Endocrine/Integumentary Flashcards
Three key features of DKA:
- Hyperglycemia
- Ketogenesis (total lack of insulin, unlike HHS)
- Acidemia (ketones, lactate)
- Hypokalemia (polyuria, H+/K+ exchange pump)
- Dehydration (polyuria, Kussmaul’s)
Three ketones and how to find them:
- Beta hydroxybutyrate (first to show, found in serum)
- Acetone (breath)
- Acetoacetate (last to show, found in urine dip)
What is the most lethal component of DKA?
-Hypokalemia will produce refractory Torsades de Pointes! (replace K+ aggressively to keep > 4.0mmol and monitor at least q. 1h. Insulin will shift more K+ back into the cell).
The 7 ‘I’s of DKA causes:
- Insulin deficiency
- Infection
- Injury
- Infarction
- Intoxication (sympathomimetics)
- Inflammation
- Idiocy (pregnancy)
DKA patients are known to have excruciating abdominal pain. What else can cause hyperglycemia and abdo pain?
- Pancreatitis
- Ileus
- Mesenteric ischemia
Management principles for DKA:
- Fluid replacement
- Aggressive potassium correction, monitor electrolytes
- Insulin to reduce BG and ketones
How to calculate corrected Na+ in the setting of hyperglycemia?
- For every 10 mmol of BG above normal (10.0mmol), there is a reduction of the calculated serum Na+ by 3mmol.
- This is because glucose and sodium are both osmotic agents. As the glucose is pushed up, sodium leaves the serum in order for it to try to maintain normal tonicity.
- Hence, a BG of 40 and a calculated Na+ of 125 will actually have a serum Na+ of 134 once the hyperglycemia is corrected.
How many mmol in 24 hours can you correct hyponatremia by?
-Don’t correct the Na+ more than 12mmol in 24 hours or it may cause osmotic demyelination.
When measuring the anion gap in DKA, what must you consider? This is a real fucking easy one…
That your anion gap is accounted for with lactate and ketones. Make sure you’re not missing another form of acidosis.
Ugh! Key features of adrenal insufficiency:
- Sudden cessation of exogenous steroids
- Septic Shock
- Low BG, Na+; high K+
- Acidemia
- Hypotension, refractory to catecholamines (>20mcg/min Levophed)
- Tanned skin
Standard dose and agent to treat adrenal insufficiency:
-50mg IV q\hydrocortisone (glucocorticoid + mineralcorticoids) q. 6h
Key features of pheochromocytoma:
- Paroxysmal release of massive amounts of endogenous catecholamines = tachycardia, HTN, mydriasis, pain, pulmonary edema.
- Generally, lasts 5-30 minutes. Consider this before treating with long-acting agents or your patient will then be hypotensive.
- Tx phentalomine, hydralazine or labetalol while minimizing any noxious stimulants
So Triiodothyronine (T3) affects almost every physiological process in the body, including growth and development, metabolism, body temperature and heart rate. How is it created and how is it managed?
- The anterior pituitary gland senses low T3/T4 levels and releases thyroid stimulating hormone (TSH). The thyroid receives this input and starts producing T4 which is then converted into T3. T3 sensitizes organs to catecholamines.
- A negative feedback loop generally keeps levels in check but pituitary tumours, Graves’ disease, thyroiditis and goiters can cause thyroid storm while Hashimoto’s and hypothyroidism can cause myexdema coma.
This is a bit of a weird and wonderful one, but what drug should you avoid in the case of a thyroid storm?
Amiodarone will increase iodine levels. Not good.
Key features of SJS/Toxic epidermal necrolysis (TEN):
- Reaction to medications cause necrosis and detachment of the epidermis. SJS has a 10% mortality while TEN has a 30%.
- SJS blisters < 10% BSA while TEN > 30% BSA
- Associated with massive insensible fluid loss. Replace fluid at 2ml/kg x BSA though fluid warmer.
- Ketamine for pain
