Endocrine Board Review

Marlaina NorrisReview 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?

• 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 concentrationsHyperglycemia decreases uterine blood flow/ fetal O2Hypokalemia 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 sulfonylureaQ6 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 IVFUrine Na <20. Rx= NS• Euvolemic: SIADH, H2O Intoxication, HypothyroidismUrine Na>20. Rx= Fluid restriction & correction of cause… • Hypervolemic: CHF, Nephotic syndrome, CirrhosisUrine 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 ANDSinus 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!