Endocrine Flashcards
Hypoglycemia, false positives (2)
Dextrose tx by age
meds
meds special situations (2)
Leukemia, polycythemia due to ongoing glycolysis by cells
D25 peds, D10 infants
glucagon coverts glycogen to glucose
sulfonyurea - “-mide/zide/ride”: octreotide -> inhibits insulin secretion
adrenal insufficiency: hydrocortisone
Kussmaul respirations?
Bicarbonate for DKA?
Pseudo? Common finding DKA
before giving insulin always check? replete if < ?
Tachypnea due to respiratory compensation of metabolic acidosis
for DKA? No
pseudo-hyponatremia down 1.6 per 100 increase in BS
check K+; when low indicates massive total body hypokalemia, given IVF only
replete K+ < 5
Hyperosmolar hyperglycemic non-ketotic state HHNS
contrast with DKA (4)
basic thyroid hormone loop
most common cause of hyperthyroid
pictured entity
No ketosis, increased hypoglycemia, increased osmolality, massive dehydration -> higher mortality
TSH stimulates production/release T3/T4 the active thyroid hormones which increase rate of cell metabolism and protein synthesis; iodine will inhibit
Graves’ disease: autoimmune antibodies resemble TSH and stimulate thyroid hormone release
other causes: thyroiditis, goiter, pituitary adenoma, access iodine
pre-tibial myxedema from graves
Hyperthyroid - treatment (3 meds+1)
clinical hallmark of thyroid storm; other sx (2), dx?
tx (general approach , additional meds* - 2)
Beta-blockers exp propanolol,PTU, radioactive iodine, surgery
AMS, fever, tachycardia out of proportion; clinical dx only
supportive care
steroids*
propanolol
PTU/Methimazole*
iodine one hour after PTU
Elderly, lethary, apathetic facies, droopy eyelids, resistent afib/CHF =
Apathetic thyrotoxicosis
Hypothyroid, common causes (3) drug causes (2)
myxedema coma triad, epidemiology
myxedema drug metabolism
myxedema drug treatment (2)
Iodine deficiency, Hashimoto’s thyroiditis, treatment of Graves’ disease
lithium, amiodarone
AMS, hypoxia, hypothermia; elderly female
drug metabolism slows
tx: steroids (possible pituitary adenoma), IV T4
Adrenal gland hormone localization
aldosterone function
primary adrenal insufficiency, cause categories (5)
drug cause
eponym cause
dx
Cortex: cortisol, sex hormones, aldosterone
Medela: epinephrine, norepinephrine
fxn: increase sodium decrease potassium
primary (Addison’s disease), infectious, infiltrative, neoplasm, infarction
drug: etomidate
eponym: Waterhouse-Friderichsen bilateral adrenal infarct from meningococcemia
dx: cortisol level, corticotropin stim
Adrenal insufficiency
secondary cause
tertiary cause
lab abnormalities
acute presentation
secondary cause: hypo pituitary
tertiary cause: steroid overuse -> adrenal atrophy
lab abnormalities: hyponatremia hyperkalemia, eosinophilia, hypoglycemia
acute presentation: fever and refractory hypotension
Adrenal crisis, TX (3)
Cushing’s disease =
most common cause +2 others
symptoms
Dextrose, hydrocortisone, pressers
Cushing’s disease = excess cortisol
cause: prolong steroids, neoplasm (adrenal or pituitary), para neoplastic
Sx: Kunkel obesity, hypertension, hyponatremia, buffalo hump, moon facies
SIADH
key lab findings (2)
cause categories (4)
tx
Concentrated urine with low serum osmolality (often hyponatremia)
paraneoplastic, CNS, lung, drugs
tx: free water restriction
Diabetes insipidus = ?
Types and test to distinguish
signature lab abnormalities (2)
sx (2)
tx for each type
drug cause
Central:Lack of ADH production; nephrogenic: renal insensitivity to ADH
central will respond to ADH
concentrated urine and elevated serum osmolality (often with hypernatremia)
sx: polyuria, polydipsia
TX:
central: DDAVP/desmopressin
nephrogenic: hydrochlorothiazide
drug cause: lithium
Pheochromocytoma =
dx
sx (5)
Adrenal medulla tumor secreting norepinephrine
dx: 24 hour urine catecholamines and metabolites (VMA)
5 Ps: pressure, pallor, pain, perspiration, palpitations
Carcinoid =
Sx (2+)
hyponatremia, three categories
pseudohyponatremia most often due to; other spurious causes (2)
G.I. tumor 10% of time secreting serotonin, prostaglandins
sx: attacks of flushing skin, watery stools, hypertension, vasodilation, edema
hypernatremia: hypo, hyper and euvolemic
due to hyperglycemia
other causes: hyperlipidemia, hyperproteinemia
Hypovolemic Hypernatremia causes (4)
tx (2)
Dehydrated: Na loss > H2O loss, G.I. (vomiting, diarrhea), renal losses (diuretics), skin loss (sweating, burns)
tx: hydrate with NS, correct underlying cause
Hypervolemic hypernatremia causes (4)
tx (3)
tx for severe, all types, Na < 120 (2)
rate of correction
CHF or cirrhosis (both cause decreased circulating volume leads to increased ADH), renal disease with nephrotic syndrome or CKD, decreased free water excretion
salt and free water restriction
loop diuretics +/- NS
severe: hypertonic saline 25-100 mL/h, lasix
goal: 0.5-1 mEQ of correction per hour to avoid central pontine myelinosis
Euvolemic hyponatremia causes (3)
tx (2+1)
SIADH, psychogenic
tx: correct underlying cause, free water restriction, consider lasix if Na < 120
central pontine myelinosis - timing
symptoms (4)
risk reduction (2)
1 to 2 days after correction
AMS, cranial nerve deficits, quadraparesis, locked-in syndrome
slow correction, concomitant use of Lasix
Hypernatremia, most common causes (3)
treatment
associated treatment formula
Limited free access to water (elderly, infants); diabetes insipidus, elevated aldosterone
tx: rehydration with NS to correct water deficit in 48 hours
formula: TBW = wt (kg) x 0.6)
water deficit = TBW x (current Na/140 - 1)
target correction 0.5 mEQ/h
Pictured entity
description of findings
cause categories (3), subcategories
Hypokalemia
•EKG changes: Decreased T waves, increased U waves, ventricular dysrhythmias
decreased intake increased output (renal losses, G.I. losses)
shift of K+ into cells (alkalosis, insulin, catecholamine)
•Renal losses
–Diuretics, osmotic diuresis
–Increased aldosterone
–Magnesium deficiency
–Renal tubular acidosis
•GI losses: Vomiting, diarrhea, NG suction
Primary symptom
Hypokalemia replacement adjuncts (2)
hyperkalemia cause categories (4)
Weakness
Correction of acid-base disturbance, magnesium
cause categories
lab error, increased intake,
decreased output - renal failure or low aldosterone
redistribution-lack of insulin, acidosis digoxin toxicity, tissue damage, succinylcholine
Hyperkalemia EKG changes (4)
dysrhythmias (4)
symptom
calcium contraindicated in management of hyperkalemia when
–EKG changes: Peaked T waves, increased PR, flattened P waves, increased QRS width
–Dysrhythmias: Conduction blocks (BBB), bradycardia, sine wave pattern, asystole
symptom: generally asymptomatic, sometimes muscle weakness
contraindication: digitalis toxicity
Parathyroid hormone function & mechanisms (3)
function of vitamin D, site of synthesis
hypercalcemia causes mneumonic review (11)
Increase calcium by Osteoclast stimulation, renal and G.I. absorption
vitamin D: allows G.I. absorption of calcium; kidney
PAM P SCHMIDT
Parathyroid: hyperparathyroidism (most common)
Addison’s disease
Multiple myeloma
Paget’s disease (during immobilization)
Sarcoidosis
Cancer
Hyperthyroidism
Milk-alkali syndrome
Immobilization
D vitamin
Thiazide diuretic
Hypercalcemia classic mnemonic
Organ based sx
neuro - reflexes?
EKG
renal
G.I.
skeletal
•Neuro: AMS, hyporeflexia, weakness
–Increased nerve and muscle resting membrane potentials
- EKG: Shortened QT, BBB, heart block
- Renal: Polyuria, polydipsia, nephrogenic DI, calculi
- GI: Abdominal pain, nausea, constipation
- PUD, pancreatitis
- Skeletal: Bone pain / fractures
- Metastatic calcifications
Hypercalcemia treatment (4)
hypocalcemia, organ-based causes (3); electrolyte cause
Normal saline, Lasix, bisphosphonates, other (calcitonin, steroids, dialysis)
pancreatitis, renal failure-> vitamin D deficiency, low Mg
Hypocalcemia symptoms (3) with eponyms (2)
EKG (2)
treatment should include
sx: hyporeflexia, paresthesia, seizure
–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, T-wave inversion
Tx: magnesium
Hypermagnesemia sx (4), tx
phosphorus has inverse relationship with
PTH effect on Phosphorus
Hyperphosphatemia tx (2)
Weakness, respiratory depression, hyporeflexia, heart blocks
TX: IV calcium
phosphorus to calcium
PTH lowers
•Treatment
–Oral phosphate binding gels
–Treat hypocalcemia if necessary
Anion gap formula
decreased anion gap (3)
increased anion gap mnemonic
Na+ minus (Cl- + HCO3-) <= 12
decreased: hypoalbuminemia, multiple myeloma, hypercalcemia, lithium
MUDPILES
Methanol
Uremia
DKA, AKA, starvation ketosis
Phenformin or paraldehyde
Iron or INH
Lactic acidosis
Ethylene glycol
Salicylates
Non-anion gap acidosis (6)
•Loss of bicarbonate and Na+
–Therefore the equation is balanced on both sides with no increase in the anion gap
•Non-gap metabolic acidosis: “HARD UP”
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Ureterosigmoidostomy
Pancreatic fistula
Metabolic alkalosis - underlying pathology
review causes
loss of H+ or HCO3 excess OR increase Na+ resoroption, K+, H+ generates bicarb
–Loss of gastric acid (vomiting, NG suction)
–Excess diuresis/volume depletion
–Mineralocorticoids
–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 alkalosis)
–Dehydration
Serum Osmolality formula
most common causes of elevated gap (3)
2Na +Glu/18 + BUN/2.8 = 280-295
ethanol, toxic alcohols, mannitol
