DKA, HHS, Hyper and Hypoglycemia Flashcards
Diabetic Ketoacidosis DKA
dehydration, system acidosis, hyperglycemia and ketosis from no endogenous insulin and increased lipolysis (free fatty acids) causing in glycogenesis and ketogenesis
breakdown of fats due to lack of carbohydrates broken down, which metabolizes into ketones, acute development
S&S of DKA
weight loss polyuria polydipsia lethargy and fatigue poor skin turgor or tenting sunken eye sockets tachypnea tachycardia ab pain weakness dry mucous membranes Kussmaul's resp hypotension and orthostatic hypotension extreme dehydration fruity breath from ketone polyphagia ketones in the urine
Hyperosmolar Hyperglycemic State HHS
typically older people with gradual development that is is from hyperglycemia from limited hyperglycemia but enough to prevent DKA for now
HHS S&S
somnolence (extreme drowsiness) dry mucous membranes poor skin toguor Kussmaul's resp acidosis as a secondary development, not part of the main disease low sodium, phosphorus, and K+ aphasia extreme dehydration polyuria
Complications of HHS
acidosis
seizure
coma
DKA
Diagnostic for DKA and HHS
Metabolic panel regular suspects Serum osmolarity urinalysis shows glucose, ketones and high spec grav Lab values of low sodium, K+, magnesium, and phosphate chest X ray ECG cardiac markers
Risk Factors for DAK and HHS
DM, diagnosed, undiagnosed or unmanaged recent infection MI or stroke Insulin omission gaining weight or losing weight without med adjustment pregnancy insulin resistance older age
Priority Nursing Diagnoses for DKA and HHS
fluid volume deficit risk for ineffective cerebral perfusion risk for electrolyte imbalance risk for decreased CO risk for ineffective renal perfusion risk for shock
TX for DKA and HHS
Balance K+ before insulin, lactated ringers and KCl for fluids insulin 0.1u/kg IV bolus or push stabilize electrolyte balance monitor all values admin glucose-based IVF once glucose is more stable to prevent the rebound hyperglycemia or hypoglycemia emotional/physical stress inactivity poor absorption corticosteriods
Hyperglycemia
too little insulin available for the glucose and carbohydrates in the body; insulin intolerance, poor diet, unknown DM diagnosis, poor personal hygiene and self-care
the body compensates by producing insulin and converting glucose into glucagon
Hypoglycemia
too much insulin for the carbohydrates and glucose in the body, lower it to 4.4mmol/L
after it suppresses insulin production, but if it continues it lowers to 3.6-8 mmol/L Alpha cells are released
if that don’t work then the neuroendocrine hormones are released and the liver produces glucose for the body
S&S of Hyperglycemia
ab cramps blurred vision increased BS headache fluctuating appetite polyuria nausea/vomiting weakness fatigue can lead to HHS and DKA if left untreated or becomes more severe
S&S of Hypoglycemia
manifestations are that you appear hammered pallor diaphoresis palpitations tremors irritability vision changes difficulty speaking difficulty with concentration confusion/weakness/fatigue nervousness and anxiety can lead to stupor, coma and seizures
Causes of Hypoglycemia
alcohol without food
food and DM meds are taken at the wrong time
missing food
loss of weight without insulin adjustment
use of adrenergic BB interfering with the recognition of the early warning signs
TX of Hyperglycemia
checking for DKA and HHS CONSTANTLY Insulin increased fluid intake monitoring intake and output adjusting meds DM diagnosis
