Endocrine Flashcards
Diabetes mellitus
chronic disorder of impaired carbohydrate, protein, and lipid metabolism; primarily carbohydrate; deficiency of insulin results in hyperglycemia
sub-categories of diabetes
Type 1, Type 2, and metabolic syndrome (pre-diabetes)
complications associated with diabetes
microvascular complications, macrovascular complications, reduced healing causing increased risk of infection
how does diabetes destroy vasculature
glucose interacts with endothelial vascular wall causing damage, thrombi can form d/t damage of walls, all organs with vascular system experience damage
type I diabetes
nearly absolute deficiency of insulin due to autoimmune primary beta cell destruction (negligible insulin); if insulin is not given then fat is metabolized for energy causing DKA; genetic
type II diabetes
relative lack of insulin or resistance t the action of insulin; insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate; develops over time
metabolic syndrome
coexisting risk factors for developing type II diabetes; risk factors include abdominal obesity, hyperglycemia, HTN, high triglyceride levels, low HDL
assessment of diabetes
polyuria, polydipsia, polyphagia, hyperglycemia, weight loss, blurred vision, slow wound healing, vaginal infections, weakness/parasthesias, signs of inadequate circulation of feet, signs of accelerated atherosclerosis
A1C diagnostic for diabetes
> 6.5
dietary reccomendation for diabetes
consistency every day in timing and amount to control blood glucose levels, following american diabetic association diet, carb counting
exercise recommendations for diabetes
exercise at same time each day when glucose is peaking from meal; monitor levels before during and after; do not exercis if >250 mg/dL and urinary ketones present
oral hypoglycemic medications
sulfonyureas- increase insulin secretion; thiazolidinediones- improve insulin sensitivity; biguanides- decrease liver glucose output; alpha-glucosidase inhibitors- delay intestinal glucose absorption; GLP-1 receptor agonists-enhance incretin activity; SGLT-2 inhibitors- promote renal glucose excretion
primary intervention for type II diabetes
exercise, diet, and lifestyle; if not working after 6 months than oral hypoglycemics and maybe insulin prescribed
only oral hypoglycemic not contraindicated in Type I diabetes
SGLT-2 inhibitors
insulin
increases glucose transport into cells and promotes conversion of glucose to glycogen causing decrease in serum glucose levels; primarily acts in the liver, muscle, and adipose tissue
dawn phenomenon
hyperglycemia on morning awakening resulting from excessive release of GH and cortisol early in morning; treatment is increase in insulin dose or change in administration timing
somogyi effect
normal/elevated glucose at bedtime, hypoglycemia around 2am causing increase in production of counterregulatory hormones; blood glucose rebounds by 7am in response to counterregulatory hormones and pt is hyperglycemic; treat with decreased insulin and or having large bedtime snack
common scenarios in Type I diabetes
dawn phenomenon and somogyi effect
how much insulin can a pump store?
about 3 days worth
hypoglycemia
<70 mg/dL or rapid drop from elevated level; caused by too much insulin, too much oral hypoglycemic, too little food, or too much exercise
hypoglycemia unawareness
warning signs of hypoglycemia are not evident until blood glucose is dangerously low; commonly seen in those with frequent hypoglycemia episodes, older patients, or those taking beta-adrenergic blockers
hypoglycemia s/s
cold, clammy, headache, lethargy, AMS, hungry, tachycardia, jittery, angry
hypoglycemia assessment
mild is 40-70: fully awake with neurogenic symptoms like tremors, palpitations, sweating, hunger; moderate is 20-39: s/s of worsening hypoglycemia like dizziness, drowsiness, and weakness; severe is <20: severe neuroglycopenic symptoms like delirium, seizure, coma, and death
hypoglycemia interventions
check BGL, 15/15 rule- if symptomatic or below 70mg/dL give 15 gram of simple carbs (4oz juice), recheck BGL in 15 min and administer another 15g, if still below 70 after 45 g sugar admin 15-50 ml of 50% dextrose or 1mg glucagon; pt should then eat snack
if pt found with altered LOC from hypoglycemia
first line is IV dextrose or IM glucagon
glucagon
hormone secreted by alpha cells in pancreas that increases blood glucose; increased after 5-20 minutes
DKA
life threatening complication of type I that can occur with severe insulin deficiency; too much breaking down of fats producing ketones which are acidic; hyperkalemia can be seen (H into cell and K out into blood stream)
assessment of DKA
precipitated by infection, stress, inadequate insulin, or can be sudden; glucose >300 Cr > 1.5, urine has ketones, K elevated with acidosis, ABG show acidotic, dehydrated, polydipsia, polyuria, weight loss, dry skin, sunken eyes, lethargy, coma
DKA interventions
restore blood volume, IV insulin with infusion of NS or 1/2 NS with dextrose added; monitor K and correct imbalances in electrolyte; cardiac monitoring if needed
IV insulin for DKA
only use short acting
HHS- hyperosmolar hyperglycemic syndrome
extreme hyperglycemia without ketosis/acidosis; more often inn Type II diabetes; enough insulin is present to prevent breakdown of fts for energy (no ketosis); need to have neurological side effects present
assessment of HHS
gradual onset precipitated by infection, stressors, poor fluid intake; neurological symptoms from altered CNS function; dehydration and electrolyte imbalance from high glucose displacing electrolytes; polyuria, polydipsia, weight loss, sunken eyes, dry skin, lethargy, coma; glucose >800, hypokalemia, hyponatremia, elevated creatinine, negative urine ketones; ABD does not show acidosis
HHS interventions
similar treatment to DKA; fluid and electrolyte repletion; insulin is less critical as there is not ketosis/acidosis
diabetic retinopathy
chronic progressive impairment of retinal circulation leading to eventual rupture of small microaneurysms in retinal blood vessels; vision changes can be permanent and can result in loss
assessment of diabetic retinopathy
vision changes, blurry vision from macular edema, sudden vision loss d/t retinal detachment (cant fix), cataracts lens opacity
interventions for diabetic retinopathy
ensure safety/promote early prevention with HTN management and glucose control, laser therapy to remove hemorrhagic tissue, vitrectomy to remove vitreous hemorrhages, cataract removal with lens implant
diabetic nephropathy
progressive kidney function decline d/t damage of vascular walls causing blood supply issue to kidneys
diabetic nephropathy assessment
fatigue, thirst, weight loss, anemia, microalbuminuria, malnutrition, UTIs, neurogenic bladder (incontinence), elevated creatinine
interventions for diabetic nephropathy
early prevention with HTN control and glucose management, monitor VS/IOs, monitor BUN creatinine and urine albumin, restrict dietary potassium sodium and protein, avoid nephrotoxic medications, prep fir dialysis kidney transplant or pancreas transplant
diabetic neuropathy
generalized deterioration of nervous system complicated by nonhealing ulcers on feet, gastric paresis, erectile dysfunction
diabetic neuropathy assessment
parasthesias, decreased/absent reflexes, decreased sensation, pain/aching in lower extrem., diminished peripheral pulses, skin breakdown with infection, weakened sensation to cranial nerves III/IV/V/VI, diarrhea/constipation, impotence, hypoglycemia unawareness, incontinence
diabetic neuropathy interventions
early prevention (glucose control), foot care, pain management, bladder training, estrogen containing lubricants, penile injections, surgical decompression
diabetes and surgery
prior- may need to hold oral hypoglycemics, may need to hold long acting insulin, monitor BGL levels; post- admin glucose/insulin as needed until oral intake resumes, admin short acting insulin as needed, risk for impaired wound healing
