Luokat: Kaikki - insulin

jonka Claire Bostic 4 vuotta sitten

215

Endo Emerg

Hyperglycemia presents with elevated fasting blood glucose or postprandial blood glucose levels. Initial assessment involves a thorough history and physical examination, urine analysis for ketones, and basic metabolic panel to check for metabolic acidosis.

Endo Emerg

Thyroid Storm:

Endo + Electrolyte Emerg.

Myxedema coma- life-threatening hypothyroidism - hallmark= AMS - precipitated by: sepsis, cardiac dz, resp. distress, CNS dz, cold exposure, drug use, non-compliance w/tx

Tx: Thyroxine IV bolus
s/sx: severe hypothermia, hypoventilation, hyponatremia, hypoglycemia, hytoTN, rhabdo, AKI

Pituitary apoplexy- spontaneous hemorrhage or infarction of preexisting pituitary adenoma - SUDDEN, severe headache

Tx: admit ICU + CS + neurosurg consult + endo, ophthalmology, and neurology
CT (non contrast) and MRI may show sellar mass and hemorrhage
RF: pregnancy, head trauma, pituitary radiation, dopamine agonist tx

Pheochromocytoma- catecholamine secreting tumor in adrenal medulla - more common in women - episode often precipitated by: abd movement, trauma, drugs, idiopathic - HALLMARK = HTN

Tx: Control HTN w/alpha blocker; BB AFTER alpha blockage *avoid BB alone
Dx: Fhx, elevated urinary catecholamine; CT or MRI of abd/pelvis; MIBG scan to detect tumors not seen on CT or MRI
s/sx: Catecholamine EXCESS= HTN crisis- HA, CP, palp, SOB, sweating
Subtopic

Hyperkalemia: serum K >5.5 mEq/L MC is pt w/missed dialysis w/ESRD - changes electrochemical gradient of cells, making muscles weak and cardiac dysrhythmias potentially fatal outcomes ***Can be d/t lab error, so repeat labs

Tx: if ECG manifestations or pt is hemodynamically unstable then first tx is STABILIZE MYOCARDIUM 1. Stabilize myocardium w/Calcium gluconate or Ca chloride - this will reverse ECG changes 2. intracellular K transfer w/regular insulin 3. decrease total K w/Furosemide - can also use Kayexelate (binds K, not used much), Hemodialysis (if hemodynamically unstable, or if pt is dialysis dependent), or Patiromer (binds K)
EKG: marker for clinically significant hyperkalemia 1. tall, peaked T waves (>6.5) 2. flattening of p wave, prolongation PR interval and widening of QRS (>7) 3. loss of p waves leading to sine-waves: fusion of wide QRS w/ST-T segments (8-10)
Etiol:
altered transfer to intracellular space- acidosis, insulin deficiency, succinylcholine
increased release from intracellular space- hemolysis, rhabdo, burns, crush injury
Decreased renal clearance- CKD, AKI
Pres: can be underwhelming! - weakness and/or paresthesias - SEVERE? = cardiac (significant), neuromuscular- muscle cramps, generalized weakness; GI: N/V/D PE: extrasystoles; pauses/bradycardia; decreased DTR; decreased strength on neuro; look for fluid overload and dialysis access sites
Cardiac pres: 2nd or 3rd degree heart block; wide complex tachycardia; progression to vFib; asystole

Hypoglycemia: serum glucose <70mg/dL - clinical syndrome of altered autonomic dysfunction and impaired cognition - sx of hypoglycemia appear at varying glucose levels

Hyperglycemia: FBG >90-130mg/dL or Postprandial BG >180 - W/U: Thorough H&P - minor sx: UA looking for ketones and BMP to see if increased gap metabolic acidosis - ill appearing/hemodynamically unstable/suspect HHS or DKA: ABCs, 2 large bore IV- NS 1-2L; cardiac monitoring

Tx: - Mild-mod: may only need IV fluids - DKA and HHS: 1. correct intravascular vol. depletion: NS 1L/hr; LR may be better option to avoid hyperchloremic non-anion gap metabolic acidosis 2. manage electrolyte abnormalities: replace K+ and Bicarb - K+ b/w 4-5 is NL >5.5= insulin infusion 3.5-5.5= add K to fluids <3.5= hold insulin, add K and restart insulin later 3. insulin replacement: IV infusion of regular insulin (preferred); at 10units/hr in 70kg pt 4. ID underlying cause and tx that - infx= abx
DDX:
DKA

MCC: infection, disruption of insulin therapy, presentation of new onset DM

usu. in T1DM; younger people

absolute insulin deficiency; hyperglycemia, anion gap acidosis; dehydration

HHS- hyperosmolar hyperglycemic state

MCC: poorly controlled T2DM w/underlying infxn

usu. in T2DM; older people

Hyperglycemia, hyperosmolar, dehydration, *WITHOUT significant ketoacidosis*

Presentation: - mild: may be asx - BG >180 (renal threshold) = polyuria/dipsia/phagia/wt loss - MOD: abd pain, Kussmaul resp, hypoTN, ketotonic breath, tachycardia - SEV: seizures, focal weakness, lethargy, coma, death
complication: cerebral edema- usually in children and young adults; preceded by HA, lethargy, neuro, bradycardia, respiratory arrest