risk fractures, osteoporosis, infection (educate abt safe environment)
risk fluid retention high
*is reversable
adrenal cortex hyperfunction (cushings)-management
monitor bp, heart rhythm for irreg, monitor Na, K, WBC, s/s infection (delayed wound healing due to think skin, impaired circ and inc glucose)
diabetic, low cal, high protein, low sodium/fat diet
meds- tapper off steroids (stopping at once = adrenal insuffciency- addisons)
surgically remove tumor
diabetes
grp metabolic dis characterized by hyperglycemia resulting frm insulin secretion, insulin action or b
insulin characteristics
anabolic (storage) horm
secreted by beta cells in pancreas
metabolizes CHO, protein and fat
insulin function
transport/ metaboli glucose
assists K+ into cells
inc. movement amino acids from protein consumed into the cells
discourages decomposition of the stored glucose, protein and fat
low bg patho
low bg triggers hormone called glucagon created in the pancreas
liver breaks down glucagon into glycogen to create glucose through process called glycogenolysis
w/8-12 hrs liver will breakdown noncarbs (ex. aa)
type 1 diab
unproductive eta cells
no insulin secretion (glucose can’t enter cells)
alpha cells damaged- no glucagon to stimulate glycogenolysis (glucose production)
causes type 1
genetic, immunologic, potential environmental
DKA
no insulin, glucose accum in blood, fat broken down for energy, ketone bodies (acidic) produced
kidneys attempt to dec glucose by inc excretion
-elevated bg
-ketosis-
metabolic acidosis
precipitating s/s dka
n/v, fatigue, polyuria. polydipsia
if untreated= stupor and coma
cause dka
dec insulin, illness, infection (spikes bg), undiag diab, stress
type 2 diab
insulin resis
impaired insulin secretion in pancreas
inc basal hepatic glucose production
type 2 risk factors
diet and lifestyle changes
age 45 older (can happen in kids)
obesity, fam hx, race/ethnicity (african, hispanic, native, asian, pacific)
htn > 140/90
high chol
hx gestational diab or delivery baby >9 lbs
hyperglycemic hyperosmolar syndrome patho
assoc w type 2
not enter DKA, only hyperglycemia
no insulin/ lack of
inc bg stimulate osmotic diuresis (loses h20 and electrolytes)
act. osmotic balance- fluid shift from ICF to ECF (blood s)
ends in- inc Na, glycosuria, dehydration
hyperglycemic hyperosmolar syndrome s/s early v late
early- polyuria, polydipsia
late- hypotension (2-3 wks), dehydration, tachycardia, Altr consciousness, seizures, hemiparesis
hyperglycemic hyperosmolar syndrome-cause
stress (CVA, MI, infection or surgery)
gestational diab- def
glucose intol in pregnancy due to placental horm inc insulin resistance
gestational diab- risk factors
fam hx dm, previous stillbirth, obesity, htn, inc maternal age >35, race/ethnicity (african, native, asian, pacific)
gestational diab- hyperglycemia risks
baby- inc insulin lvlvs, macrosomia (lrg size), birth trauma, delayed lung dev, fetal hypoxia
screen btw 24-48 wks
measures post prandial blood sugar to test insulin receptiveness
hypoglycemia
low blood glucose
(diluted kool-aid)
<70
hypoglycemia s/s
mild <70- affect sympath nervous system
sweating, tremors, tachycardia, palpitations, nervousness, hunger
severe <40- CNS
lightheaded, slurred speech,x2 vision, impaired coord, confusion, numbness, irritable, drowsy
factors type 1 and 2 (external)
alcohol (inc and dec lvls)
exercise (dec)
stress (inc)
hyperglycemia s/s
polyuria, polydipsia, polyphagia
long term- fatigue, weakness, vision changes, numbness, dry skin, delayed wound healing
fasting bg
80-110 after fasting at least 8hrs
hemoglobin A1c
% glucose attached to hemoglobin in rbc 4-6% over 3 mon period <7 for diab good < 5.9 for normal ppl
postprandial blood glucose
after eating 80-110 (can be inc)
usually 2 hrs after eating
Kidney function labs/ electrolytes
creatinine- 0.6-1.2 mg/dl
bun 7-18 mg/dl
K+ 3.5-5.5
Na 135-145
CHO compo
ex. sugars, starches, fruits
easily/fast digested macronutr
1 carb choice
15g of carbohy
1 unit of insulin/ 15g
trtment mild hypoglycemia
early- 4oz fruit juice, 2-3 glucose tabs of 15g carbs
1 tube glucose gel
later- crackers and cheese or sandwich
basal insulin (long acting)
no peak, delayed release onset- 1hr duration-24h base lvl no mixing! lantus (glargine) or levermir (dtermir)
rapid acting insulin
absorbed w/in 5-15 min subq peak-40min duration 2-4hr ac and Hs (post prandial/ nocturnal) give while eating eat w/in 15 minof admin Humalong (lispro), Novolog (aspart)
insulin pump advant- disadvan
basal rate 0.2-2 units/hr
continuous infusion w/ option for bolus
disadvan- tubing kinks, displaced cath, battery life, cost
self monitoring bg
used in hospital setting
finger stick w/ meter
oral diab meds-overview
used for type 2 if diet mod and exercise not work
not replacement for insulin for type 1
oral diab meds- sulfonylureas
glyburide, glimepiride
2nd gen sulfonylureas- stim beta cells to secrete insulin and aid in bonding of insulin-insulin receptors
side e- hypogly, weight gain, GI sympt
oral diab meds- biguanides
metformin, Glucophage
ihibit production glucose by liver, inc body sensitivity to insulin
pancreas alrdy producing insulin that isn’t working, liver producing more has no benefit
side e- hypoglyc, kidney damage (beware w/ contrast dye), lactic acidosis, drug-drug intractions
hospital monitoring for ketones
ketone body detection in urine or blood
tell if breaking down fat for energy (if not glucose is avaliable)
common diab orders
check blood g ac/hs (check w/ provider and look at prev trends if unable to check b4 pt starts eating) lab values for glucose and K skin assessment q shift monitor I and Os
factors affecting bg (external)
surgery (npo- dec) meds (steroids spike bg (prednisone)) stress (inc) K+ lvls- follow glucose, inc glucose=dec K (K leaves cells) exercise (dec lvls)
nursing considerations
auscul heart sounds (inc lvls alter vessels)
ECG (can have irreg. rhythm)
mental status assessment (drowsiness)
pedal pulse (diab assoc w peripheral vasc dis)
fluid status
specialties assoc w/ diab in care team
ophthalamist diab educator nutitionist endocrinologist pediatrist
microvasc changes w/ diab
capill basement mem thickens w/ chem rxn to inc blood glucose
narrow vessles- dec blood/nutr perfusion
ex. extremities, eyes and kidneys
macrovasc changes w/ diab
thickening, sclerosis, occlusion w/ plaque
CAD
Periph vasc dis
cerebral vasc dis
periph neuropathy
(dec blood, damage nerves, dec sensation)
glucagon injection
for outpatient type 1 w/ no IV
mix w/ saline or lidocaine
