Home > Preview
The flashcards below were created by user
on FreezingBlue Flashcards.
what is diabetes?
metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia)
what is Insulin?
a hormone produced by the pancrease (beta cells), controls levels of glucose in the blood by regulating the production & storage of glucose
hormone produced by the alpha islet cells of the pancreas, serves to complete gluconeogensis in the hypoglycemic state
stored glucose in liver and muscles
What are 1st generation sulfonylureas? what is their action?
antidiabetic; stimulates secretion of insulin.
Long lasting: 24-72 hrs
What are 2nd generation sulfonylureas and their action?
antidiabetic: stimulates the release of insulin and increases sensitivity to insulin.
Short half life, good in elderly
What is common between 1st and 2nd generation sufonylureas?
Both for Type II, both taken with first meal of the day.
Why is Glucagon given?
- raise blood sugar
- treatment of severe hypoglycemia in diabetes and adjunct for GI radiography.
What are thiazolidinediones?
- Improves insulin sensitivity in Type II in liver, muscle and fat cells.
- Pioglitazone (Actos)
- Rosiglitazone (Avandia)
what are adverse/side effects of thiazolidendiones?
hepatotoxicity: liver function, and fluid overload, edema
What are biguanides:
inhibitors of intestinal flucose production and absorption. Target is liver, small intestine and peripheral tissues. Has no effect on pancreatic beta cells
What are SE of biguanides such as metformin?
Lactic Acidosis. Must avoid it in renal failure or uncontrolled HF. Not to be used w/sulfonylureas or the pt will go hypoglycemic.
What are alpha glucosidase inhibitors such as acarbose (Precose)?
Type II- delays absorptoin of glucose from GI tract - target is small intestine. lowers BS by inhibiting alphaglucosidase in GI tract.
what are nursing implications for Acarbose/Precose (alpha-glucosidase inhibitor)?
- flatulence diarrhea, abdominal pain
- must be taken immidiatly before meal
- delays absorption of glucose in intestinal system
What are s/s of hypoglycemia?
dizziness, tremors, tachycardia, anxiety, sweating, hunger, weakness
What are Non Sulfonylureas?
- These are for Type II, and stimulates the secretion of insulin.
- Target - pancreatic beta cells.
- Fast Acting
- Repaglinide (Prandin)
- neteglide (Starlix)
s/s of ketoacidosis (DKA)?
polydipsia, polyuria, headache, N&V, ABD pain, air hunger, acetone/fruity breath, dim vision, drowsiness, unconsciousness, dehydration
causes of hypoglycemia?
- delayed or omission of a meal, excessive exercise, insulin overdose
- injection-unused tissue, ASA
causes of ketoacidosis?
infection, trauma, stress, omitted insulin, loss of pancreatic insulin secretion
Hypoglycemia compared to DKA
- BS <50, ketones 0-norm, HCO2 24-32-norm.
- BS >300, ketones 4+, HCO2 low (Met Res) 4-16
treatment for hypoglycemia?
glucose, glucagon, oral forms of sugar, D50W IVP
Treatment for DKA?
insulin, HCO2, fluid replacement, Potassium replacement is usually required after acid/base balance, Foley catheter
Difference between Type I and Type II?
- T1DM: is no insulin production, HLA (destruction of beta cells)
- T2DM: is decreased insulin or insulin resistant
difference between DKA and HHNS?
- DKA: hyperglycemia in a Type 1
- Hyperglycemic hyperosmolar nonketotic syndrome: Type 2: hyperglycemia, no ketones are produced.
chronic complications of diabetes mellitus?
- Macrovascular: coronary artery disease, cerebrovascular disease, peripheral vascular disease
- Microvascular: Kidney and eye disease, Neuropathic complications
what stimulates the liver to make glucose available to cells?
Where is glucose stored and as what?
liver as glycogen
what are some other functions of insulin?
- enhance storage of dietary fat in adipose tissue
- accelerates transport of amino acids into cells
- inhibits breakdown of stored glucose, protein and fat
what happens during fasting such as sleeping at night in regards to insulin?
during fasting, the pancreas releases a small amount of insulin on a continuous basis for our basal levels
what happens during fasting in regards to glucose?
glucose is released by the liver to provide energy to keep us breathing such as using the diaphragm
production of glucose from glycogen
glucose from the breakdown of non carb substances such as proteins
T1DM has a possible genetic tendency called ___, environmental factors of _____?
HLA human leukocyte antigen
virus and toxins
- glucose spilled in the urine 180-200 mg/dl
- Also loss of electrolytes
When you have glycogenesis (production of new glucose from amino acids) ___ are produced from the breakdown of fats
- Increasing the Acid balance = DKA
who ususally gets DKA?
- usually under 30. They have no insulin, are very dehydrated and they feel like they have the flu - vomiting, no energy
- Caused by: absence or inadequate amount of insulin, Hyperglycemia, acidosis, electrolyte loss. amount of glucose entering cells is reduced & liver produces more glucose.
treatments for DKA?
- fluid replacement Normal Saline
- tx of hyperglycemia
- electrolyte stabilizaiton
- tx of underlying risks such as lack of education.
What is the concern with K+ in DKA?
usually K+ will correct when fluid replacement and regular insulin is given. Don't replace K+ until pt has stabalized
Who normally gets type 2 diabetes?
over 30 and obese
How quickly does Type 2 advance?
- slow and insiduous process of glucose intolerance or insulin resistance
- 75% of cases dx incidentally
What is pimary treatment of type 2?
- weight loss (as most pts obese)
- oral antidiabetic medications
- then insulin if other measures are ineffective
What is primary treatment of Type 1
Does HHNS have a slower or faster onset than DKA? Is insulin present? What about Dehydration?
- HHNS is slower in onset
- some insulin is present
- profound dehydration
treatment of a HHNS Crisis?
- Fluid replacement if indicated
- trmt of hyperglycemia, electrolyte stabilization
Type 1 S/S?
Fatigue, weak, sudden vision changes, tingling or numbness in hands or feet. dry skin and sores that are slow to heal due to poor circulation.recurrent infections, ABD pain , Nausea, Vomiting
3 clinical manifestations of diabetes?
Fasting plasma glucose for diagnosis of DM ___ Random plasma glucose levels > ____ on more than one occasion
- >126mg/dl FPG
- >200 mg/dL Random PG
What is the level of HgbA1C confirming hyperglycemia?
what is HgbA1C?
- glycosylated hemoglobin measured every 3 months. It gives a tale of the last 90 days.
- Normal is 4.4% - 6.4%
- 12 is very bad
What assessments & labs can be done for assessment and diagnosis of Diabetes?
History (3 P's), Physical examination (eyes, cardiovscular, renal impairment), Labs: HgbA1C, Microalbuminuria or 24 hr urine q year (notes renal failing), Fasting lipids annually
- 1. nutrition therapy
- 2. exercise
- 3. monitoring
- 4. Phrmacologic therapy
- 5. education
Main goal of diabetes?
normalize insulin activity and blood glucose level to reduce the incident of vascular and neuropathic complications
what are some important considerations on Sick Days in DM?
- Take insulin/oral med as usual
- test BS & urine ketones q 3-4 hrs
- call MD if BS >300 or ketones present in urine
- make sure to eat, take liquids
What are advantages of patient control of DM? Disadvantages?
- adv - allows pt control
- dis - requires fine motor skills, visual acuity
possible causes of elderly who have hyperglycemia are:
poor nutrition, decrease in lean body mass, alterred insulin secretions, decrease in circulation
dm pts need referrals to other health professionals such as (3):
nutritionist, podiatrist, ophthalmologist
how does exercise effect blood sugar?
exercise lowers blood glucose levels by increasing uptake of glucose
pts with blood glucose levels of > ___ or _____ in their urine should not begin exercising
rapid acting insulins?
- Humalog, Novolog, Regular Insulin.
- Onset 10-15 minutes
- Peak 1-2 hrs
- Duration 3 hrs
intermediate acting insulins?
- NPH & Lente (cloudy) must eat food near the onset and peak of action
- Onset 3-4 hrs
- peak 4-12 hrs
- Duration 16-20 hrs
SLOW acting insulins?
- Long lasting: Ultralente
- Onset is 6-8 hrs
- peak 12-16 hrs
- duration is 20-30 hrs
- Needs to be supplemented w/short acting insulin
What are complications of insulin therapy?
- local & systemic allergic reactions
- lipodystrophy, insulin resistance, morning hyperglycemia
What do sulfonureas Type II oral antidiabetic agents do?
stimulate pancreas to secrete insulin
What do Biguanides T2DM oral antihyperglycemic agents do?
- delay absorption of glucose
- decreases glucose prodcution in liver (metformin) Glucophage
long term complications of diabetes includes macrovascular complications such as
- heart- coronary arteries
- brain- cerebral vascular accident
- main veins- peripheral vessels of lower limbs
long term complications of diabetes includes microvascular complications such as
retinopathy, nephropathy, neuropathies
what may develop in a pt when ketone bodies accumulate?
What are s/s of DKA?
ABD pain, nausea, vomiting, hyperventilation, fruity odor of breath
a fasting plasma glucose greater than or equal to ____mg/dL would support checking blood levels for the diagnosis of DM
what type of T2DM Oral antidiabetic agents inhibit production of glucose by liver?
what type of T2DM oral antidiabetic agent enhance insulin sensitivity in cells but not increasing insulin stimulation of pancreas?
Thiazolidinediones such as Actos and Avan
how do alpha-glucosiadase inhibitors work?
- delay of absorption of glucose in the GI such as Acarbose (Precose)
- lowers BS by inhibiting alphaglucosidase in GI tract
when a pt has signs of hypoglycemia such as nervousness, tachycardia, diaphoresis and hunger, the nurse should provide what?
15 g of fast acting simple carbs such as 3-4 commercially prepared glucose tabs. 6 oz fruit juice, regular soda, 6-10 hard candies
What is considerred a macrovascular complication of DM?
- Stroke, MI
- cerebrovascular disease
- peripheral vascular disease
a normal pt BS level is
60-120 in diabetic
s/s of DKA?
Kussmaul's respirations, dry skin, hypotension, and bradycardia are signs of diabetic ketoacidosis
Cardinal signs of DM?
Polyuria, polydipsia, polyphagia, and weight loss are classic signs
s/s of hypoglycemia?
anxiety, restlessness, headache, irritability, confusion, slurred speech, incoordiantion, diaphoresis, cool skin, tremors, coma, and seizures
type 2 diabetes is described as:
- insulin resistance (decreased sensitivity)or impaired insulin secretion
- body tries to compensate by increasing the production of insulin
- no ketones, rare
- pts typically obese
- pt has no islet antibodies
- > 30
Type 1 diabetes is described as:
- glucose derived from food cannot be stored in the liver and remains circulating in the blood, leading to postprandial hyperglycemia
- desctruction of beta cells results in unchecked glucose production by the liver and fasting hyperglycemiapt usually thin at Dx
- pt needs insulin to preserve life
- pt often has islet cell antibodies
- onset can occur at any age
what is lipotrophy?
Lipotrophy is loss of subcutaneous fat and appears as a slight dimpling or more serious pitting of subcutaneous fat.
Clinical manifestations of HHNS?
- profound dehydration
- neuro- seizures
leading cause of blindness in US in ages 20-74?
sensory neuropathy causes?
loss of sensation to pain and pressure
Autonomic neuropathy causes?
- increased skin dryness
- formation of skin fissures
Motor neuropathy causes?
how does peripheral vascualar disease affect the progression of a foot infection and ulcer formation?
inadequate and compromised lower extremity circulation interfers with ability to get nutrients to wound to promote healing and prevent gangrene.
how does hyperglycemia affect the spread of a foot infection?
hyperglycemia impairs leukocytes ability to destroy bacteria, thus lowering resistance to infection
explain how insulin regulation is altered in the diabetic state
insulin regulates the procution and storage of glucose: in diabetes the pancreas stops making insulin or the cells stop responding to it. hyperglycemia results and can lead to acute metabolic complications (DKA, HHNS)
Describe the pathophysiologic difference between type 1 and type 2
- type 1: characterized by an absence of insulin production and secretion due to autoimmune destruction of the beta cells
- type 2: characterized by deficiency of insulin production and decreased insulin action as well as insulin resistance
describes how much a given food increases the BG level compared with an equivalent amount of glucose