Diabetes Flashcards
what is insulin?
peptide hormone produced in the pancreas by beta cells in islets of Langerhaans
function of insulin
- regulates metabolism of CHO and fats
- promotes absorption of glucose from blood to skeletal muscle and fat tissue
pancreas
gland in abdomen that aids digestion and regulates metabolism
secretes enzymes into SI to help break down CHO, proteins and fats
secretes hormones insulin and glucagon into bloodstream to maintain glucose levels
diabetes patho
- effects of diabetes result from insulin deficiency or resistance to endogenous insulin
- normally insulin allows glucose transport into cells for energy or storage as glycogen
- also stimulates protein synthesis and free fatty acid storage in adipose tissue
type 1 DM causes
- autoimmune disease
- certain infections
type 2 DM causes
- impaired insulin secretion
- peripheral insulin resistance
- increased basal hepatic glucose prod
- obesity
- hormonal contraceptives
- pregnancy
- insulin antagonists (phenytoin)
- steroids, abx, infection
which hormone decreases blood glucose?
insulin
high blood glucose -> insulin secreted. Turned off when blood glucose is normal/low
which hormone increases blood glucose?
glucagon
low blood glucose -> glucagon secreted. Turned off when blood glucose is normal/high
where is glucagon released from?
stored glycogen in liver
how is glucagon secretion inhibited?
by increasing glucose levels only when insulin is present
bc insulin is not present to help glucose into the cells, the cells continue to stimulate glucagon to create and release more glucose (from any source including fats via gluconeogenesis)
DKA and HHS occur in what kind of environment?
where there is a lack (relative or absolute) of insulin so that glucagon cannot be turned off thereby increasing blood glucose
similarities between DKA and HHS
- Glucagon secretion not inhibited
- Elevated glucose levels continue to rise
- State of absolute or relative lack of insulin
HHS key points
insulin is present, so gluconeogenesis and lipolysis is inhibited
ketones mild/absent and pH normal/mild but typically greater fluid loss
DKA key points
no insulin, so gluconeogenesis and lipolysis occurs
ketone bodies prod (acetone breath)
ketoacidosis (can be severe)
results of DKA and HHS
- Hyperglycemic state
- Osmotic diuresis (mainly d/t glucose)
causes of DKA and HHS
- infection
- stroke
- trauma
- MI
- treatment errors with insulin
- pancreatitis
- unknown etiology
DKA
- Occurs in type 1 and 2 diabetics
○ More common in type 1 - Can develop quickly (< 24hrs)
- Blood glucose > 13.9 mmol/L
DKA diagnostics
- Elevated blood glucose - severity of DKA is not necessarily r/t blood glucose
- Low bicarb levels
- Accumulation of ketones (blood and urine)
- Electrolyte levels (K+, Na+)
- Elevated creatinine, BUN, Hgb, Hct (post rehydration continued elevation present in the pt with renal insufficiency)
what happens when you are dehydrated?
Hgb and Hct levels increase
HHS
- Occurs predominantly in type 2 diabetics (in some cases type 1)
- Develops more slowly than DKA (days to weeks)
- Blood glucose >33.3 mmol/L
- Older people with no history of diabetes or mild T2 DM
mortality rate for DKA and HHS
- DKA < 5%
- HHS approx 10-40%
HHS diagnostics
- Blood glucose
- Electrolytes
- BUN
- CBC
- Serum osmolality
- ABGs
diabetic emergencies in children
- Common emergency in peds
- Most commonly associated with newly diagnosed T1 DM
- Usually concerns in childhood or adolescence
- Leading cause of death in children with T1 DM
- Cerebral edema accounts for 50% of DKA-related deaths
- Fluid balance important to monitor
causes of diabetic emergencies in children
- Delayed diagnosis: can be difficult to discern key symptoms (polyuria, polydipsia)
- Omission of insulin: when child or caregiver fails to comply with insulin
- Delivery failure; device fails
- Infection
- Type 2 diabetes can present as DKA
- Controlling weight - children use their diabetes to drop weight
- Religion
management of diabetic emergencies in peds
- Raising awareness of public and professionals
- Fluid resuscitation: rapid fluid resus is associated w/ cerebral edema
- Electrolyte management: potassium shifts, Na+ levels
- Insulin
- Ketosis and acidosis
- Infection
- Cerebral edema managed with Mannitol
treatment of DKA
• Medical management
○ Rehydration: may require 6-10L of IV fluids to replace losses (polyuria, hyperventilation, diarrhea, and vomiting)
○ Normal saline at a rapid rate for 2-3 hrs. NS (0.45%) may be used for HTN or hypernatremia
• Restoring electrolytes: the major electrolytes of concern is K+. Initial plasma [ ] of K+ may be low, normal, or even high - but there are major losses of body stores.
- Serum K+ levels drop throughout treatment as K+ re-enters the cell
treatment of HHS
○ Medical management
- Similar to DKA - Fluid replacement - Correct electrolyte imbalances - Insulin admin - Consider age/factors - If neuro symptoms present, may take 3-5 days to clear - Other modalities are determined by underlying illness of the pt
nursing care for DKA
○ Monitor I&O, electrolytes, blood glucose
○ Administer IV fluids
○ Administer insulin, potassium
○ Administer - other meds (dependent on underlying cause)
○ Monitor: fluid overload, adequate
○ Renal function (hyperkalemia)
○ ECG: monitored for dysrhythmia at risk bc you do not have longer refractory period
○ VS, ABGs
○ Documentation
nursing care for HHS
ing Care
○ Monitor: I&O, lytes, blood glucose
○ Admin IV fluids
○ Admin insulin, K+
○ Admin - other meds (dependent on underlying cause)
○ Monitor: fluid overload, adequate
○ Renal fx (hyperkalemia, creatinine, BUN, GFR)
○ ECG: monitored for dysrhythmia
○ VS, ABGs
○ Careful assessment: CVS, pulmonary etc (r/t aging)
○ Documentation
Education when recovered
