Endocrine Flashcards

1
Q

Hypoglycemia, false positives (2)

Dextrose tx by age

meds

meds special situations (2)

A

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

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2
Q

Kussmaul respirations?

Bicarbonate for DKA?

Pseudo? Common finding DKA

before giving insulin always check? replete if < ?

A

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

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3
Q

Hyperosmolar hyperglycemic non-ketotic state HHNS

contrast with DKA (4)

basic thyroid hormone loop

most common cause of hyperthyroid

pictured entity

A

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

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4
Q
A
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5
Q

Hyperthyroid - treatment (3 meds+1)

clinical hallmark of thyroid storm; other sx (2), dx?

tx (general approach , additional meds* - 2)

A

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

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6
Q

Elderly, lethary, apathetic facies, droopy eyelids, resistent afib/CHF =

A

Apathetic thyrotoxicosis

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7
Q
Hypothyroid, common causes (3)
drug causes (2)

myxedema coma triad, epidemiology

myxedema drug metabolism

myxedema drug treatment (2)

A

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

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8
Q

Adrenal gland hormone localization

aldosterone function

primary adrenal insufficiency, cause categories (5)
drug cause

eponym cause

dx

A

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

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9
Q

Adrenal insufficiency

secondary cause
tertiary cause
lab abnormalities
acute presentation

A

secondary cause: hypo pituitary
tertiary cause: steroid overuse -> adrenal atrophy
lab abnormalities: hyponatremia hyperkalemia, eosinophilia, hypoglycemia
acute presentation: fever and refractory hypotension

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10
Q

Adrenal crisis, TX (3)

Cushing’s disease =

most common cause +2 others

symptoms

A

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

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11
Q

SIADH

key lab findings (2)

cause categories (4)

tx

A

Concentrated urine with low serum osmolality (often hyponatremia)
paraneoplastic, CNS, lung, drugs

tx: free water restriction

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12
Q

Diabetes insipidus = ?

Types and test to distinguish

signature lab abnormalities (2)

sx (2)

tx for each type

drug cause

A

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

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13
Q

Pheochromocytoma =

dx

sx (5)

A

Adrenal medulla tumor secreting norepinephrine

dx: 24 hour urine catecholamines and metabolites (VMA)

5 Ps: pressure, pallor, pain, perspiration, palpitations

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14
Q

Carcinoid =

Sx (2+)

hyponatremia, three categories

pseudohyponatremia most often due to; other spurious causes (2)

A

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

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15
Q

Hypovolemic Hypernatremia causes (4)

tx (2)

A

Dehydrated: Na loss > H2O loss, G.I. (vomiting, diarrhea), renal losses (diuretics), skin loss (sweating, burns)

tx: hydrate with NS, correct underlying cause

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16
Q

Hypervolemic hypernatremia causes (4)

tx (3)

tx for severe, all types, Na < 120 (2)

rate of correction

A

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

17
Q

Euvolemic hyponatremia causes (3)

tx (2+1)

A

SIADH, psychogenic

tx: correct underlying cause, free water restriction, consider lasix if Na < 120

18
Q

central pontine myelinosis - timing
symptoms (4)

risk reduction (2)

A

1 to 2 days after correction
AMS, cranial nerve deficits, quadraparesis, locked-in syndrome

slow correction, concomitant use of Lasix

19
Q

Hypernatremia, most common causes (3)

treatment

associated treatment formula

A

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

20
Q

Pictured entity
description of findings
cause categories (3), subcategories

A

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

21
Q

Primary symptom

Hypokalemia replacement adjuncts (2)

hyperkalemia cause categories (4)

A

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

22
Q

Hyperkalemia EKG changes (4)

dysrhythmias (4)

symptom

calcium contraindicated in management of hyperkalemia when

A

–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

23
Q

Parathyroid hormone function & mechanisms (3)

function of vitamin D, site of synthesis

hypercalcemia causes mneumonic review (11)

A

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

24
Q

Hypercalcemia classic mnemonic

Organ based sx

neuro - reflexes?
EKG
renal
G.I.
skeletal

A

•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
25
Q

Hypercalcemia treatment (4)

hypocalcemia, organ-based causes (3); electrolyte cause

A

Normal saline, Lasix, bisphosphonates, other (calcitonin, steroids, dialysis)

pancreatitis, renal failure-> vitamin D deficiency, low Mg

26
Q

Hypocalcemia symptoms (3) with eponyms (2)

EKG (2)

treatment should include

A

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

27
Q

Hypermagnesemia sx (4), tx

phosphorus has inverse relationship with

PTH effect on Phosphorus

Hyperphosphatemia tx (2)

A

Weakness, respiratory depression, hyporeflexia, heart blocks
TX: IV calcium

phosphorus to calcium
PTH lowers

•Treatment

–Oral phosphate binding gels

–Treat hypocalcemia if necessary

28
Q

Anion gap formula

decreased anion gap (3)

increased anion gap mnemonic

A

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

29
Q

Non-anion gap acidosis (6)

A

•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

30
Q

Metabolic alkalosis - underlying pathology

review causes

A

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

31
Q

Serum Osmolality formula

most common causes of elevated gap (3)

A

2Na +Glu/18 + BUN/2.8 = 280-295

ethanol, toxic alcohols, mannitol