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Endocrine Board Review. Marlaina Norris Review from Tintinalli Section 17 Endocrine Emergencies pp 1283-1318 Section 3 Fluids & Electrolyte Problems pp 168-174. Sugar…. Which one of the following statements regarding potassium balance in diabetic ketoacidosis (DKA) is TRUE?.
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Endocrine Board Review Marlaina Norris Review from Tintinalli Section 17 Endocrine Emergencies pp 1283-1318 Section 3 Fluids & Electrolyte Problemspp 168-174
Which one of the following statements regarding potassium balance in diabetic ketoacidosis (DKA) is TRUE? • A. Approximately 20% of total-body potassium is intravascular • B. Initial hyperkalemia in DKA is common • C. Initial treatment of DKA often causes hypokalemia • D. Initial serum potassium levels >3.3mEq/L and <5.0mEq/L alleviate the need for potassium supplementation
Which one of the following statements regarding potassium balance in diabetic ketoacidosis (DKA) is TRUE? • A. Approximately 20% of total-body potassium is intravascular (2%) • B. Initial hyperkalemia in DKA is common (Initial normal/ high because acidosis intracellular K+ exchange for H+, & total body fluid deficits) • C. Initial treatment of DKA often causes hypokalemia • D. Initial serum potassium levels >3.3mEq/L and <5.0mEq/L alleviate the need for potassium supplementation
Which of the following is a contraindication to Metformin use? • A. Chronic obstructive pulmonary disease • B. Pre menopause • C. Renal Insufficiency • D. Sulfonylurea use • E. Warfarin use
Which of the following is a contraindication to Metformin use? • A. Chronic obstructive pulmonary disease • B. Pre menopause • C. Renal Insufficiency • D. Sulfonylurea use • E. Warfarin use
DKA, DKA, dka, DKA, dKa, DKA, DKA • We know it! We love it! • Incidence 15/ 1000 patients; 24% of DM admissions • Pathophysiology: No Insulin Osmotic diuresis and AG acidosis • Rx: 1) IVF 2) Insulin(0.1u/kg/hr) 3) Find the ‘stressor’/ Stimulant *4) K+ maintenance [Goal glucose reduction~ 50-70 mg/dl in 1st hr] • *Important notes: • Pregnancy: DKA triggered @ lower glucose concentrations Hyperglycemia decreases uterine blood flow/ fetal O2 Hypokalemia fetal arrhythmia >Meformin= Anti hyperglycemic agent (not hypo glycemic) In setting of IV contrast dye, infection, CRI, ETOH can cause life threatening metabolic acidosis
You are treating a 4yr old male with new onset diabetes and DKA when he suddenly becomes confused and agitated. What is the first step in addressing this change in patient condition? • A. Obtain a head CT • B. Intubate the patient • C. Restrict the patient’s intake of fluids • D. Administer mannitol
You are treating a 4yr old male with new onset diabetes and DKA when he suddenly becomes confused and agitated. What is the first step in addressing this change in patient condition? • A. Obtain a head CT • B. Intubate the patient • C. Restrict the patient’s intake of fluids • D. Administer mannitol
For children undergoing treatment for DKA, which of the following has been shown to be most strongly associated with the development of clinically significant cerebral edema? • A. Administration of an insulin bolus prior to a continuous drip • B. Degree of hyponatremia on presentation • C. Elevated BUN on presentation • D. Height of the serum glucose concentration on presentation • E. Known history of diabetes with a record of poor compliance
For children undergoing treatment for DKA, which of the following has been shown to be most strongly associated with the development of clinically significant cerebral edema? • A. Administration of an insulin bolus prior to a continuous drip • B. Degree of hyponatremia on presentation • C. Elevated BUN on presentation • D. Height of the serum glucose concentration on presentation • E. Known history of diabetes with a record of poor compliance
Pediatric DKA • Pediatric DKA suspects: • Polyuria, polydipsia, polyphagia - • Anorexia • Weight loss • “acetone” smell • Kussmal respirations • (vague) Abd pain • General Management: • 10-20 ml/kg IVF boluses • K+ supplements if <5.5mEq/dl and pt urinating • Regular insulin @ 0.1u/kg/hr for decline glucose 50-100/hr • Dextrose to IVF if BS <250 • Q 2hr electrolytes, Q 1 hr glucose evaluations
Feared Complication~ Cerebral Edema • Although most treatment of children with DKA is uneventful, approximately 1% will become critically ill from developing cerebral edema • Studies have shown mortality/ permanent neurologic damage in ~50% of these patients • Usu. age <5yo • Recent studies evidence: • 1) Rapid infusion rate/ osm concentrations are not causative • 2) Causative factors: High BUN @ presentation, Treatment with Bicarbonate, Cerebral Ischemia from severe acidosis or hypocarbia, Intubation w/ Hyperventilation <22 mm Hg Rx: ABCS, Mannitol, Head CT. No role for steroids.
Which one of the following statements regarding the treatment of hypoglycemia is true? • A. Hypoglycemia that occurs in alcoholics and the elderly generally does not improve with glucagon • B. Octreotide is the first –line treatment for hypoglycemia caused by sulfonylurea ingestion • C. Steroid administration should be considered for hypoglycemia thought to be associated with sepsis • D. Controlled hypoglycemia improves outcome in patients with significant closed head injury
Which one of the following statements regarding the treatment of hypoglycemia is true? • A. Hypoglycemia that occurs in alcoholics and the elderly generally does not improve with glucagon • B. Octreotide is the first –line treatment for hypoglycemia caused by sulfonylurea ingestion • C. Steroid administration should be considered for hypoglycemia thought to be associated with sepsis (adrenal insufficiency) • D. Controlled hypoglycemia improves outcome in patients with significant closed head injury
Hypoglycemia • Finger stick= 1st Cardiac/ resuscitation room intervention • Risks= ETOH use, elderly/ poor pos, DM therapies • *Metformin alone does not hypoglycemia • Management: • D50 -D5W infusion • **Complex carbohydrates • Special Rx Considerations: • Glucagon~ 1 mg IM/IV slower reaction than dextrose, and shorter lived **ELDERLY & ETOH ABUSERS have no glycogen stores, thus do not respond to glucagon • Octreotide~ Use it for persistent hypoglycemia with sulfonylurea Q6 dosing (50ug) x 24hrs… Thiamine with glucose, esp. in ETOH to prevent Wernike’s
Which of the following classes of medications is known to adversely affect glycemic control? • A. Anticonvulsants • B. Antihistamines • C. Antidepressants • D. Calcium Cannel Blockers
Which of the following classes of medications is known to adversely affect glycemic control? • A. Anticonvulsants AND Steroids, Sympathomimetics, Diuretics, Salicylates... • B. Antihistamines • C. Antidepressants • D. Calcium Cannel Blockers
A well known alcoholic patient presents to your ED with anorexia, vomiting, and abdominal pain. He does not have a “surgical abdomen”. He is found to have a blood glucose of 250 mg/dl and a wide anion gap metabolic acidosis. Which of the following is TRUE? • A. A negative urinary ketone test effectively rules out alcoholic or DKA • B. The patient should be aggressively hydrated with NS • C. The patient should be aggressively hydrated with D5NS • D. The patient should immediately receive a loading dose of insulin
A well known alcoholic patient presents to your ED with anorexia, vomiting, and abdominal pain. He does not have a “surgical abdomen”. He is found to have a blood glucose of 250 mg/dl and a wide anion gap metabolic acidosis. Which of the following is TRUE? • A. A negative urinary ketone test effectively rules out alcoholic or DKA (no, nitroprusside test misses BHB) • B. The patient should be aggressively hydrated with NS • C. The patient should be aggressively hydrated with D5NS • D. The patient should immediately receive a loading dose of insulin (no, insulin can be dangerous)
Alcoholic Ketoacidosis • Definition • Wide anion gap acidosis • Often associated with acute cessation of chronic ETOH abuse • Results from metabolism of ETOH with little glucose sources • Pathophysiology • Ingestion of large ETOH, relative starvation, volume depletion • ETOH metabolism ~(graph)~ • Glycogen stores depleted Anaerobic Metabolism • Stress • Low NAD Acetyl coA ketones • Ketones • **B- hydroxybutyrate >>>> Acetoacetate ***usu. found in u/a • Treatment:D5 NS, replace glucose & hydrate
Which of the following is a diagnostic criteria for hyperosmolar hyperglycemic non-ketotic syndrome? • A. Plasma glucose >250 mg/ dL • B. Arterial pH >7.25 • C. Serum bicarbonate >15 mEq/L • D. Anion gap>12
Which of the following is a diagnostic criteria for hyperosmolar hyperglycemic non-ketotic syndrome? • A. Plasma glucose >250 mg/ dL • B. Arterial pH >7.25 • C. Serum bicarbonate >15 mEq/L • D. Anion gap>12
Hyperosmolar Hyperglycemic State • Only ~10% present as coma • Definition • Serum Glucose >600, - Plasma Osmolality > 315 mOsm/kg • Serum Bicarbonate >15 - Arterial pH >7.3 • Serum ketones negative/ weakly positive [2nd to tissue hypo-perfusion /starvation] - Anion Gap <12 • Pathophysiology • Decreased insulin utilization - Impaired renal glucose excretion • Increased hepatic gluconeogenesis • Clinical Features • Usually: elderly, weak, fatigued, Acute on Chronic AMS (baseline dementia) • Treatment • Hydration, hydration, Hydration • Electrolyte corrections • Search & treatment of underlying stimulus
A 69y woman presents with R-sided hemi-paresis of 4 hour duration. She is aphasic and not following commands. She does not appear to recognize her family. Her daughter reports no PMH/ drug use. She has had productive cough x 1 week. Vital signs: BP 103/68, P 112, RR 26, O2 91% RA, Finger stick= high. Na= 138, K=3.6, Cl= 98, HCO3= 20, BUN= 56, Cr= 3.6, Glucose= 986. U/A= trace ketones, and >1000 glucose. The calculated serum osmolarity= • A. 250 mOsm/kg • B. 275 mOsm/kg • C. 300 mOsm/kg • D. 325 mOsm/kg • E. 350 mOsm/kg
A 69y woman presents with R-sided hemi-paresis of 4 hour duration. She is aphasic and not following commands. She does not appear to recognize her family. Her daughter reports no PMH/ drug use. She has had productive cough x 1 week. Vital signs: BP 103/68, P 112, RR 26, O2 91% RA, Finger stick= high. Na= 138, K=3.6, Cl= 98, HCO3= 20, BUN= 56, Cr= 3.6, Glucose= 986. U/A= trace ketones, and >1000 glucose. The calculated serum osmolarity= • A. 250 mOsm/kg • B. 275 mOsm/kg • C. 300 mOsm/kg • D. 325 mOsm/kg • E. 350 mOsm/kg
Hyperosmolar Hyperglycemic State • Calculating Osmolarity: = 2 (serum Na) + (Blood Glucose)/ 18 + (BUN/2.8) = 2 (138) + (986/18) + (56/2.8) = 276 + 54 + 20 = 350 mOsm/ kg water
A 68y M with a PMHx of DM, HTN, presents with cellulitis following a cat scratch. He has noticed bilateral progressive leg edema for several weeks. No N/V/D, SOB, c/p, h/a. VS= BP 165/89, P 78, R 18, T 38.5. PE reveals obese male with erythema, swelling warmth R upper ext and lymphangitis. Labs= NA 125 mEq/L, K 4.5 mEq/L, Cl 95 mEq/L, HCO3 24 mEq/L, BUN 18 mg/dL, Cr 1.4 mg/dL, glu 135 mg/dL. In addition to IV antibiotics initial management includes: • A. Dexamethasone 8 mg IV • B. Hypertonic Saline 400 ml • C. Normal Saline 1,300 ml • D. Saline 0.45% 400 ml • E. Water restriction
A 68y M with a PMHx of DM, HTN, presents with cellulitis following a cat scratch. He has noticed bilateral progressive leg edema for several weeks. No N/V/D, SOB, c/p, h/a. VS= BP 165/89, P 78, R 18, T 38.5. PE reveals obese male with erythema, swelling warmth R upper ext and lymphangitis. Labs= NA 125 mEq/L, K 4.5 mEq/L, Cl 95 mEq/L, HCO3 24 mEq/L, BUN 18 mg/dL, Cr 1.4 mg/dL, glu 135 mg/dL. In addition to IV antibiotics initial management includes: • A. Dexamethasone 8 mg IV • B. Hypertonic Saline 400 ml • C. Normal Saline 1,300 ml • D. Saline 0.45% 400 ml • E. Water restriction
Hyponatremia • Definition: Na < 135 mEq/L • H2O gain ~vs.~ Na loss • Symptoms related to rate of Na change confusion, lethargy, N/V, muscle cramps, seizures, coma • Pathophysiology: • As serum Na decreases, osmotic gradient of BBB H2O into brain • Types • Hypertonic Hyponatremia (Plasma osm >295) * esp. Hyperglycemia • Rx= NS • Isotonic Hyponatremia(Plasma osm 275-295)*Hyper-proteins/lipids • Rx= nothing
*Hypotonic Hyponatremia*(Plasma osm <275) • Hypovolemic: Diuretic use/ volume replacement using hypotonic IVF Urine Na <20. Rx= NS • Euvolemic: SIADH, H2O Intoxication, Hypothyroidism Urine Na>20. Rx= Fluid restriction & correction of cause… • Hypervolemic: CHF, Nephotic syndrome, Cirrhosis Urine Na >20. Rx= Fluid restriction & correction of cause… • Na Deficit= ([Desired Na]- [Actual Na]) x TBW • Complications of Therapy • OSMOTIC DEMYLINATION SYNDROME or CENTRAL PONTINE MYELINOLYSIS (CPM) • CNS disturbances: AMS, Dysarthria, Dysphagia, Pseudobulbar palsy, Quadriparesis (transient/ permanent) • Symptoms related to rate of NA correction • In Chronic Hyponatremia correct no faster than • 0.5 mEq/L per hour (12 mEq/ L per day)
A 54 y woman with known Graves disease presents with delirium, dyspnea, and fecal soiling. Vital signs: BP 168/65, P 134, RR 35, T 38.9, O2 91% RA. An EKG reveals atrial fibrillation without evidence of ischemia. In addition to supportive care the most appropriate treatment order is: • A. Dexamethasone, iodine, propylthiouracil, propranolol • B. Propranolol, iodine, dexamethasone, propylthiouracil • C. Propranolol, iodine, propylthiouracil, hydrocortisone • D. Propranolol, propylthiouracil, dexamethasone, cefotaxime • E. Propranolol, propylthiouracil, iodine, dexamethasone
A 54 y woman with known Graves disease presents with delirium, dyspnea, and fecal soiling. Vital signs: BP 168/65, P 134, RR 35, T 38.9, O2 91% RA. An EKG reveals atrial fibrillation without evidence of ischemia. In addition to supportive care the most appropriate treatment order is: • A. Dexamethasone, iodine, propylthiouracil, propranolol • B. Propranolol, iodine, dexamethasone, propylthiouracil • C. Propranolol, iodine, propylthiouracil, hydrocortisone • D. Propranolol, propylthiouracil, dexamethasone, cefotaxime • E. Propranolol, propylthiouracil, iodine, dexamethasone
Thyroid Storm • Life Threatening hyper-metabolic state • Etiology • 25% unknown • Surgery, DKA, MI, Iodine, Trauma, CVA, Sepsis… • Symptoms • Fever, Tachycardia, CNS dysfunction Agitation, Delirium, Seizure, Coma • Treatment • ABCs • 1) Prevent Peripheral Effects [PROPANOLOL and slows T4 to T3] • *ESMOLOL if asthmatic • 2) Decrease de novo Synthesis [PTU and inhibits T4 to T3] • 3) Prevent Release of Hormone [IODINE or Lithium] • 4) Other considerations… Glucocorticoids prevent adrenal insufficiency, Cooling Blanket, Tylenol
An 86y woman presents with a 6 month history of fatigue and lethargy, confusion, constipation, poor appetite, slowed speech, and dyspnea. Vital signs: BP 105/60, P 55, T 33.5, O2 91% RA. Physical exam= lethargic, obese woman oriented to person & place only. She has evidence of bilateral pleural effusions and non-pitting edema. Potential iatrogenic causes of this condition include: • A. Amiodarone • B. Digoxin • C. Diltiazem • D. Flecainide • E. Procanimide
An 86y woman presents with a 6 month history of fatigue and lethargy, confusion, constipation, poor appetite, slowed speech, and dyspnea. Vital signs: BP 105/60, P 55, T 33.5, O2 91% RA. Physical exam= lethargic, obese woman oriented to person & place only. She has evidence of bilateral pleural effusions and non-pitting edema. Potential iatrogenic causes of this condition include: • A. Amiodarone • B. Digoxin • C. Diltiazem • D. Flecainide • E. Procanimide
Which of the following is an EKG change consistent with myxedema coma? • A. Prolongation of QT interval • B. Premature ventricular contractions • C. Premature atrial contractions • D. Left ventricular hypertrophy
Which of the following is an EKG change consistent with myxedema coma? • A. Prolongation of QT interval AND Sinus Bradycardia, low voltage with flattening of t-waves • B. Premature ventricular contractions • C. Premature atrial contractions • D. Left ventricular hypertrophy
Hypothyroidism & Myxedma Coma • Etiologies of Hypothyroidism~ • Hashimoto thyroiditis, Post-Partum thyroiditis [3-6mos post delivery], Pituitary/ Hypothalamic disease, • Medications [*AMIODARONE 1-30% users, Lithium via iodine release] • Myxedma Coma =Life threatening decompensation of pre-existing hypothyroidism • Findings: Hypothermia, Bradycardia, Hypoventilation, Hypo Na, Hypoglycemia, AMS, Non-pitting edema, Peri-orbital edema… • Treatment: • ABCs • Supportive Therapy • Thyroid replacement with Levothyroxine IV • Glucocorticoids to prevent adrenal insufficiency • Electrolyte replacements
Which of the following is the most common infectious cause worldwide of primary adrenal insufficiency? • A. Human Immunodeficiency Virus • B. Cytomegalovirus • C. Tuberculosis • D. Pseudomonas organisms
Which of the following is the most common infectious cause worldwide of primary adrenal insufficiency? • A. Human Immunodeficiency Virus * in USA • B. Cytomegalovirus • C. Tuberculosis • D. Pseudomonas organisms
Adrenal Insufficiency • During periods of stress [trauma/ burns/ sepsis] body should increase steroid production 5-10x in minutes. Failure to do so, esp. Glucocorticoids, ADRENAL CRISIS • Electrolyte Changes: [Low NA, High K, Low Glucose] • Adrenal Crisis: • 1st manifestation= Hypotension • Dx:We don’t do cortisol stimulation testing… • Rx: Dexamethasone will not interfere with their stimulation testing… • Don’t forget Dexamethasone in our EGDT protocol • Also Don’t forget: Waterhouse-Friderichsen syndrome, hemorrhage/ thrombosis of adrenals/ DIC; or Sheehan syndrome, post-partum pituitary hemorrhage
In the treatment of hyperkalemia induced cardiac arrest, which of the following treatment modalities provides the most rapid reduction in serum potassium levels? • A. Calcium gluconate • B. Insulin • C. Magnesium Sulfate • D. Sodium Bicarbonate • E. Sodium Polystrene Solfonate
In the treatment of hyperkalemia induced cardiac arrest, which of the following treatment modalities provides the most rapid reduction in serum potassium levels? • A. Calcium gluconate [No, Stabilizes cardiac membrane, but does not change serum K+ levels] • B. Insulin [onset 20-30 min., lowers 1 mEq/L in 1-2 hrs] • C. Magnesium Sulfate • D. Sodium Bicarbonate ~ onset 5-10 minutes, lasts 2 hrs • E. Sodium Polystrene Solfonate [onset >2hrs] • **(F.) Albuterol nebulizer = same onset as sodium bicarbonate
Hyperkalemia • We know it! We love it! • Goals of Therapy: • 1) Membrane Stabilization • 2) Shift K+ into cells • 3) Remove K+ from body • Buyer Beware! • Digitalis toxicity, as Ca+ may potentiate cardiac toxicity!