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Endocrine / Electrolyte / Acid Base

Hypoglycemia (1)
? Glucose is the sole energy source for the brain
? Symptoms of hypoglycemia depend on the
glucose level and the rate of glucose drop
? Hypoglycemia can mimic stroke,TIA, epilepsy,
MS, psychosis, Stokes-Adams
? Counterregulatory hormones (glucagon and
epinephrine) cause the release of glycogen
from the liver

Hypoglycemia (2)
? Sympathomimetic symptoms: sweating, tremor,
pal or (vasoconstriction), anxiety, nausea
? Sympathomimetic symptoms can be masked by
beta blockers
? Neuroglycopenia symptoms: dizziness,
psychosis, confusion, coma
Always consider hypoglycemia in an
unresponsive patient ? check a rapid
blood glucose level

Hypoglycemia (3)
? Differential diagnosis
?Medications / drugs / alcohol
?Extrapancreatic neoplasm
?Hepatic disease (depletion of glycogen stores)
?Deficiency of counterregulatory hormones
?Critical y il , stressed infants, hypothermia
?Dumping syndrome
? Artifactual
?Continued glycolysis by WBCs in lab tube
?Leukemia, polycythemia

Hypoglycemia (4)
? Distinguishing excess endogenous insulin from
excess exogenous insulin
?Pancreas cleaves proinsulin to insulin plus
immunoreactive C-peptide
?Excess endogenous insulin has measurable
C-peptide (not so with excess exogenous

Hypoglycemia (5)
? Standard treatment options
?D25 (peds)
?D10 (neonates)
?Glucagon 1 mg IM/IV (converts liver glycogen to
?D10 drip if recurrent or overdose
?Hydrocortisone (adrenal insufficiency)
?Octreotide ? inhibits insulin secretion and
helps prevent rebound hypoglycemia in the setting
of glucose infusion treatment of refractory
sulfonylurea-induced hypoglycemia

Oral Agents In Diabetes Treatment (1)
? Two classes: hypoglycemics & antihyperglycemics
? Hypoglycemic agents:
Sulfonylurea agents
?Chlorpropamide, tolbutamide, acetohexamide
tolazamide, glipizide, glyburide, glimepiride
?Stimulate pancreatic insulin secretion
?Cause profound hypoglycemia in overdose
?Long duration of action
?Chlorpropamide also can cause SIADH
Repaglinide (Prandin)
?Can also cause hypoglycemia

Oral Agents In Diabetes Treatment (2)
? Antihyperglycemic agents
? Less likely to cause hypoglycemia in overdose
?Rarely causes lactic acidosis
Alpha-glucosidase inhibitors
?Inhibit intestinal hydrolysis of polysacharides
?Oral sucrose wil not be absorbed
Thiazolodenediones (Avandia/Actos)
?Limited overdose experience
?Can worsen CHF
?Other side effects

Hypoglycemia Pearls
? Always admit if sulfonylurea overdose
? Most symptomatic in 4 hours (can be delayed)
? Octreotide inhibits insulin secretion
? Give thiamine with glucose in hypoglycemic
malnourished patients
? Glucagon may not be effective in chronic
alcoholics, those with liver disease or infants
with low, liver glycogen stores

Diabetic Ketoacidosis Pathophysiology
? Relative lack of insulin + stressors causes
? Hyperglycemia-induced osmotic diuresis
causes polyuria, dehydration, hypovolemia,
electrolyte loss (K, Mg, Phos)
? Switch over to fat breakdown for energy
source causes ketonemia (acidosis)
? Metabolic acidosis causes compensatory
hyperventilation (Kussmaul respirations)

Precipitants of DKA
? The "I's" have it!
?Infection (UTI, pneumonia, pancreatitis)
?Infarction (e.g. AMI)
?Infraction (noncompliance)
?IUP (pregnancy)
?Ischemia (CVA)
?Il egal (substance abuse)
?Iatrogenic (drug interactions)
?Idiopathic (new onset DM)

Fluids / Bicarbonate in DKA
? Initial fluid resuscitation for hypovolemia
? Replace electrolytes (phosphate, potassium)
? Insulin drip (after checking potassium)
? Sodium bicarbonate is rarely indicated
? The hazards of bicarbonate use include
? Paradoxical CSF acidosis
? Decreased oxygen-hemoglobin dissociation (shifts
curve to left)
? Overload of sodium
? Hypokalemia, hypophosphatemia
? Cerebral edema in children

Sodium / Phosphate in DKA
? Pseudohyponatremia
(*Hyperosmolar as opposed to hypoosmolar state)
?Sodium is artifactual y 1.6 mEq/L for every 100 mg/
dL glucose over 100
Hypophosphatemia is possible:
Respiratory depression, muscle
CHF, decreased mental status
(failure to generate adequate ATP)

Potassium in DKA
? Serum K+ level may be elevated, normal or low
? Initial hypokalemia indicates massive total body
depletion (usual deficit is 3-7 mEq/L)
? Replacement recommendations
? K < 3.3: Hold insulin, give 40 mEq per hour until 3.3
? K 3.3 but < 5.0: give 20-30 mEq in each liter IVF to
keep K 4-5 mEq/L
? K 5.0: No replacement but check Q2 hr
? Serum potassium will decline with insulin
and correction of acidosis (drives K+ into cel s)
? Cardiac arrest in DKA is often 2? to precipitous
hypokalemia (insulin therapy, acidosis correction
or fluid therapy with increased urinary losses) 14

Complications of DKA Treatment
? Hypoglycemia due to excess insulin
?Add glucose administration when
glucose = 250 mg/dl
? Hypokalemia is associated with insulin
administration, bicarbonate, hydration
? Bicarbonate therapy causes CSF acidosis
? Cerebral edema
? Patients at risk: Young, new onset DM
?Controversial: Possibly 20 to over-hydration,
rapid osmotic changes, hypoxemia, sodium

Alcoholic Ketoacidosis (1)
? Binge drinking with heavy alcohol
consumption and decreased food intake
for several days (starvation ketosis)
? Imbalance of insulin levels and counter-
regulatory hormones
? Ethanol metabolism inhibits
? Abdominal pain, nausea, vomiting,
dehydration, disorientation

Alcoholic Ketoacidosis (2)
? Alcohol levels are usual y low or negative and
glucose is often mildly elevated with low
bicarbonate and high anion gap
? Urinary ketones may be weakly positive
? Treatment: Glucose + saline (D5NS), thiamine
and potassium repletion
The major and earliest ketone produced from fat
breakdown is beta-hydroxybutyrate, but the
lab-measured ketone is acetoacetate.
Therefore, lab tests for
ketones may be falsely negative.

Hyperosmolar Hyperglycemic
Non-ketotic State HHNS (1)
? Similar to DKA but has ? Precipitating factors
important distinctions
?No ketoacidosis
?Infection, especial y
?Glucose is usual y
higher, often >1000
?Myocardial infarction
?Serum osmolality is
often greater than 350
?GI bleed
?Most often occurs with
?Higher mortality than
?Subdural hematoma
?DKA has shorter onset
?Peripheral vascular

Hyperosmolar Hyperglycemic
Non-ketotic State HHNS (2)
? Common comorbid ? Common associated
?Renal insufficiency
?Vascular disease
?Poor access to water ?Corticosteroids
?Calcium channel
is often
the initial
presentation of

Hyperosmolar Hyperglycemic
Non-ketotic State HHNS (3)
Physical findings
Normal saline
? Average fluid deficit 8-12
? Altered sensorium
? Focal neurologic
? ? of deficit in first 12
findings (often
hours, rest over next 24
mistaken for a
? Initial 1-2 liter bolus as
clinical y indicated
? Coma is rare
? Insulin infusion (usual y
lower doses than in DKA)
Cerebral edema possibly 2? to rapid fluid
replacement or the severity of the condition

Thyroid Hormones
? TRH from hypothalamus stimulates TSH release
from anterior pituitary
? TSH stimulates thyroid gland
?Thyroid hormones (T3, [20%]T4 [80%]) are
synthesized and released
?Thyroid hormone production depends on iodine
intake. Excess iodine blocks hormone release
? T is biological y 4x more active than T
? T and T
4 provide feedback inhibition of TSH
? T and T
4 act on cel s
?Increase rate of cel metabolism
?Increase rate of protein synthesis

Hyperthyroidism (1)
? Causes
?Graves' disease (most common):
? An autoimmune disorder (thyroid-stimulating
immunoglobulins mimic the action of TSH)
?Toxic thyroid adenoma, toxic multi-nodular goiter
?Pituitary adenoma
?Excess iodine in diet

Hyperthyroidism (2)
? Signs and symptoms
?Nervousness, tremor, insomnia
?Heat intolerance, sweating
?Weakness, weight loss,
hair loss
?Tachycardia, palpitations
?Irregular menses
?Goiter / thyroid bruit
?Exopthalmos (Grave's only), lid lag (the lids
move more slowly than the eyes)

Hyperthyroidism (3)
Pre-tibial Myxedema
? Rare manifestation of
Graves' disease
? Bilateral, elevated, firm
dermal nodules and plaques
? Skin yel ow or waxy
? Accumulation of

Hyperthyroidism (4)
? Risk factors: female, family history, other
autoimmune disease
? Lab: Increased T3 and T4, decreased TSH
? Treatment
?Beta blockers
?Radioactive iodine

Thyroid Storm (1)
? A life-threatening complication of
hyperthyroidism. May not be directly related
to magnitude of excess thyroid hormone
? Precipitating events include
?Withdrawal of antithyroid medications
?Administration of IV contrast
?Thyroid hormone overdose
?Pulmonary embolus
?Toxemia of pregnancy

Thyroid Storm (2)
Thyroid storm is a clinical diagnosis
The hal mark is CNS dysfunction
? Other diagnostic criteria include
?Temperature > 38 ?C
?Tachycardia out of proportion to the fever
?Exaggerated peripheral manifestations of
thyrotoxicosis, including tremor and weakness
? No laboratory tests distinguish thyroid storm
from simple hyperthyroidism ? it is a clinical

Thyroid Storm (3)
? Thyrotoxicosis / thyroid storm is associated
?Elevated free T4 level
?Decreased TSH level
?Elevated LFTs
?Low cholesterol

Thyroid Storm Treatment
? Five step ORDERED approach
1. General supportive care: IV fluids, correct
electrolyte imbalance, corticosteroids (decrease
peripheral conversion of T4 to T3), no ASA
(displaces thyroid hormone from thyroglobulin)
2. Blockade of peripheral thyroid hormone effects:
Propranolol 1 mg to 10 mg titrated to symptoms
3. Blockade of thyroid hormone synthesis: PTU
(also inhibits peripheral conversion of T4 to T3)
4. Blockade of thyroid hormone release: iodine
given one hour after PTU
5. Identification and treatment of precipitating

Apathetic Thyrotoxicosis
? Rare disorder seen in elderly patients
? Lethargy, slowed mentation, apathetic facies
? Goiter is usual y present
? Droopy eyelids are common
? No exophthalmos, stare or lid lag
? Symptoms of apathetic hyperthyroidism may be
masked because of underlying organ dysfunction
? Resting unexplained tachycardia
? Resistant atrial fibril ation and CHF are common

Hypothyroidism (1)
? Causes
?Treatment of Graves' disease
?Iodine deficiency in diet
?Autoimmune destruction of thyroid gland (e.g.
?Lithium therapy for bipolar disorder
?Pituitary and hypothalamic disorders (rare)

Hypothyroidism (2)
? Signs and symptoms
?Weakness, lethargy
?Cold intolerance
?Weight gain
?Dry, thick skin
?Generalized nonpitting edema (myxedema)
?Prolonged, heavy periods

Hypothyroidism (3)
? Clinical signs of severe hypothyroidism include
?Dermatologic: coarse, waxy skin, loss of lateral
third of eyebrows, scant pubic hair, puffy face
and extremities (myxedema)
?CNS: slowed mentation, altered
mental status, psychosis ("myxedema
madness"), coma
?Cardiac: CHF, bradycardia,
hypotension, cardiomegaly,
pericardial effusion, low voltage

Hypothyroidism (4)
? Lab
?Low T4, elevated TSH (unless problem with
hypothalamus or pituitary)
?Elevated lipids
?Hyponatremia (dilutional)
? Myxedema coma

Myxedema Coma (1)
? The end of the spectrum of hypothyroidism
? Life-threatening, rare, elderly females, winter
? Precipitating factors include
?Stressors: MI, infections, trauma, cold exposure
?Drugs are metabolized slower and therefore
have increased effects (narcotics, tranquilizers,
beta blockers, amiodarone)
?Non-compliance with thyroid replacement

Myxedema Coma (2)
? Signs
?"Hung up" reflexes (prolonged relaxation
phase of DTRs)
?Non-pitting periorbital edema
(puffy eyelids)
?Generalized non-pitting edema

Myxedema Coma (3)
? Treatment
?Supportive care: Rewarming, fluid support,
search for underlying cause
?Specific treatment
?IV thyroxine (T4). May require large doses
?IV T3 is not recommended (can cause V-tach)
?Corticosteroids (because of possible
unrecognized adrenal or pituitary insufficiency)

Adrenal Gland
? Clinical manifestations primarily due to
?Cortisol (affects metabolism of most tissues,
glucose regulation, increases blood glucose)
?Aldosterone (renal Na+ reabsorption & K+ excretion)
Sex hormones
Medul a

Adrenal Insufficiency (1)
Primary Adrenal Failure
? Idiopathic (autoimmu ne): Hyperpigmentation
Addison's Disease
is seen in
Infiltrative, infectious
Sarcoid, amyloid
?TB, fungal, septicemia
? Hemorrhage, infarction
? Neoplastic
? Drugs (etomidate)
? Bilateral adrenal failure is associated with
meningococcemia (Waterhouse-Friderichsen)
?Presents with abdominal pain, vomiting, fever,
? Diagnosis by serum cortisol level or corticotropin
stimulation test

Adrenal Insufficiency (2)
? Secondary adrenal fail ure
?Due to hypopituitarism
? Tertiary adrenal failure
?Usual y iatrogenic from prolonged steroid use (most
common cause overall)
?Causes adrenal atrophy
?Usual y due to oral steroids; rarely may be due to
inhaled or topical steroids
? Laboratory abnormalities include
?Hyponatremia (most common abnormality) +/-
hyperkalemia, eosinophilia (al most common in chronic
insufficiency), hypoglycemia
? Acute presentation
?Fever and refractory hypotension
?Consider in malignancy

Adrenal Crisis (Insufficiency)
? Treatment
?D5NS +/ - D50%
? Mortality from adrenal crisis due to
?Dysrhythmias (hyperkalemia)
?Underlying disease

Hyperadrenalism (Cushing's Syndrome)
? Excess cortisol
?Prolonged steroid use (most common)
?Adrenal neoplasm, pituitary microadenoma
?ACTH-secreting carcinoma (smal cel ,
pancreatic, bronchial carcinoid)
? Signs and Symptoms
?Truncal obesity, hypertension, hirsutism,
edema, glucosuria, Na+
?Moon facies, buffalo hump, purple striae
?Treatment: Stop steroids, treat cause

Syndrome of Inappropriate
Secretion of Antidiuretic Hormone
? Normal y, ADH is secreted in states of dehydration
?ADH increases renal H20 reabsorption
?ADH is inhibited in over-hydration (dilutes urine)
? SIADH: Inappropriate ADH secretion (inhibits urine
production resulting in fluid retention and dilutional
? Inappropriately concentrated urine in the setting
of low serum osmolality (low sodium) and
normovolemia = SIADH
? Causes include CNS (tumor, infection, CVA, injury),
Lung (infection including TB, fungal), Drugs
(chlorpropamide, vasopressin, diuretics, vincristine,
thioridazine, cyclophosphamide)

Diabetes Insipidus
? Symptoms similar to DM ? excess urination and
increased thirst and fluid intake
? Lack of ADH activity
?Central: Failure to secrete ADH (head trauma, neoplasm,
pituitary surgery)
?Nephrogenic: Kidney not responding to ADH (lithium
toxicity, hypokalemia, hypercalcemia, nephrotoxic drugs)
? Presents with polydipsia, polyuria
? Lab: Dilute urine in the face of concentrated serum
(hypernatremic and hyperosmolar)
? Central DI wil concentrate urine with ADH; nephrogenic
DI wil not respond
? Treatment
?Central = Desmopressin (synthetic vasopressin = DDAVP)
?Nephrogenic = Hydrochlorothiazide

? Rare cause of treatable hypertension
? Often diagnosed at autopsy
? Can be malignant
? Tumor of adrenal medul a cel s (secretes
? Diagnosis: catecholamines and metabolites
(VMA) in 24 hour urine
? 5 Ps (paroxysmal spel s) in a 20-45 y/o patient
? Pressure (sudden increased hypertension)
? Pain (headache, chest pain, abdominal pain)
? Perspiration
? Palpitations
? Pallor

Carcinoid Syndrome
? Carcinoid tumor: Circumscribed tumors
occurring in smal intestine, appendix,
stomach, colon
? Tumor secretes serotonin,
prostaglandins and other
bioactive substances
? Attacks of skin flushing,
watery stools, hypotension,
vasodilation, edema, ascites
and bronchoconstriction
? Attacks can last from minutes to days
? Occurs in 10% of carcinoid tumor patients

Electrolyte / Acid Base

? Usual y due to too much water relative to
? Symptoms depend on level and rate of drop
?Early: Nausea, headache
?Late: Lethargy, seizures
?Symptoms often start
around 120 mEq/L

Classification of Hyponatremia
? Hypovolemic hyponatremia (clinical y dehydrated)
?Na+ loss > free water loss
?GI losses (vomiting, diarrhea)
?Renal losses (diuretics)
?Excess skin losses (sweating, burns)
? Hypervolemic hyponatremia (edematous states)
?CHF (decreased effective circulating volume leads to
ADH release)
?Liver cirrhosis (same as CHF)
?Renal disease (nephrotic syndrome, renal failure)
?Decreased free water excretion
? Euvolemic hyponatremia
?SIADH (syndrome of inappropriate ADH secretion)
?Psychogenic polydipsia

? Hyperglycemia
?Free water osmotical y drawn out of cel s and
into serum, leading to lower serum Na+
(Remember Na+ drops 1.6 mEq/L for every
100 mg/dL increase in glucose over 100
? Hyperlipidemia, hyperproteinemia
?Displaces sodium from the lab specimen

Hyponatremia Treatment (1)
? Depends upon etiology, chronicity and
? Hyponatremia that develops slowly should be
corrected slowly
? Hypovolemic hyponatremia
?Replace fluid deficits with NS
?100-150 mL/hr
? Euvolemic hyponatremia
?Correct underlying cause
?Water restriction (+/- furosemide if Na+ < 120)

Hyponatremia Treatment (2)
? Hypervolemic hyponatremia
?Goal is to increase Na+ and H2O loss
?Salt and water restriction
?Diuretics to increase Na+ loss
? Caveat: May worsen hyponatremia because water
leaves in excess of Na+
?Faster correction: IV NS & loop diuretics

Hyponatremia Treatment (3)
Life-threatening symptoms
? Severe hyponatremia (Na+ < 120 PLUS
CNS abnormalities)
?Goal is to raise level to >120 mEq/L
?Rise in Na+ should be no greater than
0.5-1.0 mEq/L per hour (1-2 mEq/L per
hour if seizures)
?Hypertonic saline (3%) 25-100 mL/hr
?Furosemide (Lasix) 20-40 mg IV
?Too-rapid correction
?Central pontine myelinolysis (CPM)

Central Pontine Myelinolysis
Results from too rapid
correction of hyponatremia
? Occurs 24-48 hours after rapid correction
? Symptoms include confusion progressing to
cranial nerve deficits to quadriparesis to
locked-in syndrome; dysphagia, dysarthria,
? Concomitant use of furosemide (Lasix) has
been shown to decrease incidence of CPM

? Too little water relative to Na+
? Most commonly due to free water loss or
decreased intake
? Common in infants and debilitated elderly
(limited access to water or impaired thirst)
? Also seen with elevated aldosterone levels or
diabetes insipidus
? Irritability, doughy
skin turgor, coma

Treatment of Hypernatremia
? May calculate total body water by formula
?TBW = Wt (kg) x 0.6
Water deficit in liters =
TBW x ( [current Na/ 140] -1)
? Replace calculated water deficit over 48 hours
?Start with NS not D5W
?May use diuretic to increase Na+ excretion
?Target 0.5 mEq/hr correction
? Severe volume depletion: NS bolus
Too-rapid correction may result in cerebral edema

Hypokalemia (1)
? Most common electrolyte abnormality in patients
with weakness
? EKG changes: Decreased T waves, increased
U waves, ventricular dysrhythmias
? Causes
?Decreased intake (e.g. NPO)
?Increased output
?Renal losses
?Diuretics, osmotic diuresis
?Increased aldosterone
?Magnesium deficiency
?Renal tubular acidosis
?GI losses: Vomiting, diarrhea, NG suction 57

Hypokalemia (2)
? Shift of K+ into cel s
?Alkalosis (protons move out of cel s to restore
pH; K+ moves in to maintain electrical neutrality)
?Insulin-mediated transport
?Catecholamine-mediated transport
? Potassium is primarily an intracel ular ion (30:1)
?Mild hypokalemia may represent severe total
body deficits (especial y in the setting of acidosis)
?Serum levels determine adverse effects

Hypokalemia Treatment
? Treat after urine output established
? Oral replacement safest
? Correct acid-base abnormality
? IV replacement: No more than 40 mEq/L and no
faster than 40 mEq/hour
? Hypokalemia often is associated with
Magnesium required for Na/K pump
? In severe hypomagnesemia, potassium
supplements wil continue to be excreted in the
? Resistant hypokalemia: Replace Mg++ & K+ 59

Hyperkalemia Causes
? Lab error: Hemolysis (most common), thrombocytosis,
leukocytosis, ischemic blood
? Increased intake (rare)
? Decreased output (renal failure
or low aldosterone)
?Aldosterone causes sodium and
water retention resulting in elevated
BP and loss of K in the urine
?Aldosterone is blocked by
spironolactone (a K-sparing diuretic)
? Redistribution (lack of insulin,
acidosis, digoxin toxicity, tissue
damage, succinylcholine)

Hyperkalemia Signs and Symptoms
? Usual y asymptomatic
? May have muscle weakness
? Cardiac
?EKG changes: Peaked T waves, increased
PR, flattened P waves, increased QRS width
?Dysrhythmias: Conduction blocks (BBB),
bradycardia, sine wave pattern, asystole

Hyperkalemia Treatment
? Correct acidosis
? Calcium gluconate 10% (10-20 mL) antagonizes
the effects of high K+,, especial y cardiac
?Quick onset, shortest acting
? D50 + insulin, bicarbonate, beta agonists
?Shift K+ extracel ular to intracel ular
? Exchange resins polystyrene (Kayexalate) oral y
or by enema to remove and lower total K+
? Dialysis if above fails
Don't use calcium in hyperkalemia with
digitalis toxicity cardiac arrest

Calcium Metabolism
? Parathyroid hormone: Increases total serum
?Osteoclast stimulation (bone resorption)
?Renal resorption
?GI absorption
? Vitamin D
?Synthesized by kidney
?Activated by skin exposure to sun
?Essential for GI absorption
? Kidneys (dual role)
?Synthesize vitamin D
?Reabsorb filtered Ca++

? Causes
Parathyroid: hyperparathyroidism (most common)
Addison's disease
Multiple myeloma
Paget's disease (during immobilization)
Milk-alkali syndrome
D vitamin
Thiazide diuretic

Hypercalcemia Features
Stones, bones, moans (psych) and groans (abdominal)
? Neuro: AMS, hyporeflexia, weakness
?Increased nerve and muscle resting membrane
? EKG: Shortened QT, BBB, heart block
? HypERcalcemia = ShortER QT
? Renal: Polyuria, polydipsia, nephrogenic DI, calculi
? GI: Abdominal pain, nausea, constipation
? PUD, pancreatitis
? Skeletal: Bone pain / fractures
? Metastatic calcifications

Hypercalcemia Treatment
? IV saline ? 2-4 L
? Dilutes calcium and increases GFR thereby increasing the
calcium load excreted by the kidney
? Bisphosphonates (zoledronic acid / pamidronate)
? Inhibit osteoclast function and decrease bone resorption ?
response seen within 2-4 days, nadir at 7 days). Used
once hydration has been completed
? Loop diuretics (furosemide)
? Facilitates calcium excretion but are advised only after
hydration achieved
? Less often used options
? Calcitonin (inhibits bone resorption)
? Steroids (increase renal losses of calcium)
? Dialysis

Hypocalcemia Causes
? Hypoparathyroidism (surgical)
? Renal failure
? Vitamin D deficiency
? Pancreatitis
? Hypomagnesemia (Mg++ necessary for PTH
? Drugs: Phenytoin, cimetidine, phosphates
(extensive list)
? DiGeorge Syndrome

Hypocalcemia Signs & Treatment
? Decreases nerve and muscle resting membrane
? Signs & Symptoms
?Paresthesias, hyperreflexia, seizures
?Chvostek's sign: Twitch of corner of mouth on
tapping facial nerve in front of ear
?Trousseau's sign: Carpal spasm when BP cuff is
inflated above systolic BP
?EKG: Prolonged QT / inverted T waves
?HypOcalcemia = LOnger QT
? Treatment
?Goal is to raise Ca++ to low normal levels
?Calcium gluconate

? Causes: Renal failure, iatrogenic
? Symptoms: Weakness, hyporeflexia,
respiratory depression, heart blocks
? Treatment: IV calcium (the same as with high
potassium), dialysis
? Causes: Malnutrition, alcoholism, diuretics
? Symptoms: Similar to hypocalcemia and
hypokalemia; serum levels can be normal in spite
of significant deficit
? Treatment: IV magnesium

Phosphorus Metabolism
? GI tract absorption
? Excreted and reabsorbed in kidneys
? PTH lowers serum phosphorous by blocking
renal resorption
? Usually inverse relationship with calcium
?Ca++ = phosphate
?Ca++ = phosphate

? Causes: PTH, renal failure, increased vitamin
D, many problems associated with Ca+ +
? K+, Mg++ and phosphate (major intracel ular
components) travel together, of one = of
the others
? Symptoms are usual y from associated
hypocalcemia and hypomagnesemia
? Treatment
?Oral phosphate binding gels
?Treat hypocalcemia if necessary

? Phosphate is involved in the function of al
hematologic cel lines (i.e. red cel s / WBC /
? Causes
? PTH, malignancies with CA+2
?Hyperventilation (respiratory alkalosis)
?Hyperalimentation (common)
?Decreased oral intake (alcoholics)
?DKA (12-24hrs s/p tx)
? Symptoms and signs
?Muscle weakness, respiratory depression, altered mental
status, CHF, hemolytic anemia, rhabdomyolysis
? Treatment
?Oral phosphate for minor cases
?IV phosphate if symptomatic

Anion Gap (1)
? Anions = negatively charged ions
? Calculates unmeasured anions
? Electroneutrality: Plasma has no net charge
? Measured cation: Na+
? Measured anions: Cl- and HCO -
? Unmeasured cations: Ca++, Mg++
? Unmeasured anions: Organic acids, proteins,
phosphates and sulfates
Calculation: Na+ ? (Cl- + HCO -) 12

Anion Gap (2)
? Decreased anion gap
?Measured: Occurs if there are less positive
charges or more negative charges
?Unmeasured: Occurs if there are more
positive or less negative charges
?Hypoalbuminemia (less unmeasured anions)
?Multiple myeloma (excess positively charged
IgG paraproteins), hypercalcemia,
hypermagnesemia, lithium toxicity
?Bromide intoxication (mistaken for chloride)

Anion Gap (3)
? Increased anion gap metabolic acidosis:
DKA, AKA, starvation ketosis
Phenformin or paraldehyde
Iron or INH
Lactic acidosis
Ethylene glycol

Lactic Acidosis
? The most common cause of metabolic acidosis
? Lactate is produced by anaerobic glycolysis
? Causes: Hypoperfusion or hypoxia
?Medical conditions: Seizures, renal
insufficiency, hepatic failure, infection,
neoplasm (especial y, leukemia, lymphoma and
?Drugs and toxins: Ethanol, toxic alcohols (also
produce organic acidosis), metformin (rare,
associated with renal failure), antiretrovirals

Non-gap Acidosis
? Normal anion gap metabolic acidosis
? Loss of bicarbonate with a corresponding
loss of Na+
?Therefore the equation is balanced on both
sides with no increase in the anion gap
? Non-gap metabolic acidosis: "HARD UP"
Renal tubular acidosis
Pancreatic fistula

Metabolic Alkalosis (1)
? H+ loss or HCO- excess
? Differential diagnosis
?Loss of gastric acid (vomiting, NG suction)
?Excess diuresis
?Increased citrate or lactate due to transfusions
of Ringer's lactate
?Antacids (e.g. milk-alkali syndrome, results
from high calcium intake + absorbable alkali-
like antacids = hypercalcemia and metabolic

Metabolic Alkalosis (2)
? Increase of renal Na+ resorption with K+ and H+
secretion causes bicarbonate generation
? Chloride-sensitive
?Chloride loss: Vomiting, diuretics
?Volume depletion
? Chloride-insensitive
?Euvolemia or hypervolemia
?Excess mineralocorticoids
?Examples: renal artery stenosis, renin-secreting

? Determined by the concentration of low
molecular weight solutes
? Primarily determinants: Sodium, chloride,
glucose and BUN
? A difference between the measured and
calculated osmolality of >10 is an osmolal gap
? An osmolal gap indicates the presence of
other, unmeasured, low molecular weight
solutes (ethanol, ethylene glycol, methanol,
isopropyl alcohol, mannitol or glycerol)
Formula to calculate serum osmolality:
2Na +Glu/18 + BUN/2.8 = 280-295 (normal)


The treatment of diabetic
ketoacidosis may result in which
of the following complications?

A. Cerebral edema
B. Hypokalemia
C. Worsening CSF acidosis
D. Hypoglycemia
E. All of the above

A patient has a 600 mg/dl serum
glucose. What is the expected serum
sodium level (normal = 140)?

A. 150mEq/L
B. 146mEq/L
C. 132mEq/L
D. 123mEq/L
E. 120mEq/L

The most common etiology
for metabolic acidosis is:

A. Lactic acidosis
B. Diabetic ketoacidosis
C. Alcoholic ketoacidosis
D. Non-ketotic hyperosmolar acidosis
E. Toxic ingestion
3 84

A 26 y/o female patient presents with an acute
onset of confusion, fever, tremor, weakness and
tachycardia. She is given propranolol 1 mg IVP.
What is the most appropriate next medication to

B. Digibind
C. Thyroxine
D. Iodine
E. Magnesium sulfate

A patient arrives after new onset
tonic/clonic seizures. The patient's
medical history includes psychogenic
polydipsia. Which is most consistent
with this diagnosis?
A. Na+ = 165; urine maximal y concentrated
B. Na+ = 142; urine maximal y concentrated
C. Na+ = 115; urine maximal y dilute
D. Na+ = 150; urine maximal y dilute
E. Na+ = 110; urine maximal y concentrated

Which of the following is
associated with a non-gap
metabolic acidosis?

A. Diarrhea
B. Pancreatic fistula
C. Renal tubular acidosis (RTA)
D. Acetazolamide
E. All of the above

Which of the following entities
causes an elevated anion gap

A. Isoniazid toxicity
B. Bromide toxicity
C. Multiple myeloma
D. Hypoalbuminemia
E. Hypoaldosteronism

The treatment of hypercalcemia
includes which of the following:

A. Hypertonic saline diuresis
B. Hemodialysis
C. Vitamin D
D. Hydrochlorothiazide
E. Pamidronate

Which of the following is the most

A. Thrombolytic administration
C. D50
D. Calcium chloride
E. Passive external re-warming

Which of the following is
typical of hypokalemia?

A. J waves on EKG
B. Magnesium toxicity
C. Peaked T waves
D. Inhibits atrial and ventricular dysrhythmias
E. Flaccid paralysis
10 91

What is the most common electrolyte
abnormality associated with adrenal

A. Hyponatremia
B. Hyperkalemia
C. Hyperglycemia
D. Decreased eosinophil count
E. Hypercalcemia
11 92

The common findings in myxedema
coma include which of the following?

A. Hyperthermia
B. Hypoglycemia
C. Hypernatremia
D. Low cholesterol
E. Elevated T4
12 93

A 78 y/o patient had a gradual onset of
confusion. The patient
's GCS = 10 and
GLC = 946. Serum ketones = neg. Which
statement is true?

A. This patient is in DKA
B. Over-aggressive glucose reduction and
hydration may result in cerebral edema
C. More common in IDDM
D. Precipitated by dietary indiscretions
E. Mortality rate lower than DKA
13 94

Which of the following statements is
correct regarding alcoholic

A. Always associated with hyperglycemia
B. Is associated with alcohol levels > 300
C. Beta-hydroxybutyrate is the predominant
ketone found in AKA
D. ETOH metabolism promotes
E. Should be treated with an insulin infusion
14 95

A 23 y/o type 1 diabetic patient quit taking
his insulin. His blood gas = 7.18/30/99/100%
RA. What should be done first for this

A. Replete his potassium
B. Administer 2 amps of NaHCO3 IVP
C. Give 2 liters of normal saline IV
D. Administer phosphate
E. Regular insulin bolus and infusion
15 96

Octreotide is effective in which
of the following situations?

A. Metformin overdose
B. Sulfonylurea overdose
C. Hypoglycemia from insulinoma
D. Hypoglycemia associated with chronic
liver disease
E. Ace inhibitor overdose
16 97

Treatment with hypertonic
saline may result in which of
the following?
A. Reflex hyponatremia
B. Diabetes insipidus
C. Hypotension
D. Hypokalemia
E. Central pontine myelinolysis
17 98

Which is true regarding
diabetes insipidus?

A. The least common drug-related cause is
B. In nephrogenic DI, the kidney responds to
exogenous infusion of ADH
C. The urine is typical y very concentrated
D. Head trauma is a rare cause
E. Results from decreased secretion or
response to ADH
18 99

A patient is documented to have true
fasting hypoglycemia with sugars
measured as low as 30. Your differential
diagnosis should include which of the

A. Smal cel lung CA
B. Diabetes insipidus
C. Cushing syndrome
D. Liver disease
E. Hyperthyroidism
19 100

Regarding adrenal
insufficiency, which of the
following is true?

A. Histamine release associated with etomidate
results in relative adrenal suppression
B. It is associated with meningococcemia
C. It rarely results in refractory hypoglycemia
D. It is never associated with hypothyroidism
E. It is a self-limited disease
20 101

Endocrine Answer Key
1. E
11. A
2. C
12. B
3. A
13. B
4. A
14. C
5. C
15. C
6. E
16. B
7. A
17. E
8. E
18. E
9. D
19. D
10. E
20. B

This post was last modified on 24 July 2021