chronic exam 1-diabetes Flashcards
beta cells produce
insulin
alpha cells produce
glucagon
functions of insulin
lowers blood glucose by: regulates rate of CHO metabolism promotes glycogen storage inhibits fats breakdown inhibits protein breakdown
functions of glucagon
raises blood sugar by promoting conversion of glycogen to glucose
name of type 1 diabetes
IDDM (insulin dependent diabetes mellitus)
previously called juvenile diabetes
name of type 2 diabetes
NIDDM (non-insulin dependent diabetes mellitus)
previously called maturity onset diabetes
type 1 diabetes is characterized by
a total lack of insulin production
suggests an autoimmune process that destroys beta cells
type 2 diabetes is characterized by
an inadequate production of insulin or increased cellular resistant to the body’s own insulin
type 1 diabetes onset
faster onset
usually before 30yo but can occur at any age
tend to be normal weight
type 2 diabetes onset
slower onset
usually 35+ years but can occur at any age
tend to be obese
% of diabetics that are type 1
10-15%
insulin required by all
% of diabetics that are type 2
85-90%
increased familial predisposition
insulin required for 20-30%
clinical manifestations
- three P’s
- weight loss-cant breakdown glucose so it’ll breakdown fat
- fatigue/weakness
- blurred vision
- frequent infections-glucose harbors bacterial growth
three P’s
polydipsia-excessive thirst
polyphagia-excessive hunger
polyuria-excessive urination
fasting blood sugar
70-110 mg/dL
Diagnosis= FBS>126 on 2 different occasions
glycoslyated hemoglobin
Hgb A1C
Hgb molecules combine with glucose to from glycohemoglobin which is stored by red blood cells
the percentage of “glycosylated hemoglobin” can be measured by a blood test (4%-6%)
indicator od an individual’s glucose level for the previous three months
6 food groups
Starch/Bread Protein/Meat Dairy/Milk Fruits Vegetables Fats
distributions of calories
50-60% Carbs
20-30% Fats
20% protein
dietary considerations
special foods are not necessary alcohol promotes hypoglycemia dont skip meals do strive for regular meal times do control fat do use sugar substitutes (equal splenda etc)
net effect of exercise
lower blood sugar by transporting glucose into the muscle cell (must be aerobic exercise)
controlling type 2 diabetes
may be controlled with diet and exercise alone, or in combination with oral hypoglycemics
original source of insulin
beef and pork pancreas
persons using synthetic insulins….
have a lower risk of insulin resistance
rapid acting types
Humalog (lispro)
Novalog (aspart)
Short Acting types
regular
Intermediate acting types
NPH (cloudy)
Long acting types
Glargine (Lantus)
Detemir (Levemir)
onset peak duration of Rapid Acting
Onset: 10-15 min
Peak: 1 hr
Duration: 2-4 hr
onset peak duration of Short Acting
Onset: 1/2 hr-1 hr
Peak: 2-4 hr
Duration: 5-7 hr
onset peak duration of Intermediate Acting
Onset: 2-4 hr
Peak: 6-12 hr
Duration: 18-24 hr
onset peak duration of Long Acting
Onset: 3-4
Peak: none for lantus; 3-14 hr for detemir
Duration:24-36 hr
insulin preparation
cloudy
clear
clear
cloudy
insulin storage
keep vial at room temp
refrigerate spare vials
protect from extreme heat, freezing
injection teaching
more rapid absorption from abdomen, then arms, then legs
lipohypertrophy
fat accumulation which occurs at sites of frequent insulin injection
injection rotation
rotate within each site, spacing injections 1 inch apart
do not se a site longer than a month
sulfonylureas
Glucatrol, Glimepiride
Stimulates beta cells to produce insulin; increase cellular receptivity
Meglitinides
Prandin
stimulates beta cells to produce insulin
Biguanides
Glucophage
Increase cellular receptivity to insulin; decrease hepatic production of glucose
Thiazolidinediones (TZDs)
Avandia, Actos
Decrease insulin resistance by increasing receptor sensitivity
Alpha-glucosidase Inhibitors
Precose
Delay digestion of complex carbs
Incretin Mimetics
decrease glucagon secretion from pancreas, increase insulin release
DDP-4 Inhibitors
Inhibit enzyme that inactivates incretin
Diabetic Ketoacidosis
usually occurs in type 1 diabetes
As a result of severe insulin deficiency, the body resorts to breakdown of fats and proteins since it cannot utilize glucose
DKA pathophysiology
ketone production (incomplete fat metabolism) acidosis profound dehydration (due to osmotic diuresis) Hyperkalemia (potassium shifts out of the cells)
DKA causes
undiagnosed Diabetes
omitting insulin especially on sick days
not enough insulin in relation to a physical stressor
DKA stressors
cause a sympathetic response which mobilizes glycogen from the liver resulting in hyperglycemia surgery infection trauma illness
DKA clinical manifestations
3P's dehydration tachycardia hypotension warm, dry skin n/v fruity breath Kussmaul Respirations
Kussmaul Respirations
increases rate and depth to blow off CO2 and raise pH
DKA diagnostics
pH 350 mg/dL
positive serum acetone
positive ketonuria
potassium >5.0
DKA management
IV fluids
IV insulin (regular only, continuous low dose)
IV K+ prn (as pH improves, K levels drop)
DKA complications
hypovolemic shock
coma
death
HHNK
hyperglycemic, hyperosmolar Nonketotic Coma
primarily occurs in T2Diabetes
insufficient insulin prevents ketoacidosis but not severe hyperglycemia
HHNK causes
often the same precipitating factors as for DKA
HHNK clinical manifestations
severe hyperglycemia (>1000mg/dL) severe dehydration hypotension tachycardia hypovolemic shock leading to coma
HHNK Management
Rapid IV fluid replacement to correct fluid deficit
continuous low dose infusion of regular IV insulin
hypoglycemia (insulin reaction)
Most common type one diabetic’s related to insulin therapy with the rapid onset
Causes of hypoglycemia (insulin reaction)
Excessive insulin, delayed or skipped a meal, alcohol usage, excessive exercise without calorie supplementation
Clinical manifestations of hypoglycemia (insulin reaction)
Shakiness, palpitations, dizziness, anxiety, hunger, headache, confusion, irritable, fatigue, diaphoresis, may appear as if person is drunk
management of hypoglycemia (insulin reaction) in conscious
orange juice
jam, honey
hard candy
“regular” soda
management of hypoglycemia (insulin reaction) in unconscious
glucagon subQ
dextrose 50% IVP
microvascular disease
Disease of the small blood vessels; more common in type one diabetics; includes retinopathy, nephropathy, and neuropathy
Retinopathy
Diabetic retinopathy increases the risk of glaucoma (increased intraocular pressure) and cataracts
Management of retinopathy
Slow the onset and progression buy near euglycemia (near normal blood glucose levels)
photocoagulation (laser therapy) to coagulate bleeding
Nephropathy
Damage blood vessels become leaky allowing proteins to form deposits in the vessels
deposits decrease oxygenation resulting in death of kidney cells
Management of nephropathy
Euglycemia (“normal” blood sugar levels)
dialysis or kidney transplant for end-stage renal disease
Neuropathy
Deterioration of nerves due to nerve hypoxia
sensorimotor neuropathy
bilateral and distal paresthesias characterized bu numbness, tingling, burning pain, or weakness
autonomic neuropathy
can affect CV, GI, Urinary, or other function
atherosclerosis
damage to blood vessels due to increased lipid and cholesterol levels with fatty plaque formation, increasing risk of coronary heart disease, HTN, MI
home blood glucose monitoring
test 1-4 times a day (before/after meals)
keep diary of results
stress good control of FBS
Sick Day care
test BS q4hr sip fluids q1hr if vomiting, take regular soda or easily tolerated foods if BS> 300mg/dL, test urine for ketones DO NOT skip insulin or oral medication
