Metabolic/Endocrine Flashcards
Which oral diabetes med drug class can cause prolonged or rebound hypoglycemia?
Sulfonylureas, such as glipizide, are a class of drugs used for glycemic control that work by blocking potassium channels in the pancreas, leading to depolarization and insulin release. Sulfonylureas have a longer half-life than many diabetes medications and thus can cause prolonged hypoglycemia that may persist for > 24 hours when ingested in overdose.
What are the symptoms of Vitamin C deficiency (Scurvey)?
↑ bleeding, anemia, loose teeth
What is the goal rate for increasing serum sodium in acute hyponatrimia?
Small increase in sodium often sufficient to resolve symptoms (ex. 2 mEq/L/hour for the first 2–3 hours or 4–6 mEq/L over 6 hours); monitor sodium closely
What is the goal rate for increasing serum sodium in chronic hyponatrimia?
Chronic: correct by 8–12 mEq/L in 24 hours
What does increasing serum sodium to fast in hyponatremia cause?
Osmotic demyelination syndrome formerly central pontine myelinolysis (dysarthria, dysphagia, paralysis, death) if corrected too fast
What lab abnormalities are seen in
Primary Adrenal Insufficiency (Addison Disease)?
Labs: hyponatremia and hyperkalemia
What is the firstline treatment for Primary Adrenal Insufficiency (Addison Disease)?
Tx: hydrocortisone or other glucocorticoid
Most patients also require mineralocorticoid (fludrocortisone)
First line treatment in Pheochromocytoma?
Alpha-blocker (phentolamine, phenoxybenzamine) prior to beta-blockade to prevent unopposed alpha-agonism.
What lab abnormalities are seen in Pheochromocytoma?
↑ 24h urinary catecholamines and metanephrines, or ↑ plasma metanephrine levels
What genetic disorder is associated with Pheochromocytoma?
MEN2 (medullary thyroid cancer, pheochromocytoma, +/- primary hyperparathyroidism)
What is the most common cause of hypercalcemia?
Malignancy (most common inpatient cause)
Primary hyperparathyroidism (most common outpatient cause, and overall)
What lab findings are seen in Hypoparathyroidism?
Labs will show low PTH, low calcium, high phosphorus.
What is Chvostek sign?
Contraction of facial muscles after tapping facial nerve
What is Trousseau sign?
Induction of carpopedal spasm by a sphygmomanometer
What are two medications that can cause hypercalcemia?
Lithium and thiazide diuretics.
Which of the following subtypes of thyroid carcinoma is associated with multiple endocrine neoplasia?
Medullary: associated with MEN2, calcitonin can be used as a tumor marker
Hashimoto thyroiditis is associated with what type of thyroid cancer?
Thyroid diffuse large-cell lymphoma.
Treatment of thyroid storm in order?
Tx:
Beta-blocker (propranolol)
Thioamide (propylthiouracil or methimazole)
Iodine solution
Glucocorticoids
Which metabolic derangements would you expect in tumor lysis syndrome?
Hyperuricemia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
What is Anion Gap?
Anion gap (AG) is the difference between the sodium, chloride, and bicarbonate concentrations (Na - [Cl + HCO3]). A normal AG is 3–11 mEq/L, whereas an increased anion gap is > 11–20 mEq/L. This represents a metabolic acidosis.
What is the most common cause of hyperthyroidism?
Graves Disease
What are common causes of hypophos?
What is the strong ion difference?
Strong ion difference = ([Na+ + K+ ] − [Cl− ]). When significantly less than 40, an acidosis is present.
What is the delta gap?
The delta gap (ΔG) = (AG − 12) − (24 − [HCO3 − ]). Its calculation determines if the anion gap is accounted for by the change in serum bicarbonate concentration. An elevated anion gap and ΔG more than 6 indicates that a metabolic alkalosis in addition to a metabolic acidosis is likely to be present.
What is the anion gap?
Anion gap = Na+ − (Cl− + HCO3 − ). Causes of an elevated anion gap include ketoacidosis, lactic acidosis, toxins metabolized to acids, and renal failure.
Symptoms of Korsakoff syndrome?
Confabulation
Anterograde Amnesia
Retrograde Amnesia
Symptoms of Wernicke encephalopathy?
Classically characterized by encephalopathy, gait ataxia, and ophthalmoplegia. Ocular findings commonly include nystagmus, lateral rectus palsy (mostly bilateral).
Symptoms of niacin or vitamin B3 deficiency (Pellagra).
Dermatitis
Diarrhea
Dementia
Multiple Endocrine Neoplasia (MEN)
Autosomal dominant
MEN1: parathyroid tumors (resulting in primary hyperparathyroidism), pancreatic tumors, and pituitary adenoma
MEN2A: medullary thyroid carcinoma, pheochromocytoma, and parathyroid hyperplasia
MEN2B: medullary thyroid carcinoma, marfanoid habitus, mucosal neuromas and pheochromocytoma
Vitamin A Deficiency
A: night vision loss, xerophthalmia, dry skin (xerosis), growth retardation, Bitot spots on the conjunctivae
Vitamin B1 Deficiency
B1 (thiamine): beriberi, Wernicke-Korsakoff syndrome, cardiac failure; alcoholism, malnutrition
Vitamin B2 Deficiency
B2 (riboflavin): cheilosis, corneal vascularization (the two Cs of B2)
Vitamin B3 Deficiency
B3 (niacin): dermatitis, dementia, diarrhea; corn-based diet (pellagra)
Vitamin B6 Deficiency
B6 (pyridoxine): sideroblastic anemia, convulsions, peripheral neuropathy; INH use
Vitamin B12 Deficiency
B12 (cobalamin): megaloblastic anemia + neurological symptoms, hypersegmented neutrophils
Vitamin C Deficiency
C (ascorbic acid): scurvy (↑ bleeding, anemia, loose teeth)
Vitamin D Deficiency
D: rickets (children), osteomalacia, tetany
Vitamin E Deficency
E: anemia, peripheral neuropathy, ataxia
Vitamin K Deficency
K: ↑ bleeding, ↑ PT/INR, ↑ PTT if severe
Folate Deficency
Folate: megaloblastic anemia, sensory neuropathy
Causes of acute respiratory acidosis?
Airway obstruction
Pulmonary disease (pneumonia, asthma, pulmonary edema, aspiration pneumonitis)
CNS depression (recreational drugs, intracranial catastrophe, neuromuscular disorders, thoracic trauma)
Causes of chronic respiratory acidosis?
Lung disease (COPD, IPF)
Neuromuscular disorders (ALS, muscular dystrophy, obesity hypoventilation)
What are the clinical features of postpartum panhypopituatrism.
What disorders cause a normal anion gap metabolic acidosis?
Most common cause of DKA and HHS is…
Most common cause of DKA and HHS is infection (30-50% of cases). Of those, UTI or PNA is the most common.
5 I’s of DKA
5 I’s- Insulin (low/absent), Insemination, Infection, Infarction, Initiation (first time presentation)
Review expected bicarb and
pCO2 levels for Metabolic
Acidosis, Metabolic Alkalosis,
Respiratory Acidosis, Respiratory
Alkalosis
M.Acid: ↓ HCO3, ↓ pCO2 (hypervent);
M.Alk: ↑ HCO3, ↑ pCO2(hypovent);
R.Acid: ↑ pCO2, ↑ HCO3 (↑ renal reabsorption);
R.Alk: ↓ pCO2, ↓ HCO3 (↓ renal reabsorption).
Normal values: pH 7.4 / HCO3 24/ pCO2 40 / AG 12 ±
What is the appropriate
metabolic compenstion for
Respiratory Acidosis and
Alkalosis?
(Delayed metabolic compensation) Acid/Alk: ‘1325’: Acute/Chronic;
R.Acid: for every ↑ of pCO2 by 10, HCO3 should ↑ by 1 (Acute) and 3
(Chronic); R.Alk: for every ↓ in pCO2 by 10, HCO3 should ↓ by 2
(Acute) and 5 (Chronic); If NOT true then a mixed disorder is present
What is the appropriate
respiratory compensation for
Metabolic Acidosis and Alkalosis
(Immediate respiratory compensation) Acid: Rule of 15s; Alk: 007;
M.Acid- 1.5 x HCO3 + 15 (±2) = PCO2 & last two digits of pH (±2);
M.Alk: for every ↑ of HCO3 by 1, pCO2 should ↑ by 0.7; If NOT true then a mixed disorder is present
What is the differential for an
anion-gap metabolic acidosis?
A CAT MUDPILE: Aspirin, Carbon monoxide, Cyanide, Caffeine,
Acetaminophen, Theophylline, Methanol, Metformin, Uremia, DKA
(AKA), Propylene Glycol, Isoniazid, Ibuprofen, Iron, Lactic Acidosis,
Ethylene glycol
What are the most common
causes of non-anion-gap
metabolic acidosis?
Diarrhea & spironolactone
What are the most common
causes of metabolic alkalosis?
Vomiting, diuretics
What is the primary difference
between Type I and Type II
diabetes?
I: insulin deficiency (auto-immune),
II: insulin resistance
What are the criteria for
diagnosis of diabetes?
Fasting blood sugar >126 (2 separate occasions),
Random glucose >200 with ssx of DM,
Glucose >200 after OGTT,
HbA1c > 6.5%
Suspected DKA and coffeeground
emesis
Erosive esophagitis & hemorrhagic gastritis in up to 9% of DKA, rarely need treatment/endoscopy
What are the keys to diagnosis
of DKA?
SSx: Polyuria, polydipsia, abd pain, vomiting, acetone (fruity) smell, ± unstable vitals/shock, AMS, possible coffee-ground emesis;
Labs: glucose > 250, pH < 7.3 (VBG ok), HCO3 <18, AG >10, +Serum/urine ketones;
Note: workup should include eval for cause of DKA (infection rule out) and EKG due to lyte abnormalities
What lab value is critical to know
prior to giving insulin for DKA?
Serum potassium: patients have an overall deficiency of K (initial labs may show high K), if initial low K and pt given insulin they will become too hypokalemia and code
What is the appropriate
approach to fluid resuscitation in
DKA?
Rx: 2L NS IVF bolus (kids: 10-20cc/kg), when glucose < 250, start
glucose-containing fluids (D51⁄2 NS)
What is the appropriate
approach to electrolyte repletion
in DKA?
Key = POTASSIUM! Know level before insulin. K<3.3: HOLD Insulin & give K, K 3.3-5.2: can start insulin but give K in each liter of IVF; K>5.2:
Start Insulin & NS, no supplemental K needed; BICARB: controversial, only Rx if severe DKA + intubated; MAG: replete with K; SODIUM: falsely low, abnormal Na will typically correct with fluids.
What is the appropriate
approach to insulin
administration in DKA?
Eval K level first, then give 0.1 U/kg/hr gtt (double if glucose not down by 50 after first hour); initial bolus not necessary; can also follow SQ regimen; **Transition to regular insulin SQ when gap closed and pH >7.3, dose 5U per 50 over 150 (max 20U), stop insulin gtt 1hr after pt given SQ insulin
How do you correct sodium for
hyperglycemia (pseudo
hyponatremia)?
Add 1.6 to Na for each glucose value of 100 over 100 mg/dL
Treatment for DKA followed by
new AMS or seizure
Cerebral edema, more common in kids and new onset type I, Rx:
mannitol (1-2g/kg)
What is the mechanism of action
and possible adverse effect of
Sulfonylureas (Glipizide, glyburide)
Stimulates insulin release from the pancreas, can cause prolonged hypoglycemia in overdose
What is the mechanism of action
and possible adverse effect of
Biguanides (Metformin)
Suppress hepatic gluconeogenesis (NO hypoglycemia), ± GI upset, lactic acidosis
What is the mechanism of action
and possible adverse effect of
Thiazolidenediones (TZDs-
Actos, Avandia)
Increase sensitivity to insulin (muscle & fat); ± hepatitis & edema; NO hypoglycemia
What distinguishes Hyperosmolar
Coma from DKA?
Occurs in Type II DM. SSx: more likely to have CNS ssx (stupor/coma).
Labs: glucose > 600, pH >7.3, HCO3 >18, ± urine ketones, AG <12, severe dehydration (8-12L deficit). Rx: IVF, insulin
What lab test can help identify
facticious hypoglycemia
(exogenous administration)?
C-peptide, value will be low 2/2 suppression of endogenous insulin
What is the rule to calculate
MIVF rate?
4cc/kg for first 10kg, 2cc/kg for second 10kg, 1cc for each additional kg to max of 120cc/hr total
What are typical causes and
appropriate treatment for
Hypervolemic, Euvolemic and
Hypovolemic Hyponatremia?
HyperV: CHF, ESRD, cirrhosis; Rx: water restrict + diuretics;
EuV: SIADH, psychogenic polydipsia; Rx: water restrict;
HypoV: vomiting, diarrhea, third spacing, diuretics; Rx: NS vs 1/2 NS
What is the approach to
correction of hyponatremia?
Overall goal correction rate 0.5 mEq/hr or 10-20 mEq/day. Note: rapid
correction risks central pontine myelinolysis/demyelination. Rx:
asymptomatic & Na >120 = no emergent treatment; Na <120 & +neuro ssx, give 3% NaCl (100cc over 10m, additional 100cc over 50m)
How and when does central
pontine myelinolysis present?
How: AMS (lethergy and coma) w/ spastic quadriplegia after treatment for hyponatermia. When: 1-6 days after treatment for hyponatremia. Pts with chronic hyponatremia (e.g. alcoholics) are most at risk for this.
What is the approach to
treatment of hypernatremia?
Overall goal correction rate 1-2 mEq/hr. Note: rapid correction risks cerebral edema.. Calculate Free Water Deficit (0.6 x wt(kg) x (Na/140 -1)) and replace with NS until euvolemic, then D5W vs D5 1/2 NS. Give 50% over 12h, remainder over the next 24hr
What is the most common cause
of hyperkalemia?
Lab error, resend lab
What EKG changes are seen in
hyperkalemia?
Peaked TW, PR long, loss of P wave, wide QRS, sine wave, VT/VF
What is the general approach to
treatment of hyperkalemia?
Cardioprotection (Calcium Gluconate or Chloride ONLY if ekg changes, K shifters: Insulin/glucose, bicarb if acidotic, albuterol), K excretion: lasix, kayexylate, HD
Dx and Tx of hypokalemia?
Most common electrolyte disturbance. 2/2 ↑ losses (GI loss or diuretics), intracellular shift.
SSx: cramps, weakness, arrhythmias, cardiac arrhythmias, rhabdo;
Rx: K repletion 100 mEq K for every 0.3 below normal, give 10-20 mEq/hr; **Note: supplement with Magnesium (↑absorption)
What is the most specific EKG
change associated with
hypokalemia?
Flattened or inverted T wave, U waves = specific, prolonged QT, STD
U Wave
Dx and Tx of Hypercalcemia
Ca > 10.5. Causes: hyperparathyroid (overall most common cause), malignancy (most common inpatient cause);
SSx: BONES (bone pain), STONES (renal, biliary), GROANS (abd pain, n/v), THRONES (polyuria) and PSYCHIATRIC OVERTONES (depression, anxiety, insomnia);
EKG: short QT;
Rx: immediate if Ca > 14 (12-14 per ssx) with IVF (first step),
Calcitonin (↑ excretion, inhibits osteoclasts), Bisphosphonates (inhibits osteoclasts, requires days to work), Steroids (↓ GI absorption), Lasix (if volume overload)
Dx and Tx of Hypocalcemia
Ca < 8.5. Causes: 2/2 hypoparathyroid (thyroidectomy = most comon cause), Vit D deficiency, high phos, low or high Mg;
SSx: paresthesias, tetany, Chvostek’s sign, Trousseau’s sign, seizure. EKG: QT prolongation;
Rx: IV calcium (if <7.5 and severe ssx), give Vit D and Mg prn
Dx and Tx of Hypermagnesemia
SSx: weakness, loss of reflexes, dysrhythmias, respiratory depression;
Rx: calcium gluconate
Alcoholic with AMS, ataxia,
nystagmus
Wernicke’s Encephalopathy 2/2 Thiamine (B1) deficiency;
Rx: Thiamine 500 mg IV, improvement in hours
Alcoholic with short term memory
loss
Korsakoff’s Psychosis 2/2 Thiamine deficiency, irreversible
Poor nutrition and high output
cardiac failure (dyspnea,
peripheral edema)
“Wet” Beriberi 2/2 chronic thiamine deficiency; Rx: Thiamine 100mg IV
Diarrhea, Dermatitis, Dementia
Pellagra 2/2 Niacin (B3) deficiency
Crohn’s patient with macrocytic
anemia and paresthesias
Cobalamin (B12) deficiency; high risk include Crohns, vegans,
alcoholics, PPIs, pernicious anemia (antibody to intrinsic factor); causes megaloblastic anemia + neuro deficits, hypersegmented neutrophils
Alcoholic with macrocytic anemia
Folic Acid deficiency. High risk: alcoholics, elderly, phenytoin; no neuro changes. Hypersegmented neutrophils seen as well.
Child with poor diet and bowed
legs
Rickets 2/2 Vitamin D deficiency (Calcium absorption); Osteomalacia: adult equivalent, normal height
Bad skin, bleeding gums and
poor wound healing
Scurvy caused by Vitamin C deficiency (collagen formation)
What vitamins are toxic in
overdose?
Fat soluable ADEK;
A: bear liver consumption, skin changes,
pseudotomor cerebri,
D: hypercalcemia, hypercalciuria,
E: ↑ bleeding,
K: hemolytic anemia, jaundice in newborns
What hormones are secreted
from the pituitary?
GOAT FLAP: Growth Hormone, Oxytocin, ADH, TSH, FSH, LH, ACTH, Prolactin;
ALL but Oxy/ADH are from anterior pituitary
What are potential causes of
hypopituitarism?
Mass lesions, bleeds (pituitary apoplexy), hypothalamic disease,
Sheehan’s syndrome; Dx: check hormone levels
Low cortisol but normal
aldosterone
ACTH deficiency, causes 2° adrenal insufficiency
Inability to lactate post-partum
Sheehans syndrome causing prolactin deficiency (and panhypopit)
Visual field deficits, headache,
hormonal abnormalities
Pituitary adenoma (macro if >1cm), Rx: transsphenoidal surgery
What is the treatment for
prolactinoma?
Most common pituitary tumor. Rx: Bromocriptine (does not require
surgery)
Dx and Tx of Cushing’s
syndrome
Cortisol excess. ACTH secreting pituitary adenoma or exogenous
steroids (most common cause):
SSx (‘CUSHING’): Central obesity, Urinary cortisol ↑, Striae, HTN/Hyperglycemia/Hirsutism, Iatrogenic, Neoplasms, Glucose intolerance.
Rx: surgery (tumor)
Headache and tunnel vision in
oversized person
Growth Hormone secreting pituitary adenoma;
Labs: ↑ GH & ILGF1.
Children: gigantism, adults: acromegaly;
Rx: surgery
What hormones are produced by
the adrenal glands?
Medulla: epinephrine & norepinephrine;
Cortex: cortisol, androgens, aldosterone
Identify the key differences
between primary and secondary
adrenal insufficiency
Deficiency of adrenal gland hormone production. 1° (adrenal disease): ↑ CRH & ACTH, Addisons dz (autoimmune) = most common cause, rapid withdrawal of steroids = most common cause in US, SSx: shock, hypoglycemia ,↓ mineralocorticoid = ↓ Na/gluc, ↑ K, HYPERpigmentation (buccal, 2/2 ↑ ACTH); 2° (pituitary dz): ↑ CRH, ↓ ACTH: ↓ Na/gluc, normal K, NO hyperpigmentation; Rx: IVF, glucocorticoids, vasopressors
Dx and Tx of adrenal crisis
Lif threatening exacerbation of adrenal insufficiency. Hallmark = shock that is refractory to IVF / vasopressors. Cause: acute stressor (infxn, trauma, MI); SSx: shock, ↓ Na/gluc, ↑ K; Rx: glucocorticoids (Hydrocortisone v Dexamethasone)
Young child with mass in
abdomen and HTN
Neuroblastoma (adrenal medulla tumor)
HTN, headache, palpitations,
elevated catecholamines
Pheochromocytoma (adrenal medulla tumor)
Review the hormone cascade
and general function of thyroid
hormones
Thyroid Releasing Hormone (hypothalamus) → Thyroid Stimulating
Hormone (Ant Pituitary) → T4 (inactive from thyroid gland) → converted
to T3 (active form) in peripheral tissues, requires iodine for conversion;
T3 functions in glucose absorption, muscle building, increases
catecholamines, increases basal metabolic rate
What are common causes of
hyperthyroidism
Graves (most common cause, young person), Toxic nodular goiter (elderly), iodine-induced (amiodarone), Thyroiditis (amiodarone)
Review common SSx and Dx of
hyperthyroid
SSx: heat intolerance, palpitations, wt loss, tachycardia, anxiety,
hyperreflexia, goiter, exophthalmos, pretibial edema; Labs: ↓ TSH level, ↑ T4/T3
Difference between
thyrotoxicosis and thyroid storm
Thyrotoxicosis: any condition that results in excessive thyroid hormone concentration. Thyroid storm: life threatening decompensation of thyrotoxicosis (hyperthyroid + acute event)
What is the appropriate
treatment for Thyroid storm?
1) Beta-blockers (Propanolol): ↓ sympathetic activity + blocks peripheral conversion of T4 → T3. 2) Antihormone Rx: PTU (if Pregnant) or Methimazole (blocks new hormone synthesis). 3) Potassium Iodine (AFTER above, blocks release of preformed hormone). 4) Steroids (blocks peripheral conversion of T4 → T3. 5) Treat precipitant & prevent decompensation (IVF, tylenol, cool prn) // The order is controversial. Some sources say give PTU before beta-blockers, but just know that PTU comes BEFORE iodine. That’s what they typically test.
What are common causes of
hypothyroid
Hashimoto’s (MCC in US, autoimmune), meds, postpartum, Iodine deficiency (MCC worldwide)
Review common symptoms,
diagnosis and treatment of
hypothyroid
SSx: fatigue, weight gain, cold intolerance, brittle hair and nails,
constipation, periorbital edema, slow reflexes, edema; Labs: TSH (↑ with 1°, ↓ with 2°), ↓ free T3 / T4; Rx: synthroid.
Hypothyroidism + AMS
Myxedema coma. Rx: steroids (for concurrent adrenal crisis), IV
Levothyroxine (T4)
Dx and Tx of Thyroid Ca
5% thyroid nodules are cancerous, common CA overall but low mortality;
Dx: FNA; Rx: thyroidectomy, radioactive iodine-131, thyroid
supplementation
Dx and Tx of
Hyperparathyroidism
↑ PTH → ↑ Ca, ↓ Phos; SSx of hypercalcemia (see above); Rx: lower Ca with IVF (first line), calcitonin, bisphosphonates, steroids, surgery
Dx and Tx of Hypoparathyroidism
↓ PTH → ↓ Ca, ↑ Phos; may be 2/2 thyroid surgery; SSx of hypoCa; Rx: replacement of Ca, Vit D
Pt w/ hx of anorexia, presents
with signs of heart failure after
starting an outpatient refeeding
program.
Refeeding syndrome. Happens when refeeding begins before
correcting electrolyte abnormalities. Leads to profound
hypophosphatemia, hypokalemia, hypomagnesium, and ultimately volume overload and CHF. Tx: stop refeeding, correct electrolyte abnormalities.
