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
Test for adrenal insufficiency
ACTH stimulation test
-24hr urine smaple for 17-hydroxycorticosteroid
Tx of adrenal insufficiency
rapid infusion of 5% dextrose and isotonic saline
- tx hypotension w/ IV fluids and pressors as needed
- Tx hyperkalemia as indicated
- Glucocorticosteroid and mineralocorticoid replacement w/ hydrocortisone = mainstay (use dexamethasone if doing concurrent ACTH stim test)
Hypokalemia findings
- areflexia, paralysis, arrhythmias, orthostatic hypotension, ileus
- U waves, t-wave flattening or inverse, ST segment depression
Tx of hypokalemia
- if 2.5 to 3.5 can be managed outpatient w/ gradual potassium repletion (follow up w/in 48h)
- If <2.5 should be admitted to th hospital
Hyperkalemia findings
- paralysis, areflexia, focal neuro deficits, respiratory insufficiency, cardiac arrest
- 1st: t waves peak, then PR prolongation, then loss of Ps and widening of QRS complex
Tx of hyperkalemia
-Administer calcium chloride and sodium bicarb
-cardiac monitor
-IV access
give insulin and IV glucose to shift potassium into the cells
-albuterol neb and sodium bicarb can additionally cause shift
-consider furosemide or kayexalate (K binding resin) to remove potassium from body
**if severe and renal filure or severe refractory hyperkalemia = consider dialysis
isotonic hyponatremia
falsely low serum sodium due to hyperproteinemia or hyperlipidemia
hypertonic hypernatremia
low serum sodiu level due to high levels of osmotically active substance (like glucose) that cause water to move into the extracellular space
Hypotonic hyponatremia
divided into hypovolemic, isovolemic, and hypervolemic
hyponatremia symp
<120 is almost always symptomatic
- disorientation and confusion, agitiation, ataxia, altered consciousness, seizures and coma
- other: HA, muscle cramps, anorexia, nausea, vomiting, and weakness
Causes of hypotonic hypovolemic hyponatremia
-GI losses (vomiting, diarrhea)
-Excessive sweating
-Renal losses (salt wasting nephropathies, diuretics)
-Addisons disease
-CF
-Third spacing (burns, peritonitis, pancreatitis)
(Tx w/ isotonic saline)
Causes of hypotonic isovolemic hyponatremia
-SiADH
-psychogenic polydipsia
-water intoxication
-hypothyroidism
-cortisol deficiency
(Tx w/ free water restriction)
Causes of hypotonic hypervolemic hyponatremia
-CHF
-Cirrhosis
-Nephrotic syndrome
-renal failure
(Tx w/ sodium and free water restriction)
Calculating Serum Osmolality
2Na + glucose /18 + Bun/2.8
(normal = 290)
**helps to separate isotonic, hypertonic, hypotonic
Tx of hyponatremia
- give hypertonic 3% saline
- correcting hyponatremia too aggressively can lead to central pontine myelinolysis or cerebral edema
Hypernatremia
results from free water deficit compared to sodium levels
-hypovolemic hypernatremia is the most common and due to loss of water and sodium but >water loss than sodium loss
Tx of hypernatremia
- 9% normal saline to improve BP and restore tissue perfusion
- once volume is restored change to D5W or hypotonic saline (0.45%)
Tx of DI
parenteral or intranasal vasopressin in addition to water deficit replacement
Hypocalcemia should be considered in
renal failure, chronic malabsorption, neck surgery and irradiation
Manifestations of hypocalcemia
- circumoral and distal extremity paresthesias
- weakness, irritability, muscle cramps
- tetany and seizures
- *QT prolongation
- ***careful in patients on digoxin
Trousseaus sign
-carpal spasm in response to inflation of BP cuff to 20mmHg above SBP for 3 min
Chvostek sign
-twitching of the facial muscles after tapping over the facial nerve
Hypercalcemia causes
primary hyperparathyroidism and malignancy
Manifestations of hyercalcemia
weakness, fatigues, confusion, obtundation, coma
nausea, vomiting, abdominal pain, constipationTx: IV fluids, furosemide, hydrocortisone, dialysis if refractory to other tx
**QT shortening, PR prolongation, widened QRS on EKG
