Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/57

Click to flip

57 Cards in this Set

  • Front
  • Back
Define Diabetes Mellitus
Siphon or flow/sweet
A complex chronic disorder characterized by disruption of normal carb, fat and protein metabolism and the development over time of MICROVASCULAR and MACROVASCULAR complications and neuropathies.
What type of cell secrete insulin, glucagon
Beta Cells/pancrease
Alpha Cells
Type I Diabetes
Insulin dependant diabetes mellitus
NO INSULIN/ need to perserve life.
onset: any but usually <30
Body weight: generally thin
Prevelance: 5-10%
Etiology:autoimmune
What is the leading cause of death in DM I
Renal Failure
Complications
DKA
Hypoglycemia
Treatment for DM I
Diet, Exercise and insulin
Type II DM
Non-insulin dependant DM
Age of onset: Usually >30
Body weight: 80% overweight
Prevelance: 90-95%
Etiology: heredity, may also be auto immune, OBESITY
Leading cause of death with Type II DM
Acute coronary syndrome
stroke
Complication Type II
neuropathy, retinopathy, prone to renal failure/disease
Treatment Type II
DIET! loss of 10-20% of body weight gives more glucose control
exercise and meds(PO)
Vyetta-SC
New medication that stimulates beta cells to produce insulin
Risk factors for DM
Family hx
obesity BMI>27
race/ethnicity
age>45
impaired fasting glucose or imparied glucose tolerance
HTN
HDL <35
Triglycerides>250
Diagnostic
Urinalysis
microalbumin in uria-NOT normal.
Pt with DM who don't know have freq. UTI's B/C DM affects leukocytes and Phagocitosis
Fasting blood glucose

Casual blood glucose
Impaired glucose intolerance is 100-125
Diabetes >126
Casual <200
Post prandial
BS below 140 is normal
impaired b/w 140-199
DM >200
done 2 hours after meals to see how body is handling glucose,
3P's
clincial manifestations of all DM
Polyuria-increased urination
polydipsia-increased thirst
polyphagia-increased appitite
Glycosylated hemoglobin
Heme A1C
Not diagnostic for DM but tests control of glucose. Glucose attaches to Hgb what they are looking for is <6
Assessment:Objective

Nutrition
Thirsty?
hungry?
Signs of DM
Assessment:Objective

Elimination
young children may see bed-wetting after previously being potty trained
Older-nocturia
Type II not diagnosed will see bowel incontinence
If have neuropathy may have urine/feces incontinence
Decreased function and drug clearance
Assessment:Objective

Neurosensory
numbness/tingling
confusion
change in vision, decreased smell, taste changes
Type II-classic sign change in consciousness, confused/disoriented
Assessment:Objective

Mobility
Fatigue and weakness
Inability to moce
Type I increase muscle cramps due to latic acid
Assessment:Objective

Circulation
when not in DKA: angina,(w/neuropathy silent angina) HTN, PVD (more arterial)
In DKA: HTN tachycardia
Diet
Qualitative
Non-concentrated sweet diet (type II) want complex carbs not simple sugars
Diet
Quantitative
CHO counting. Does not differentiatie b/w different types of carbs
Diets should be based on...
weight, sex and amount of exercise
Why would you not take PO medications for DM if pregnant or thinking of becoming pregnant?
PO meds cross the placenta. Switch to Insulin as soon as you plan or become pregnant.
Why are type II diabetics on Insulin sliding scale in the hospital?
Due to increased stress which can increase blood glucose,
Hypoglycemia

Etiology
BS <60
Delayed or omitted meal, insulin OD, excessive exercise without food or insulin adj.
CAN HAPPEN TO NON DIABETICS!
Hypoglycemia
Onset
Rapid mins to hours
If unsure if S/S are from hypo or hyper glycemia treat it as .....
HYPOGLYCEMIA
Hypoglycemia

S/s mild hypoglycemia
low blood glucose levels
SNS-sweating,tremors, tachy, palpitations, nervousness and hunger!
Why does hypoglycemia affect brain functioning?
The brain can not use ATP for energy so if no glucose the brain is deprived from the fuel it needs to function.this causes neuro changes
S/s Moderate hypoglycemia
impaired CNS function: inability to concentrate,headache,lightheadedness,confusion, memory lapses,numbness of lips and tounge, slurred speech, impaired coordination, emotionsl changes, irrational or combative behavior.double vision, drowsiness. Plus the SNS systems.
S/S severe hypoglycemia
Will need assistance from another person....
disoriented behavior, seizures, difficulty arousing from sleep, loss of consciousness and COMA
Hypoglycemia interventions
Need simple sugars ASAP
JUICE,Glucose tablets,
Icing gel
Epinephrine
Hyperglycemia
Etiology
Undiagnosed DM, neglected treatment, infection, cardiovascular disorders, physical stress, emotional stress
Hyperglycemia
Onset
Slow- hours to days
What are some Adrenergic Changes
Hunger, weakness, diaphoresis, tachycardia, pallor, anxiety, tremors, nervousness, REBOUND hyperglycemia.
Long Term Complications

Macrovascular
Blood vessel walls thicken, sclerose and become occluded. 3 main types of Macrovascular ar CAD, Cerebralvascular disease, PVD
MI, CVA, diminished peripheral pulses, intermittent claudication. PVD cause for increased levels of gangrene and Amputation
Long Term Complications
Microvascular
unique to diabetes
(The basement membrane thickens) Affects the retina and the kidneys
Define Retinopathy
Deterioration of the small blood vessels that nourish the retina.
Clinical manifestations of retinopathy
Blood vessels in the retina develop microaneurysms that leak fluid, causing swelling and forming deposits.
Nephropathy-define
Long term complication of DM, where the kidney cells are damaged. Charecterized by microalbuminuria and progressing to end stage renal disease
Long Term Complications

Neuropathys
effects all types of nerves
decreases gastric emptying, incont of urine/feces. sexual dysfunction. peripheral-esp. the feet
Define Vitrectomy
The surgical removal of the vitreous of the eye. The removed vitreous is replaced with liquid or gas.
Sick day rules
Check BS regularly/q6 hr
Check ketones/Call md is spilling
Continue to take Insulin/stress and infection
Encourage drinking juice
What do Ketones produce?
Acidosis
Why does glucose cause glycosuria and osmotic diuresis?
Because Glucose has a high osmolarity and will pull fluid from the cells! Reason why DKA pt are dehydrated and thirsty!
When should a diabetic test for Ketones in their Urine?
When their BS is >250
Where is glucose stored?
Liver
What is DKA. Etiology
Diabetic Ketoacidosis. caused by absence or markedly inadequate amount of insulin resulting in disorders of metabolism
What are the three main clinical features of DKA?
Hyperglycemia
Dehydration and electrolyte loss
Acidosis
Why is dehydration and electrolyte loss caused by DKA?
Without insulin the glucose can not get into the cell and the liver produces more glucose. The kidney then excrete the glucose in an attempt to rid the body of the excess. So out goes water and Na and K
What are the three main causes of DKA?
decreased or miss dose of insulin
illness or infection
undiagnosed or mistreated DM
S/S of DKA
Hyperglycemia, polyuria,dehydration,blurred vision,headache, weakness, increased thirst, orthostatic hypotension, GI symptoms, kussmaul resp.
LAB values for DKA
BS 300 to 800
Low serum bicarb
low PCO2
increased ketone bodies
NA and K low, normal or high depending on water loss.(monitor closely will eventually need to be replaced. Esp K
elevated BUN and creatinie
elevated H&H
What electrolyte is a major concern with regards to DKA
K due to arrhytmias