-
diabates
- hyperglycemia caused by a relative or absolute deficiency of insulin or by cellular
- resistance to insulin
- chronic, uncurable
- dx: 2 FBG of 126 or higher OR random BG > 200 with overt symptoms (3P's)
-
pancreas
- secretes endocrine and exocrine
- alpha cells: produce glucogon to increase blood sugar by stimulating breakdown of glycogen stores
- beta cells: produce insulin to decrease blood sugar by moving glucose from blood into cells
- brain, liver, intestines, renal tubules do not need insulin
- skeletal muscle, cardiac muscle and fat need insulin
-
type 1 DM
- destruction of beta cells
- little to no insulin produced
- hyperglycemia when 80-90% of beta cells destroyed
- ketois: accumulation of ketone bodies produced during the oxidation of fatty acids
- etiology: autoimmune or idiopathic
- risk factors: genetic, environmental (virus, chemicals)
-
type 1 DM manifestations
- hyperglucemia
- polyuria: high serum osmolality due to excess glucose molecules in blood -> osmosis from intracellular space to vascular space -> increased renal blood flow -> increased urine output
- polydipsia: dehydration due to polyuria triggers thirst
- polyphagia: lack of glucose in cells (because no insulin to transport) triggers hunger
- glucosuria: BGL > 180, excess is excreted in urine
- weight loss: buring protein and fat for energy
- malaise
- fatigue
-
type 2 DM
- insulin resistance in peripheral tissues
- non-ketotic form of DM
- risk factors: obesity, family hx, inactivity, race, hx of gestational diabetes, HTN, metabolic syndrome
-
type 2 DM manifestations
- slow onset
- polyuria
- polydipsia
- blurred vision
- fatigue
- paresthesia
- skin infections
- older adults - orthostatic hypotension, periodontal disease, infection, stroke, slow gastric emptying, impotence, neuropathy, confusion, glaucoma
-
DM testing
- 2 fasting blood glucose > 126
- random BG > 200 with overt symptoms (3P's)
- HbA1C
- --3 month average of BDL
- -- > 6.5% can Dx DM
- -- < 7% is goal
- UA for glucose (hyperglycemia), ketones (hyperglycemia), albumin (kidney damage)
- self-monitoring: AC/HS or daily
-
insulin
- required for type 1
- some type 2's who can control with oral antidiabetics
- physical stress/taking corticosteroids
- DKA/HHS
- tube feeding/parenteral nutrition
- most insulin is synthesized human form, but can be from pork pancreas
-
rapid acting insulin
- lispro (Humalog), aspart (Novolog)
- onset: 5-15 mins
- peak: 1-2 hours
- duration: 3-4 hours
- administer 15 minutes before a meal
- may lower risk of nocturnal hypoglycemia in Type 1
-
short acting insulin
- regular (Humalin R, Novolin R)
- only insulin to give IV
- onset: 30 mins to 1 hour
- peak: 2-3 hours
- duration: 4-8 hours
-
intermediate insulin
- NPH (Humalin N, Novolin N)
- onset: 1-2 hours
- peak: 6-12 hours
- durtaion: 12-18 hours
-
long acting insulin
- glargine (Lantus), detemir (Levemir)
- onset: 1-2 hours
- peak: none
- duration: 14-24 hours (Lantus 24 hours)
- given at night
- do not mix
-
oral antidiabetics
- stimulate or increase insulin secretion
- prevent breakdown of glycogen to glucose by the liver
- make cells less reisstant to insulin
-
sulfonylureas
- glimepiride (Amaryl)
- glipizide (Glucotrol)
- glyburide (Diabeta, Micronase)
- tolazamide (Tolinase)
- tolbutamide (Orinase)
- for mild type 2
- stimulate insulin secretion from pancrease
- increase sensitivity of peripheral tissues
- side effects: hypoglycemia, weight gain
-
biguanides
- metformin (Glucophage)
- decrease overproduction of glucose by the liver
- increase sensitivity of peripheral tissues
- for obese patients or those who do not respond to sulfonylureas
- d/c with renal insufficiency
- d/c before procedure with contrast dye
-
aspirin therapy
- cardiovascular disease common in DM - sticky blood r/t increased sugar
- prevent clots and strokes
- 81mg - 325mg aspirin daily for prophylaxis
- contraindicated for anticoagulant therapy, GI bleed, liver disease
-
nutrition
- carb controlled diet
- limit sugars - eat complex carbs
- eat carbs with protein and fiber
- portion control
-
exercise
- promotes WL
- decreases insulin resistance
- monitor BGL before/after exercise
- exercising at peak insulin time can cause hypoglycemia
-
dawn phenomenon
- rise in BGL between 4am and 8am
- not a response to hypoglycemia
-
somogyi phenomenon
- hypoglycemia at night
- rebound hyperglycemia in AM
-
hypoglycemia
- s/s: shaking, cold, irritability, sweating, restlessness, nausea, hunger
- severe s/s: AMS, decreased LOC, slurred speech
- tx: check BGL, 15g carbs (4oz OJ), recheck in 15 min, give carb+protein/fat
- severe tx: parenteral glucose/glucagon/D50
-
DKA
- diabetic ketoacidosis
- Type 1
- absolute deficiency of insulin and increase in cortisol
- glucose production increases, peripheral glucose usage decreases, fat is mobilized, ketones
-
form
- increased ketones cause loss of bicarb -> metabolic acidosis
- CNS depression -> death
-
DKA metabolic problems
- 1. hyperosmolality r/t hyperglycemia and dehydration
- 2. extracellular volume depletion r/t osmosis
- 3. metabolis acidosis r/t increased ketoacids
- 4. electrolyte imabalances r/t osmosis (loss of potassium/sodium)
-
DKA s/s
- dehydration
- --thirst
- --skin turgor
- --tachycardia (weak)
- --hypotension
- --AMS
- metabolic acidosis
- --fruity breath
- --lethargy
- --coma
- --N&V
- abd pain
- Kussmaul respirations (compensatory)
-
DKA manifestations
- BGL > 250
- pH < 7.3
- bicarb < 15
- serum ketones
- urine ketones
- urine glucose
- abnormal Na, K, Cl
-
DKA tx
- IV insulin to reverse acidosis and lower BGL
- IV fluids (NSS) until BGL 250 then detroxe
- electrolytes (insulin carries K into cells -> hypokalemia)
- BGL q hour
-
HHS
- hyperosmolar hyperglycemia state
- Type 2
- higher mortality that DKA
- precipitating factors: infection, therapeutic agents, procedures, acute or chronic illness
- hyperglycemia causes increased urine output -> decreased plasma volume and GFR -> glucose
-
retained -> hyperosmolarity -> dehydration (osmosis)
no metabolic acidosis - sufficient insulin to prevent metabolism of fats
-
HHS manifestations
- plasma osmolarity > 340
- BGL > 600
- dehydration
- --dry skin
- --thirst
- --AMS
-
HHS tx
- IV fluids to decrease serum osmolality
- IV insulin
- electrolytes
-
DM complications
- macrovascular (r/t atherosclerosis):
- --CAD -> MI -> CHF - leading cause of death for type 2 DM
- --HTN - 75% of DM
- --CVA - 2-4x higher risk with DM
- --PVD - gangrene
- microvascular (decreased tissue perfusion r/t thickening of the basement membrane):
- --nephropathy - albumin in urine (microalbuminuria), HTN, edema, renal insufficiency -> ESRD, tx with antihypertensives (ACE inhibitors), low salt diet, WL, exercise
- --retinopathy - retinal ischemia -> blindness
- neuropathy (decreased nutrients to nerves r/t thickened BV, demyelinization of nerves):
- --peripheral:
- ----polyneuropathies - bilateral - toes/feet and progresses upward - lack of sensation
- ----mononeuropathies - isolated single nerve
- --visceral - ANS:
- ----sweating dysfunction
- ----abnormal pupillary function
- ----gastropareisis - delayed stomach emptying - N&V - Reglan, gastric pacemaker
- ----bladder function changes - incomplete emptying, UTIs
- ----impotence
-
DM teaching
- foot hygiene: wash feet daily, mild soap, dry between toes
- inspect feet daily
- yearly eye exams
- know your meds (name, dose, side effects)
- treatment of hypoglycemia
-
DM nursing dx
- risk for infection r/t vasular insufficiency (limited inflammatory response)
- risk for impaired skin integrity
- risk for injury r/t neuropathy, blurred vision
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