Endocrine Board Review

Raghu Seethala MD

1/7/2009

Endocrine

• 10/410 questions from PEER VII (2.5%)

• Some overlap with Renal and Fluids and Electrolytes

Question 1A 68 year old man with COPD presents with hypotension, abdominal pain, and confusion. He was recently discharged from another hospital with his long-term prednisone prescription and a new prescription for azithromycin, but he admits he did not have them filled. Vital signs are blood pressure 89/48, HR 110, RR 24, and temp. 37.5C. Lab test results are serum sodium 125 meq/L, potassium 6.3 meq/L, and glucose 55 mg/dL. In addition to fluid resuscitation and glucose replacement, immediate management should include:

A. Abdominal CT scan and surgical consultation

B. ACTH 0.25mg IVThe pt needs stress dose steroids not ACTH stim test

C. Fludrocortisone 0.1 mg IVThis is a mineralocrticoid, you need to replace with a glucocorticoid

D. Hydrocortisone 100 mg IV

E. Surgical consultation and laparotomy

Adrenal pituitary axis

Adrenal Insufficiency and Adrenal Crisis

• Primary adrenal insufficiency– Addison’s disease, TB, HIV, infiltrative disease,

hemorrhage• Secondary adrenal insufficiency

– Most common cause exogenous steroid therapy– Infiltrative disease, tumour, head trauma,

• Clinical presentation– Abdominal pain,nausea, vomiting, fatigue,

hypotension, hyponatremia, hyperkalemia, hypoglycemia

• Dx: ACTH stimulation test– Dexamethasone will not interfere

Adrenal Insufficiency and Adrenal Crisis

• Adrenal Crisis– Life threatening emergency, primary

manifestation is hypotension non-responsive to fluids and catecholamines

– Coagulopathies, Sepsis, (Waterhouse-Friderichsen Syndrome), catastrophic failure of HPA axis (head trauma, hemorrhage of pit. tumour, Sheehan syndrome)

– Tx: 100 mg hydrocortisone IV

Question 2

A 54 year old woman with known Graves disease presents with delirium, dyspnea, and fecal soiling. Vital signs are BP 168/65, HR 134, RR 35, T 38.9C, O2 sat 91 % on RA. ECG reveals atrial fibrillation without evidence of ischemia. In addition to general supportive care, the most appropriate treatment order is:

A. Dexamethasone, iodine, propylthiouracil, propranololB. Propranolol, iodine, dexamethasone, propylthiouracilC. Propanolol, iodine, propylthiouracil, hydrocortisoneD. Propanolol, propylthiouracil, dexamethasone, cefotaximeE. Propanolol, propylthiouracil, iodine, dexamethasone

Thyroid pituitary axis

Hyperthyroidism

• 10 times more common in women• Most common cause from Grave’s disease• Symptoms – nervousness, sweating, hyperdefecation,

dyspnea, weight loss• Signs – lid lag, tremor, tachycardia, systolic

hypertension, widened pulse pressure, fever, hyperreflexia

• EKG - Afib• Dx: low TSH, high T4, if T4 normal check T3• Apathetic hyperthyroidism – in 7th – 8th decades of life

characteristic symptoms are absent, slowed mentation, apathetic facies

Thyroid Storm• Thyroid storm – life threatening manifestation of

thyrotoxicosis• Fever, tachycardia, CNS dysfunction agitation, delirium,

seizure, coma• Precipitants – unknown 25%, infection, trauma, DKA, MI,

PE, surgery • Treatment – 5 goals, in the following order

– General supportive care (ABC’s)– Block peripheral effects of hormone (propanolol)– Block synthesis of hormone (PTU, methimazole)– Block release of hormone (iodine, lithium)– Block peripheral conversion of T4 to T3 (dexamethasone)

• 1. propanolol 2. PTU 3. iodine 4. dexamethasone• Prognosis

– Untreated 100% mortality– Treated 10% – 20% mortality

Question 3An 86 year-old woman presents with a 6 month history of fatigue and lethargy, increasing confusion, constipation, poor appetite, slowed speech, and dyspnea. Vital signs include BP 105/60, HR 55, T 33.5C, O2 sat 91% on RA. Physical examination reveals a lethargic, obese woman who is oriented to place and person. She has evidence of bilateral pleural effusions and has nonpitting peripheral edema. Potential iatrogenic causes of this condition include:

A. Amiodarone

B. Digoxin

C. Diltiazem

D. Flecainide

E. Procainamide

Hypothyroidism

• 5 – 10 times more common in women• Etiology – most common autoimmune (Hashimoto’s

thyroiditis), iatrogenic s/p surgery or RAI ablation, drugs – amiodarone, lithium, secondary (pituitary problem), tertiary (hypothalmus problem)

• Symptoms – fatigue, weight loss, cold intolerance, depression constipation

• Signs – hypothermia, bradycardia, cool rough dry skin, non-pitting edema, periorbital puffiness, goiter, effusions

• Dx: elevated TSH, low T4, T4 can be normal early on

Myxedema Coma• Life threatening state• Etiology – infection, cold exposure, drugs, inadequate

thyroid replacement• Altered mental status, hypothermia, bradycardia,

hypoventilation, cardiovascular collapse• Hypoventilation, hypercapnia, hyponatremia,

hypoglycemia• EKG – bradycardia, prolonged QT• Tx:

– General support (ABC’s)– Thyroid replacement drugs: IV T4 (thyroxine), AVOID IV T3

because can cause ventricular arrhythmias– Correct metabolic abnormalities (hypoventilation, hyponatremia,

hypoglycemia)– Stress dose of steroids (may also have hypoadrenalism)– Find precipitating factor

Amiodarone induced Thyroid disease

• Amiodarone is an iodine-rich benzofuran derivative. Approximately 37% of amiodarone (by weight) is organic iodine; 10% of the latter is deiodinated to yield free iodine.

• Can cause either thyrotoxicosis or hypothyroidism• Incidence of thyrotoxicosis has been reported to be 1%

to 23%• Incidence hypothyroidism has been reported to be 1% to

32% • Amiodarone-induced thyrotoxicosis prevails in areas with

low iodine intake, and hypothyroidism is prevalent in areas with high iodine intake.

Question 4A 17 year old boy with Type I diabetes mellitus presents with diabetic ketoacidosis. A venous blood gas analysis is conducted, and the pH is 7.09. Treating this patient with bicarbonate could result in which of the following complications:

A. CSF alkalosiscauses CSF acidosis

B. Hypokalemia

C. Hypotonicitycauses hypertonicity

D. Increased work of breathingtheoretically can decrease work of breathing

E. Rightward shift of the oxyhemoglobin dissociation curvecauses leftward shift of the curve

DKA• Pathophysiology – lack of insulin -> hyperglycemia ->

osmotic diuresis -> severe dehydration/shock, ketoacidosis because can’t metabolize glucose

• Dx: blood glucose >250 mg/dl, arterial pH <7.3, bicarbonate <15 mEq/l, and moderate ketonuria or ketonemia

• Precipitant – ANY stressor, infection, not taking insulin, MI, pregnancy

• Signs and Symptoms – Kussmaul’s respiration, abd. pain, nausea, vomiting, fruity acetone odor

• Electrolyte disturbances– Sodium – Falsely decreased. Standard teaching 1.6 meq added

for every 100 mg of glucose over 100mg/dl. New teaching 2.4 meq esp. for glucose over 400mg/dl.

– Potassium – usually present with profound total body potassium deficit. Serum potassium may be low, normal, or high.

– Phosphate – hypophosphatemia most severe 24 – 48 hr after tx

DKA• Tx: IVF, insulin, potassium repletion, when glucose

below 250 switch to D5 ½ NS, potassium repletion• Should check K+ prior to instituting insulin therapy, have

been reports of fatal arrhythmia from instituting insulin therapy in K+ < 3.3 meq

• Bicarbonate therapy– Use is controversial recommendations vary in usage from pH

<7.1 - <6.8– Complications

• Shifts O2- Hb curve to left• CSF acidosis • Hypokalemia• Hypertonicity and sodium overload

• DKA in pregnancy– Triggered at lower glucose levels

Question 5For 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 complianceMany of the cases are in new onset diabetics under the age of 5

Pediatric DKA

• No insulin bolus• Feared complication CEREBRAL EDEMA!!!

– Rare occurring in 1% of pediatric DKA– Mortality 40% – 90%– Clinical features – severe headache, change in MS, seizures– Old theory – excessive rate of IVF infusion led to brain swelling

because of idiogenic brain osmoles– Recent work suggests that it is a vasogenic process not an

osmotic process– Factors related to development of cerebral edema

• Low arterial pCO2 on presentation• High BUN on presentation• Treatment with bicarbonate• Intubation with hyperventilation to pCO2 < 22 mm Hg

– Tx: Mannitol, ABC’s, Head CT, no role for steroids

Question 6A 69 year old women presents with right sided hemiparesis of 4 hours duration. She is aphasic and not following commands. She does not appear to recognize her family. Her daughter reports no prior medical history and no medications or over-the-counter drug use. She has had a productive cough for 1 week. Vital signs include blood pressure 103/68, HR 112, RR 26, O2 sat 91% RA. Fingerstick blood glucose level is high; laboratory test results are as follows: sodium, 138 meq/L; potassium 4.5 meq/L; chlorine, 98 meq/L, HCO3, 20 meq/L, BUN, 56 mg/dL, creatinine, 3.6 mg/dL and blood glucose, 986 mg/dL. UA reveals trace ketones and greater than 1,000 mg/dL of glucose. The patient’s calculated serum osmolarity is:

A. 250 mosm/kgB. 275 mosm/kgC. 300 mosm/kgD. 325 mosm/kgE. 350 mosm/kg

HyperosmolarHyperglycemic State (HHS)

• Used to be known as HHNC but only 10% present in coma

• Rarer than DKA but mortality rate much higher• Dx: glucose > 600, pH > 7.3, bicarb >15, serum

osm > 320, small urine and serum ketones• Clinical features – typically elderly patient with

poor access to water, signs of volume depletion, altered mental status, CNS symptoms, hemiparesis, hemisensory defects, seizures

• Tx: IVF, IVF, IVF, insulin, electrolyte correction, search for precipitant

• Serum Osmolality– 2 (Na) + Blood Glucose/18 + BUN /2.8

Question 7

In an awake patient with uncomplicated hypoglycemia, which of the following will provide a sustained improvement in serum glucose level?A. 50 mL D50WB. AppleC. Cheese and turkey sandwichD. Chocolate barE. Orange juice

Hypoglycemia• Etiology: insulin, oral hypoglycemics, sepsis, etoh

intoxication, toxic ingestions, liver failure • Clinical features – Wide array of symptoms

– Neuroglycopenic – glucose is main energy source for CNS function -> altered MS, lethargy, confusion, agitation, unresponsiveness, seizure, focal neuro defecit

– Hyperepinephremic – decreased glucose causes release of catecholamines and some cholinergic activity -> anxiety, nervousness, nausea, vomiting, palpitations, tremor, sweating

• Dx: finger stick!• Tx:

– Initial 1 g/kg dextrose, 1 amp (50g) D50W = 25g dextrose– Oral replacement therapy provides most sustained treatment for

hypoglycemia if able to tolerate po, Tintinalli recommends 300g of carbs in a meal containing complex carbs, fat, protein.

– Glucagon can be used in individuals with no IV access, works via stimulating hepatic gluconeogenesis through glycogenolysis

• Glucagon wont work in alcoholics, elderly or other individuals with depleted glycogen stores

Hypoglycemia

• Administer thiamine in your alcoholics to avoid Wernicke’s encephalopathy

• Insulin in the body made as proinsulin then cleaved into insulin and c-peptide– Insulinoma – elevated c-peptide– Exogenous insulin overdose – decreased c-

peptide level

Question 8

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

Oral hypoglycemics• Sulfonylurea – increases insulin secretion

– Causes hypoglycemia– In overdose use octreotide after initial glucose therapy to reduce

recurrence of hypoglycemia• Biguanides (Metformin) – decreases hepatic production

– No hypoglycemia– Contraindicated in renal failure pt, can develop fatal metabolic

acidosis• Nonsulfonylurea secretagogues (Prandin) – increases

insulin secretion – Causes hypoglycemia

• Thiazolidinediones (-glitazones, Actos) – increases peripheral tissue glucose use– No hypoglycemia

• Alpha-Glucosidase inhibitors – decreased GI tract absorption of glucose– No hypoglycemia

Question 9

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?

Unknown Indian Male

A. A negative urine ketone test effectively rules out alcoholic or DKA

Urine nitroprusside test only tests for acetoacetate, will miss ketones in the B-hydroxybutyrate form

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

Can be dangerous, because they have low glucose, and depleted glycogen stores

Alcoholic Ketoacidosis• An acute metabolic acidosis that typically occurs in

people who chronically abuse alcohol and have a recent history of binge drinking, little or no food intake, and persistent vomiting.

• Labs – High anion gap– Ketones

• Acetoacetate and B-hydroxybutyrate are elevated, initially mostly in B-hydroxybutyrate

• Urine nitroprusside test only tests for acetoacetate, so can be negative in 15% of AKA

– pH maybe low, normal, or high– Blood glucose low to mildly elevated– Etoh usually negative

• Clinical features – nausea, vomiting, diffuse abdominal pain

Alcoholic Ketoacidosis

EMCrit.org

Alcoholic Ketoacidosis

• Treatment– Administer D5 NS

• Crystalloid restores volume• Glucose stimulates insulin release which inhibits

ketosis

– Electrolyte repletion– Thiamine administration prevent Wernicke’s

Question 10

A 52 year-old woman presents complaining of generalized fatigue and weakness for the past week. She admits to a 40-pack-year history of smoking and occasional alcohol use. Over the past several weeks she has noticed that her clothes have become loose fitting and that she has lost 20lb. PE is unremarkable except for an intermittent, hacking cough. A chest radiograph demonstrates a mediastinal mass, and serum electrolytes are as follows: sodium, 116 mEq/L; potassium, 4.7 mEq/L; chloride, 90 mEw/L; bicarbonate, 18 mEq/L; BUN, 10 mEq/L; and creatine, 0.6 mEq/L. What is this the most appropriate initial management?

A. DemeclocyclineShould be reserved for pt’s with chronic SIADH in whom water restriction has failed

B. Fluid restriction

C. Hospital admission

D. Hypertonic salineShould be reserved for severe hyponatremia with seizing or significant altered mental

status

E. Intravenous furosemide

SIADH

• The body is producing too much ADH• Etiology

– CNS – tumor, trauma, infection– Lung – tumor, infection, PE– Drugs

• Clinical features – anorexia, nausea, vomiting, headache, irritability, weakness

• Lab – hyponatremia, hypotonicity, elevated urine sodium, concentrated urine

• Tx: Fluid restriction, demeclocylcine

Question 11

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 Should be reserved for severe hyponatremia with seizing or coma

C. Normal Saline 1,300 ml Pt is not dehydrated does not require aggressive fluid tx

D. Saline 0.45% 400 ml Pt is hyponatremic, this would worsen the condition

E. Water restriction

Question 12

A 36-year-old man is transferred to the emergency department from a psychiatric facility following a witnessed seizure. He previously had been observed drinking large amounts of water. In the emergency department, he is somnolent but arousable to voice, with normal vital signs. Laboratory results are sodium, 106 mEq/L; potassium, 3.5mEq/L; chlorine; 94 mEq/L; bicarbonate, 22 mEq/L; BUN, 4; creatinine 0.5; and glucose, 90. The patient weighs approximately 70kg. Shortly after lab tests return, he has a generalized tonic-clonic seizure that does not resolve with lorazepam 2 mg IV. The next therapeutic intervention should be:

A. Benzotropine 2 mg IVTreatment for dystonic reaction, no role in hyponatremia

B. Hypertonic saline 400 mL

C. Normal saline 1300 mLRequires aggressive tx because of seizures

D. Phenytoin 1000 mg IVSeizures from hyponatremia do not respond to normal anticonvulsants

E. Sodium bicarbonate 100 mEqNot indicated, can worsen by causing intracellular acidosis, hypokalemia

Hyponatremia

• Hypertonic (P osm > 295) - hyperglycemia• Isotonic (P osm 275 – 295) – hyperlipidemia,

hyperproteinemia• Hypotonic (P osm <275)

– Hypovolemic – Diuretics, volume replacement using hypotonic IVF, GI loss, sweating

• Tx: Correction of dehydration– Euvolemic – SIADH, hypothyroidism, drugs,

psychogenic polydypsia • Tx: Water restriction and underlying condition

– Hypervolemic – renal failure, CHF, nephrotic syndrome, liver failure

• Tx: water restriction and underlying condition

Hyponatremia

• Treatment of severe hyponatremia– Hypertonic saline for seizures or coma– Rise in sodium should not exceed 2 mEq/L per hour– Formulas

• Required Volume = (Na Desired – Na Current)(Total Body Water) (Na Fluid – Na Current)

• Total Sodium Deficit – (Na Desired – Na Actual)(TBW)

– In chronic hyponatremia correct no faster than 0.5 mEq/L per hour

• Complications – from correcting Na too fast– OSMOTIC DEMYLINATION SYNDROME or CENTRAL PONTINE

MYELINOLYSIS (CPM) • CNS disturbances: AMS, Dysarthria, Dysphagia, Pseudobulbar palsy,

Quadriparesis (transient/ permanent)

THE END