Endocrine Emergencies Flashcards
Diabetic Ketoacidosis (DKA)
Body’s response to cellular starvation - not enough insulin to transport glucose into the cell
Starving cells resort to lipolysis and form ketoacids, which are excreted
Causes ketonuria, anion gap metabolic acidosis w/ compensation, vomiting
Dehydration by efforts to excrete increased serum glucose - oncotic pressure draws fluid into the interstitium
DKA Hypotension
Initially, oncotic increase results in increased fluid in vasculature
However, once glucose is absorbed into the urine, it causes massive osmotic diuresis where the water is following the glucose in the urine
Glucose starts to be spilled in the urine >200
DKA Presentation
Hyperglycemia with polydipsia and polyuria
Acidosis from ketoacids - tachypnea, fruity breath odor
Volume loss with dehydration and HOTN
DKA Management
Aggressive fluid therapy (NS) early - single most important step
Blood gas, CBC, CMP, BG, UA, ECG
Insulin - 0.1 units/kg/hour after bolus - continuous infusion ideal with frequent monitoring - never IM/subQ in dehydrated pt
Potassium therapy: deficient due to acidosis, osmotic diuresis, vomiting - give gradually over time; insulin drives into cell
No phosphate or bicarb replacement at this time
DKA Complications
Hypoglycemia
Cerebral edema
Hypokalemia
Hypophosphatemia
Adult Respiratory Distress Syndrome
Hyperosmolar Hyperglycemic State
Patients with poorly controlled/undiagnosed Type 2 DM
Severe hyperglycemia with elevated plasma osmolality, bicarb, and pH (alkalotic)
-Hyperglycemia >600, Bicarb >15, with mild ketone elimination is what differentiated from DKA
Ketones are negative to mildly positive
Much more rare and much more deadly than DKA
MC in nonambulatory nursing home patient
Hyperosmolar Hyperglycemic State (HHS) Presentation and Treatment
Cognitive impairment with weakness, anorexia, fatigue, dyspnea, abdominal pain
-May by precipitated by pneumonia or UTI
Treatment: volume repletion, correct electrolyte abnormalities with gradual hyperglycemia correction
Hypoglycemia
Neurogenic (sweating, pallor, tachycardia) and Neuroglycopenic (HA, drowsiness, lightheadedness) symptoms
Adrenal Insufficiency
Adrenal Crisis
Insufficiency: failure of adrenal glands to produce essential basal steroid secretion - insidious wasting disease
Crisis: failure of adrenals to respond to increased demands by stress or sudden inability to secrete essential steroids
-life-threatening
Two Forms of Adrenal Insufficiency
Primary: destruction/dysfunction of adrenal cortex
-Addison’s disease
Secondary: inadequate stimulation of cortex by ACTH
-exogenous steriods
Stimulated by Cortisol
Gluconeogenesis
Protein metabolism
Fat mobilization
Stabilize lysosomes
Aldosterone Functions
Increases Na reabsorption by renal cells
Stimulates potassium secretion by renal principal cells
Conn’s Syndrome
Primary Aldosteronism
Excess production of aldosterone by adrenal glands
Adrenal Crisis Management
Give IV Steriods
Any elderly pt - HOTN post op; HOTN after an accident
If patient is nonresponsive to volume repletion or dopamine, try steroids
Pheochromocytoma
Tumor of neural crest cells of SNS - usually in adrenal medulla
Releases catecholamines -> episodic HTN emergencies with palpitations, sweating, HA, fainting
Catecholamines hit b1 receptor on heart - Increases HR and contractility
Hit blood vessels - vasoconstriction cutaneous (alpha1) and vasodilation skeletal (b2)
90%: adrenal medulla, unilateral, benign, adults
