nutrition and fluid balance (class 6) Flashcards
Type 1 diabetes
10-15%
auto-immune-body attacks beta cells in pancrease that produce insulin.
occurs before age 30.
no insulin is produced.
Type 2 diabetes
85-90%.
risk factors: obesity, family hx, inactivity, middle age or older. insulin resistance, inadequate insulin production.
hyperglycemia s/s
polydipsia, polyuria, polyphagia, weight loss, fatigue.
DM monitoring: capilary glucose monitoring
frequency of monitoring individualized. isopropyl alcohol, food residue, & some locations will alter the results.
HGB A1C or HBA1C or glycosylated hemoglobin (A1C)
represents average glucose level during 2-3 month period.
A1C >/= 6.5% diagnostic for diabetes
hypoglycemia: blood glucose < 60.
s/s
anxiety, shaky, irritability, tachycardia, difficulty thinking, poor concentration, slurred speech, blurred vision, decrease LOC, seizures, coma, pale cool skin, sweaty.
hypoglycemia treat
need sugar. alert?: oral juice, glucose gel/tabs, reg soda.
unresponsive?: IV D50.
hypoglycemia in elderly
speech disorder, slurring, confusion, disorientation
hypoglycemia vs stroke
hypoglycemia can produce symptoms similar to stroke. blurred vision, weakness, dizziness, slurred speech..
** all suspected strokes should receive hypoglycemia treatment just in case.
diabetic ketoacidosis
a state of insulin deficiency resulting in hyperglycemia and an accumulation of ketones in the blood.. fat stores used for energy results in metabolic acidosis.
diabetic ketoacidosis: causes/risk factors
sick or infection.
decrease or omission of insulin
labs for DKA
ketones elevated in bloor or urine, blood glucose > 250 pH > 7.30, bicarb < 15.
symptoms DKA
lethargy, coma, kussmauls respirations, warm, dry, poor turgor, fruity breath from ketones, hypotension
somogyi phenomenon
combo of hypoglycemia in the night with rebound hyperglycemia in the morning.
caused by too much insulin.
treat by slowlyg reducing insulin. more common in type 1 DM.
dawn phenomenon
rise in blood gluocose between 4-8 am that is not a response to hypoglycemia.
cause: unknown thought to be r/t nocturnal release of counter-regulatory hormones that increase blood sugar.
can occur in DM 1 & 2
correct with timing of insulin or increase dose.
COMPLICATIONS DM:
macrovascular
manifested thru atherosclerosis results in HTN, CAD, PVD, Cerebral & carotid artery damage
complications DM
microvascular
basement membrane of smaller blood vessels & capillaries thickens eventually leading to decreased tissure perfusion.
complications DM:
retinopathy
micro-vascular damage & hemorrhage lead to scarring of retina. leading cause of blindness in DM.
complications DM
nephropathy
thickening of basement membrane of glomeruli impairing renal function
complication of DM
neuropathy
thickening of blood vessels that supply nerve endings. causes change in sensations, pain, teach importance of visuallty inspecting feet.legs daily to look for injury.
diabetic foot care
teach daily foot inspection.
avoid crossing legs.
non-restrictive shoes and good quality socks.
do not self-treat foot problems.
avoid dry skin, cracks, infections.
pdiatrist evaluation.
buy shoes late afternoon-feet at largest size.
RAPID ACTING INSULIN
lispro, humalog, aspart, novalog.
onset: 15 mins.
peak: 1-1.5 h, 40-50 min Aspart
duration: 3-4hrs, 3-5 hrs. give 15 min before meals
short acting insulin
regular, novolin r, humalin r.
onset 30-60 mins. peak 2-3 hrs. duration 4-6hrs. give 30 min before meals.
** only insulin that can be given IV.
may give IM in emergency.
intermediate acting insulin
NPH(humulin N, novolin N)
Detemir (levemir)
onset 2hr, gradual.
peak 6-8h, 6-8h.
duration 12-16hr, 17-24 hr.
long acting insuline
glargine (lantus)
onset 1.1 h
peak 3-4 h
duration 10-24 h
QD or BID more constant levels no true peaks do not mix with other insulin types.
metformin (biguanides)
reduces FBG & postprandial hyperglycemia.
often suspended during hospitalization r/t increase risk of lactic acidosis
stopped prior to & 48 h after us of contrast media & surgery r/t risk of renal failure.
sulfonylureas
treat type 2 DM in non-obese pts. stimulate pancreatic cells to secrete more insulin making peripheral tissues. usually suspended during hospitalizations r/t dose adjustments must be made slowly.
common side effect hypoglycemia from NPO status
teaching SICK DAY rules
M- monitor blood sugar levels more frequently.
D_ do not stop taking insulin.
C- check urine for ketones if glucose > 240,
B- be careful with over-the-counter medications
H- have a game plan & ask for help if needed
F- force fluids 8oz each hour
C- call provider if unable to eat > 24 hr, vomitting, diarrhea > 6h, urine ketones mod/lg for >4hr.
medulla
inner portion of adrenal glad.
epinepherine and norepinephrine
cortex
outer portion adrenal gland, produces hormones essential to life.
mineralcorticoids (release controlled by renin when b/p or Na is low)
glucocorticoids: cortisol & cortisone released in time of stress affect CHO metabolism & regulates glucose use in body tisuess.
androgens- sex hormones- loss of cortex hormones=death.
cushings syndrome
excessive cortisol produced, chronic disorder, taking corticosteroids long time=increased risk. treated: meds to supress coritsol or adrenalectomy.
cushins disease diagnoistics
increase: serum cortisol, sodium, glucose, urine free cortisol.
decrease: potassium
treatment: meds to suppress activity of adrenal cortex, adrenalectomy
addisons disease
adrenal insufficiency- corisol deficiency.
autoimmune most common cause.
slow onset s.s occur after 90% adrenal function lost.
addisons disease
deficient cortisol effects
sodium is lost & potassium retained. extracellular fluid depleted and blood volume decreased
addisons disease s/s
postural hypotension & syncope, dysrhythmias, dizziness, confusion, lethargy, emotional lability, weakness, muscle wasting, hyperpigmentation of skin, hyperkalemia, hyponatremia, hypoglycemia.
addisons disease diagnostics
decrease levels: serum cortisol, blood glucose, serium sodium.
increased: serum potassium.
addisons disease treatment
meds to replace corticosteroids and mineralocorticoids. hydrocortisone, fludrocortisone, prednisone, dexamethasone, methylprednisolone.
addisons teaching
meds needed for life, diet low K+ high Na+ and protein.
addisonian crisis
life threatening adrenal insufficiency abruptly withdrawn from corticosteroid meds or hemorrhage into adrenal glans.
S/S high fever, weakness, severe penetrating pain in abdomen lower back legs, severe vomitting, diarrhea, hypotension, circulatory collapse, shock, and coma.
treatment: rapid IV replacement of fluids & glucocoricoids.
