final Flashcards
pancreas hormones
- insulin
- glucagon
target cells of insulin
cells of body to lower blood glucose levels by moving insulin into cells
glucagon target cells
- liver and muscles
- promotes glycogenolysis by increasing blood glucose levels by conversion of glycogen to glucose
exocrine function
secretion of pancreatic juices into the small intestine that aid in digestion
endocrine function
blood glucose control by the islet cells; insulin (beta cells) and glucagon (alpha cells)
when blood glucose gets high…
the pancreas releases insulin to stimulate the liver to convert glucose into glycogen for storage to LOWER blood glucose levels
if blood glucose is too low…
glucagon causes liver to turn stored glycogen back into glucose and release it to INCREASE blood glucose levels
risk factors of diabetes
- age >30 years for type 2 and <30 years for type 1
- elevated HDL and triglyceride levels
- hx of gestational diabetes or delivery of baby >9lb
HTN - family hx of diabetes
- obesity
- previously impaired fasting glucose test
- african americans, hispanics, native americans, asians, pacific islanders
pre-diabetes
- impaired fasting glucose, impaired glucose tolerance
- warning for development to type 2 DM
fasting blood glucose pre-diabetes
100-125 mg/dL
a1c prediabetic
5.7-6.4%
oral glucose tolerance test prediabetic
140-199mg/dL
type I DM
- autoimmune disorder causing beta cells of pancreas to be destroyed resulting in no insulin production
- children and young adults
- total insulin deficiency occurring within 1 year
- lifelong insulin therapy needed
- surgery induced diabetes
type II DM
- insulin resistance: body tissues do not respond to insulin’s action due to unresponsiveness or insufficient numbers of insulin receptors
- inadequate insulin secretion: cell of pancreas become fatigued and so insulin production is decreased
diagnosing diabetes
- fasting blood glucose >126
- A1C >6.5%
- oral glucose tolerance test >200mg/dL
- random glucose test >200mg/dL
testing must be repeated before diagnosis
clinical manifestations of diabetes
- polyuria (increased urination)
- polydipsia (increased thirst)
- polyphagia (increased hunger)
- glucosuria
- fatigue
- unexplained weight loss (type I)
medical management of diabetes
maintenance of glycemic levels and prevention of complications
type I medical management
- glucose monitoring
- insulin
- diet
- patient education
- disease management
type II medical management
- glucose monitoring
- medications
- diet
- exercise
- weight loss
- patient education
- disease management
assessing glycemic control
- self monitoring w/ finger stick (before meals and at bed time)
- continuous glucose monitor (skin impant or close loop system, insulin pump)
- Hgb A1C (2x/year q3 months if targets haven’t been met)
diet for diabetics
- weight, meds, activity, and comorbidities should be taken into account
- consistency in times for meals
- carb counting
- incorporate diet individually
exercise for diabetics
- exercise lowers glucose levels and encourage weight loss as well as many other health benefits
- dietary adjustments
- if glucose >250 and urinary ketones are present, do NOT exercise until levels are normal
- try to exercise at same time each day
- insulin shouldn’t be injected in area that will be worked out
- monitor levels before, during, and after workout
insulin therapy
- regular insulin
- lispro
- glargine
- determir
regular insulin
use of this insullin increases change of hypoglycemia if give 3-4x/day due to action overlap
lispro (humalog) and aspart (Novolog)
should be held if patient is NPO or unable to tolerate food or caloric intake
glargine (lantus) and detemir (levemir)
basal insulins administered daily and given regardless of nutritional intake and not held if glucose levels are within normal limits
rapid-acting and short-acting insulin should be taken
at mealtimes to cover incoming carbs
correction insulin is determined by
random glucose stick prior to eating
prandial and correctional insulins are administered
prior to eating
insulin administration
- subq
- insulin pump or patch
insulin injection sites
- abdomen
- arm
- thighs
- hips
insulin injections
- rapidly absorbs in subq layer of stomach
- systemic rotation to prevent lipodystrophy
- injection should be 1-1.5in apart
- heat, massage, and exercise of injected area to increase absorption
- hypoglycemia may occur
storing insulin
- avoid extreme temps
- do not freeze or keep in direct sunlight
- before injection, insulin should be room temp
- if vial of insulin will be used in 1 month ,it may be kept at room temp but if not it needs to be refrigerated
complications of insulin admin
- allergic reactions (redness, swelling, tenderness, induration)
- insulin lipodystrophy (fibrous fatty massess at injection site caused by repeated use of an injection site)
- dawn phenomenon (high BS in am)
- somogyi effect (low glucose overnight, high glucose in am)
meds for type II diabetes
- biguanides
- sulfonylureas
- meglitindes
- thiazolidineodiones
- a-glucosidase inhibitors
- dipeptidyl peptidase-4 inhibitors
- sglt2 inhibitors
- glp-1 receptor agonist
- insulin
biguanides
metformin
most effective med for type II
cannot be used if KF, liver disease, or HF
metformin must be withheld when?
before and for 48hrs after having radiology studies done due to increased risk of lactic acidosis with dye
sulgonylureas
glyburide, glipizide
meglitinides
repaglinide, nateglinide
thiazolidineodioens
rosiglitazone, pioglitazone
a-glucosidase inhibitors
acarbose, miglitol
depeptidyl peptidase4 inhibitors
sitagliptin, linagliptin, saxagliptin
sodium glucose co-transporter 2 (SGLT2) inhibtors
dapagliflozin, empaglioflozin
GLP1 receptor agonists
semaglutide
liraglutide
nursing management for diabetes
- vitals
- glucose monitoring
- I&Os
- carb intake at meals
- labs: K, WBC, BUN/Creatinine
- perform neuro assessment
- skin assessment
- assess perfusion
- administer insulin/meds
- administer IV fluids
- dietician referral
- diabetic educator referral
- assess ability to manage diabetes at home
nursing interventions (teaching) for diabetes
- signs of hypoglycemia and hyperglycemia
- complications (DKA, HHS)
- insulin admin
- med education
- blood glucose moitoring
- a1c monitoring
- health lifestyle
- medical alert
- sick days
- foot care
- eye exams
- annual physical
diabetics during illness
- take insulin or antidiabetics as prescribed
- determine blood glucose levels and ketones q3-4hrs
- if meals cannot be followed, substitute soft foods 6-8x/day
- if vomiting, diarrhea, or fever consume liquids q30-60min
- notify HCP of illness and if levels are >250-300 or when ketonuria is present >24hrs or unable to ingest food
diabetic foot care
- provide proper care
- inspect feet daily
- notify HCP if break in skin occurs
- avoid thermal injuries
- wash feet with warm water
- avoid treating blisters
- do not cross legs or restrict blood flow
- apply moisture
- prevent accumulation of moisture between toes
- wear clean gloves and socks
- avoid wearing same shoes
- avoid smoking
complications of diabetes
- vascular damage
- nerve damage
- hyperglycemia
- hypoglycemia
- diabetic ketoacidosis
- hyperosmolar hyperglycemic state
vascular damage from diabetes
- atherosclerosis causing decreased circulation/perfusion causing inschemia leading to ulcers, amputation, poor wound healing, increase risk of infection and organ damage or disease
vascular damage secondary to diabetes can lead to
- nephropathy (KF)
- retinopathy (blindness)
- carotid artery disease (stroke)
- coronary artery disease (myocardial infarction)
- hypertension (cardiomyopathy and HF)
hyperglycemia in hospitalized patient
- changes in usual treatment
- meds
- IV dextrose
- overly vigorous treatment for hypoglycemia
- inappropriate witholding or use of sliding scales
- mismatched timing of meals and insulin
hypoglycemia
- acute or life-threatening emergency
- blood glucose levels fall below <65mg/dL or drops rapidly from elevated level
- caused by too much insulin, too little food, excessive activity
- more circulating insulin than is needed to handle amount of circulating glucose
signs of hypoglycemia
- shaking or trembling
- tachycardia
- extreme hunger
- sweating
- confusion/difficulty concentrating
- dizziness
mild hypoglycemia
awake and alert
glucose <70
moderate hypoglycemia
client shows s/s of worsening hypoglycemia
blood glucose <40
severe hypoglycemia
showing neuroglycopenic s/s
glucose <20
mild s/s
hunger
nervousness
palpitations
sweating
tachycardia
tremor
moderate s/s
confusion
double vision
drowsy
emotional changes
headache
impaired coordination
inability to concentrate
irrational or combative behavior
light-headed
numbness of lips and tongue
slurred speech
severe s/s
difficult to arouse
disoriented behavior
loss of consciousness
seizures
carbs to treat hypoglycemia
- 6-10 lifesavers
- 4tsp of sugar
- 4 sugar cubes
- 1tsp of honey or syrup
- 1/2 cup fruit juice
- 8oz of low fat milk
- saltine crackers (6)
- 3 graham crackers
diabetic ketoacidosis causes
- intentional or unintentional missed or reduced dose of insulin
- inadequate insulin due to increased insulin needs secondary to stress, infection, illness, trauma
- new onset of type 1 diabetes
s/s of DKA
- blood glucose >250
- acidosis (pH <7.35)
- kussmaul respirations
- ketosis (fruity smelling breath)
- ketonuria
- hyperkalemia
- dehydration
- hypotension
- tachycardia
treatment for DKA
- fluid replacement and electrolytes
- correct hyperglycemia (IV insulin)
- treat electrolyte imbalances (K+, cardiac monitor)
- monitor neuro status (increased ICP- cerebelar edema)
hyperosmolar hyperglycemic syndrome cause
- extreme hyperglycemia and dehydration occur without ketosis or acidosis
- blood glucose >600
s/s of HHS
- glucose >600
- negative ketones
- glycosuria
- profound dehdyration
- altered LOC
- increased BUN/Creatinine
treatment of HHS
- ID and treat cause
- fluid replacement
- insulin admin (if hyperglycemia not correct by fluid replacement)
- correction of imbalances
- monitor neuro status
DKA occurs more in
type 1
HHS occurs more in
type 2
main funciton of urinary system
- eliminate of waste
- fluid and electrolyte balance (blood volume, blood pressure, increase or decrease in electrolytes)
- acid base balance
kidneys are the primary
organs responsible for maintaining water balance in the body
volume in = volume out
with low intake, dehydration or hypovolemia…
- thirst is stimulated
- ADH is released increasing water reabsorption and decreasing urine output
- these processes increase solutes in urine
increased intake, fluid overload, and hypervolemia
- lowers ADH release to increase urine output and fluid release
- this decreases solute in urine
anuria
less than 100mL urine output in 24hrs
dysuria
painful urination
enuresis
involuntary urination at night
frequency
increase in incidence of voiding, usually only small amounts
hematuria
blood in urine
hesistancy
difficulty starting flow of urine
nocturia
frequent urination at night
oliguria
decreased urine output
<400mL/24hrs
polyuria
increased urine output >2,000mL/24hrs
renal colic
pain radiating to perineal or groin area
retention
inability to completely empty bladder
urgency
sudden onset of urge to void
normal UA findings
- color: pale yellow
- turbidity: clear
- odor: faint ammonia smell
- specific gravity: 1.005-1.030
- osmolality: 250-900
- pH: 4.5-8
- protein: 30-150
- glucose: -
- ketones: -
- bilirubin: -
- RBC: 0-4
- WBC: 0-5
- casts: few or none
- bacteria: <1000
renal function tests
- renal concentration (specific gravity (1.005-1.030) and urine osmolality (300-900mOsm))
- 24hr Creatinine Clearance (M=55-146, F=52-134)
- creatinine level (M=0.5-1.2, F=0.4-1.0)
- BUN (8-20mg/dL)
- BUN/creatinine ratio (10:1)
cytoscopy
- cystoscope inserted through urethra into the bladder
- preop: educate, informed consent, assess allergies to contrast, iodine, shellfish, if done under anesthesia, NPO @ midnight
- postop: monitor urine output, monitor s/s of infection, expect pink tinged urine and frequency, educate on signs and symptoms of infection and adequate output, when to call
red flags for GU
- decerasing urine output
- pain in bladder or flank
- difficult or painful urination
- burning w/ urination
- felling like bladder is not emptying
- hematuria
- elevated BUN/Cr
- elevated K+
- EKG changes related to K+ (tall T waves, ST segement depresion)
acute kidney failure
sudden short term loss of kidney function
if not stopped and reversed, can lead to chronic renal failure
chronic kidney failure
long term chronic damage to kidneys, year of destruction leading to permanent damage
stage 1 CKD
90%+ of normal kidney function
stage 2 CKD
60-89% normal kidney function
stage 3 CKD
30-59% of normal kidney function
stage 4 CKD
15-29%
kidney function low and treatment for kidney failure may be needed soon
stage 5 CKD
<15% normal kidney function
no longer removing wastes effectively leading to renal failure, end stage kidney disease or renal disease
CKD causes
- long-term disease or medical comborbities like HTN, DM, untreated AKI
- poorly managed or untreated AKI
- reduces independence shortnes life, and decreases quality of life
diagnosis of CKD
- low GFR (ESRD <15mL/min)
- low urine output (may be anuric)
- increased BUN/creatinine
- ultrasound shows scarring/damage
clinical manigestation of renal failure
- neurological weakness and fatigue
- increased BP
- pitting edema
- periorbital edema
- increased CVP
- preicarditis
- SOB
- depressed cough
- thick sputum
- ammonia odor to breath
- metallic taste
- mouth/gum ulcers
- anorexia
- weight loss
- n/v
- anemia
- bleeding tendencies
- increased K+
- dry flaky skin
- uremic frost
- weight related to fluid retention
- cramps
medical managment of CKD
- anemia: epoetin alfa (synthetic EPO)
- hyperkalemia: monitor K+, tele, K+ lowering meds (Kayexalate, insulin and dextrose)
- hyperphosphatemia: phosphate binders to lower phosphorous levels
- hypocalcemia: calcium carb, vit D
- HTN: antihypertensives, diuretics, diet
- diet: low protein, K+, Na+, PO34, fluid restriction
- dialysis
- transplant
- weight loss and exercise
- smoking cessation
- avoid NSAIDs and aspirin