Non-vascular complications of DM Flashcards
Diabetic Ketoacidosis -which type of DM gets this? -Characterized by what 3 things? -MOA -
- T1D
- Characterized by hyperglycemia, ketonemia, and anion gap metabolic acidosis*
MOA: reduction in effective concentration of circulating insulin, elevation of counter-regulatory hormones (glucagon, cortisol, GH) Since glucose cannot get into cells the body starts breaking down protein and fats for energy leading to excess free fatty acids in circulation, this leads to production of ketones and ketonuria.
What are some of the most common precipitating factors leading to DKA?
-pneumonia, urinary tract infection, severe dehydration, MI, CVA, pancreatitis, *New onset of diabetes, inadequate insulin therapy
Clinical Presentation of DKA
- thirst, polydipsia
- polyuria
- n/v
- Abd pain
- weakness, fatigue
- tachycardia (from low blood volume)
- ortho hypotension
- kussmauls respirations
- fruity breath
- AMS
Lab findings in DKA
-Blood Glucose 250-800
-Anion gap greater than 12
-pH less than 7.3 (acidotic)
-Ketones +
^^^Need these to dx DKA.
May also find:
- serum Na low
- serum K+ high (glucose pulls K+ out of cells)
- Serum bicarb low (less than 20)(you have all the ketones in your system leading to acidity, all of your bicarb is being used to lower its acidity)
Hyperosmolar Hyperglycemic State (HHS)
- which type of diabetes does this occur with?
- cause?
- Distinguished from DKA by
- T2D most common
- caused by limited access to free water.
- Distinguished by:
- sever hyperglycemia (greater than 600)
- Hyperosmolality (increased solutes, hypovolemic)
- Greater degree of dehydration
- absence of acidosis and keetones
Causes of Hyperosmolar Hyperglycemic State
-clinical presentation
- catabolic stress
- infection
- non-compliance with medications
- drugs
Presentation:
- polyuria
- polydipsia
- weight loss
- vomiting
- dehydration
- weakness
- AMS
- Tachycardia
- Hypotension
- coma
Lab findings in HHS? How do these lab findings differ from DKA?
- blood glucose greater than 600
- serum Na normal to high* (so dehydrated that now you have more Na in your body than water)
- serum K+ normal
- serum bicarb greater than 20
- pH greater than 7.3
- ketones negative
Differ form DKA:
DKA Na = low and HHS Na = high
-DKA Serum K+ = high and HHS Na= normal
-DKA bicarb less than 20 and HHS bicarb greater than 20
-DKA pH less than 7.3 and HHS pH greater than 7.3
-DKA= ketones and HHS = no ketones.
Tx DKA and HHS.
Both are medical emergencies!
-initial assessment: airwary, breathing, and circulation (ABC’s)
- assess volume status: IV fluid and electrolyte replacemente
- slower rate and greater volume needed for HHS
- insulin replacement sstarts after rehydration is in progress.
- make sure serum K+ is greater than 3.3 before giving insulin otherwise insulin will push back all K+ back into the cells leading to hypokalemia.
- Give fluids first (should drop blood sugar), watch their sugars, check K+, if thats all good you give them insulin and dextrose so y ou dont make them hypoglycemic.
Hypoglycemia
- most common in which type of diabetes
- causes
- clinical presentation
- T1D most common
- causes: insulin injections, oral hypoglycemic agents, gastroparesis, hepatic and renal dysfunction, malnutrition
-Presentation:
*Diaphoresis, pallor, tachycardia, elevated blood pressure
–neurogenic sx: catacholamine-mediated: tremor, palpitations
acetylcholine-mediated: sweating, hunger, paresthesias
–Neuroglycopenic sx: cognitive impairment, behavioral changes, seizure, coma in severe cases.
Hypoglycemia unawareness in DM caused by?
- result of reduced sympathoadreal responses to a given degree of hypoglycemia caused by:
- -loss of autonomic warning (recent antecedent hypoglycemia, prior exercise, or sleep
- -autonomic neuropathy: epinephrine response diminished or lost
- -Medications: beta blockers
Management of Hypoglycemia
- Outside of Hospital: oral, SQ, or IM glucose
- Inside Hospital: IV; 1amp D50
Non-diabetic Hypoglycemia
-whipples triad
-causes
-
-Whipples: sx of hypoglycemia, low plasma glucose, resolution of hypoglycemia sx after carb intake.
Cause: drugs, critical illness, endocrine deficiency, nonislet cell tumor.
Factitious Hypoglycemia
- what causes this?
- endogenous hyperinsulinemia, what are the levels of C-peptide and insulin?
- exogenous insulin factitious hypoglycemia, what are the levels of c-peptide and insulin?
- surreptitious (secret) use of insulin or insulin secretagogues.
- in ENDOGENOUS hyperinsulinemia the levels of c-peptide and insulin are secreted in equimolar fashion, the plasma concentrations are equal.
- in EXOGENOUS insulin factitious hypoglycemia the plasma concentrations of the two peptides are inversely related, plasma insulin is high while peptide-c is low.
hypoglycemic coma
- unconciousness lasting more than 30 minutes after plasma glucose is corrected is called?
- tx
- post hypoglycemic coma
- Tx: IV mannitol, glucocorticoids(dexamethasone)
