nutrition and fluid balance (class 6)

Question 1

Type 1 diabetes

Answer 1

10-15%
auto-immune-body attacks beta cells in pancrease that produce insulin.
occurs before age 30.
no insulin is produced.

Question 2

Type 2 diabetes

Answer 2

85-90%.

risk factors: obesity, family hx, inactivity, middle age or older. insulin resistance, inadequate insulin production.

Question 3

hyperglycemia s/s

Answer 3

polydipsia, polyuria, polyphagia, weight loss, fatigue.

Question 4

DM monitoring: capilary glucose monitoring

Answer 4

frequency of monitoring individualized. isopropyl alcohol, food residue, & some locations will alter the results.

Question 5

HGB A1C or HBA1C or glycosylated hemoglobin (A1C)

Answer 5

represents average glucose level during 2-3 month period.

A1C >/= 6.5% diagnostic for diabetes

Question 6

hypoglycemia: blood glucose < 60.

s/s

Answer 6

anxiety, shaky, irritability, tachycardia, difficulty thinking, poor concentration, slurred speech, blurred vision, decrease LOC, seizures, coma, pale cool skin, sweaty.

Question 7

hypoglycemia treat

Answer 7

need sugar. alert?: oral juice, glucose gel/tabs, reg soda.

unresponsive?: IV D50.

Question 8

hypoglycemia in elderly

Answer 8

speech disorder, slurring, confusion, disorientation

Question 9

hypoglycemia vs stroke

Answer 9

hypoglycemia can produce symptoms similar to stroke. blurred vision, weakness, dizziness, slurred speech..
** all suspected strokes should receive hypoglycemia treatment just in case.

Question 10

diabetic ketoacidosis

Answer 10

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.

Question 11

diabetic ketoacidosis: causes/risk factors

Answer 11

sick or infection.

decrease or omission of insulin

Question 12

labs for DKA

Answer 12

ketones elevated in bloor or urine, blood glucose > 250 pH > 7.30, bicarb < 15.

Question 13

symptoms DKA

Answer 13

lethargy, coma, kussmauls respirations, warm, dry, poor turgor, fruity breath from ketones, hypotension

Question 14

somogyi phenomenon

Answer 14

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.

Question 15

dawn phenomenon

Answer 15

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.

Question 16

COMPLICATIONS DM:

macrovascular

Answer 16

manifested thru atherosclerosis results in HTN, CAD, PVD, Cerebral & carotid artery damage

Question 17

complications DM

microvascular

Answer 17

basement membrane of smaller blood vessels & capillaries thickens eventually leading to decreased tissure perfusion.

Question 18

complications DM:

retinopathy

Answer 18

micro-vascular damage & hemorrhage lead to scarring of retina. leading cause of blindness in DM.

Question 19

complications DM

nephropathy

Answer 19

thickening of basement membrane of glomeruli impairing renal function

Question 20

complication of DM

neuropathy

Answer 20

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.

Question 21

diabetic foot care

Answer 21

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.

Question 22

RAPID ACTING INSULIN

Answer 22

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

Question 23

short acting insulin

Answer 23

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.

Question 24

intermediate acting insulin

Answer 24

NPH(humulin N, novolin N)
Detemir (levemir)

onset 2hr, gradual.

peak 6-8h, 6-8h.

duration 12-16hr, 17-24 hr.

Question 25

long acting insuline

Answer 25

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.

Question 26

metformin (biguanides)

Answer 26

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.

Question 27

sulfonylureas

Answer 27

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

Question 28

teaching SICK DAY rules

Answer 28

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.

Question 29

medulla

Answer 29

inner portion of adrenal glad.

epinepherine and norepinephrine

Question 30

cortex

Answer 30

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.

Question 31

cushings syndrome

Answer 31

excessive cortisol produced, chronic disorder, taking corticosteroids long time=increased risk. treated: meds to supress coritsol or adrenalectomy.

Question 32

cushins disease diagnoistics

Answer 32

increase: serum cortisol, sodium, glucose, urine free cortisol.
decrease: potassium
treatment: meds to suppress activity of adrenal cortex, adrenalectomy

Question 33

addisons disease

Answer 33

adrenal insufficiency- corisol deficiency.
autoimmune most common cause.
slow onset s.s occur after 90% adrenal function lost.

Question 34

addisons disease

deficient cortisol effects

Answer 34

sodium is lost & potassium retained. extracellular fluid depleted and blood volume decreased

Question 35

addisons disease s/s

Answer 35

postural hypotension & syncope, dysrhythmias, dizziness, confusion, lethargy, emotional lability, weakness, muscle wasting, hyperpigmentation of skin, hyperkalemia, hyponatremia, hypoglycemia.

Question 36

addisons disease diagnostics

Answer 36

decrease levels: serum cortisol, blood glucose, serium sodium.

increased: serum potassium.

Question 37

addisons disease treatment

Answer 37

meds to replace corticosteroids and mineralocorticoids. hydrocortisone, fludrocortisone, prednisone, dexamethasone, methylprednisolone.

Question 38

addisons teaching

Answer 38

meds needed for life, diet low K+ high Na+ and protein.

Question 39

addisonian crisis

Answer 39

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.