7) Immune, Endocrine, Electrolyte Flashcards
What type of run is anaphylaxis
Type I; IgE antibodies bind to mast cells or basophils
Tx of Anaphylaxis
Secure airway
IV Epi
IV fluids
pressors
**all patients should receive corticosteroids to prevent late phase reactions
**everyone should also receive antihistamines both H1 and H2 blockers (diphenhydramine and ranitidine)
**must monitor for at least 6hrs
Angioedema causes
IgE mediated, also can occur with ACEI, hereditary, idiopathic
Tx of Angioedema
Same as anaphylaxis
**known hereditary angioedema should also receive C1 esterase inhibitor or FFP
Predisposing factors to DKA
- noncompliance w/ insulin
- infectious process
- stress
- pregnancy
- trauma
- alcohol use
- MI
- new onset DM
- CVA
- GI bleeding
Labs dx of DKA
- glucose >250
- HCO3 less than 15
- pH <7.3
Tx of DKA
- 0.8% normal saline
- Insulin drip to revers ketogenesis and allow glucose to be used
- *once the glucose level is below 250 switch to glucose containing solutions to avoid hypoglycemia
- *insulin drip can be tapered once vicar increases and anion gap resolves
labs dx of Hyperosmolar hyperglycemic nonketotic syndrome
glucose >600
osmolarity >320
Prerenal azotemia in the absence of ketoacidosis
Tx of HHS
- fluid resuscitation w/ NS
- insulin drip
- once glucose is <250 switch to glucose continuing solutions and reduce insulin accordingly
Tx of thyroid storm
- suppress thyroid hormone synthesis w/ PTU
- inhibit thryoid hormone release w/ potassium iodine
- block peripheral effects w/ Beta blockers
- prevent conversion of T4 to T3 with dexamthasone
Presentation of myxedema coma
- altered mental status
- respiratory insufficiency
- myxedema (non pitting dry, waxy swelling of skin caused by deep of mucopolysaccarides in the dermis)
- **hyponatremia, hyopchloremia, hypoglycemia
Tx of myxedema
- cardiac monitor
- IV fluids
- rewarming as indicated
- hydrocrotisone to avoid precipitating and/or exacerbating possible underlying adrenal insufficiency
- IV levothyroxine
What is primary adrenal insufficiency
aka Addison’s Dz
-due to disease of destruction of adrenal cortex (no cortisol or aldosterone so no feedback to pituitary gland and thus HIGH levels of ACTH)
What is secondary adrenal insufficiency
disease or destruction of pituitary gland (LACK OF ACTH secretion)
Presentation of adrenal insufficiency
weakness, fatigue, nausea, vomiting, diarrhea, abdominal pain, weight loss
Labs in adrenal insufficiency
hyponatremia, hyperkalemia, hypoglycemia
***cortisol and ACTH to confirm adrenal insufficiency are not readily available to should treat based on suspicion