THE THYROID IS THE ONLY ENDOCRINE GLAND THAT STORES LARGE QUANTITIES OF HORMONE, T/F
TRUE
WHAT CLINICAL SIGN "TYPIFIES" THYROID STORM?
AMS OR COMA
THYROID STORM IS THE MOST SEVERE MANIFESTATION OF HYPERTHYROIDISM
GIVE 3 SYMPTOMS OF HYPERTHYROID IN A GAM GAM
WEIGHT LOSS, SHOB, DEMENTIA, AFIB, THYROTOXIC PERIODIC PARALYSIS
THYROID DISORDERS ARE THE MOST COMMON ENDOCRINE DISORDERS AFTER DIABETES, T/F
TRUE
HYPOTHYROIDISM IS THE THE MOST COMMON DISORDER OF THE THYROID
MAJORITY OF CASES ARE DUE TO INTRINSIC GLAND FAILURE
T3 OR T4 IS MORE BIOLOGICALLY ACTIVE?
T3
ONLY ABOUT 20% OF CIRCULATING T3 IS DIRECTLY RELEASED BY THE THYROID. THE REST IS FROM PERIPHERAL CONVERSION OF T4 TO T3
OVER 99.5% OF THYROID HORMONES ARE PROTEIN BOUND TO THYROXINE-BINDING GLOBULIN MAKING THEM METABOLICALLY INACTIVE. ONLY FREE T4 AND T3 ARE CLINICALLY RELEVANT
TYPICALLY OCCURS SECONDARY TO SOME SORT OF STRESSOR, T/F
TRUE
ACUTE REACTION TO SURGERY, TRAUMA, INFECTION, IODINE LOAD, CHILD BIRTH, MI, PE, HYPEREMESIS GRAVIDARUM, PREECLAMPSIA, DKA
WHICH DIRECTION OF GAZE MAY BE AFFECTED BY GRAVES DISEASE?
UPWARD GAZE
INFILTRATION OF INFERIOR RECTUS MUSCLE
OPTIC NERVE MAY BE INVOLVED DUE TO ENLARGED, INFLAMED ORBITAL CONTENTS CAUSING VISUAL LOSS
EYELID EDEMA, HYPEREMIA, CHEMOSIS, RESTRICTED EYE MOVEMENT, EXOPHTHALMOS
WHAT IS THE MOST COMMON CAUSE OF CENTRAL HYPOTHYROIDSM?
PITUITARY ADENOMA
WHAT IS THE BASIC FUNCTION OF THYROID HORMONE?
INFLUENCE METABOLISM OF CELLS BY INCREASING BASAL METABOLIC RATE
IF LEFT UNTREATED MORTALITY APPROACHES 100%, T/F
TRUE
MORTALITY LOWERED TO 10-30% WITH PROMPT TREATMENT
YOUNGER PATIENTS TYPICALLY PRESENT WITH SIGNS OF SYMPATHETIC STIMULATION VS OLDER ADULTS BECAUSE...
OLD PEOPLE LACK THE SAME DEGREE OF ADRENERGIC RESPONSE THAT YOUNGER PATIENTS HAVE
OLDER PATIENTS WILL HAVE MORE VAGUE SYMPTOMS LIKE WEIGHT LOSS, FATIGUE
GIVE 8 SYMPTOMS OF HYPOTHYROIDISM...
WHAT 2 PARTS OF THE BRAIN REGULATE THYROID HORMONE PRODUCTION?
GIVE 3 SYMPTOMS OF THYROID STORM...
PYREXIA (104-106), EXTREME TACHYCARDIA (OFTEN OUT OF PROPORTION TO FEVER), ALTERED MENTAL STATUS
BURCH-WARTOFSKY POINT SCALE IS OVER 30 YEARS OLD, BUT MAY BE OF BENEFIT
PRETIBIAL MYXEDEMA
CONFLUENT, PAINLESS, REDDISH RAISED NUDLES AND PLAQUES OVER PRETIBIAL AREA AND DORSUMS OF FEET, OFTEN DESCRIBED AS ORANGE SKIN
WILL FEEL INDURATED, BUT WON'T PIT
TYPICALLY SEEN IN CONJUNCTION WITH GRAVES OPHTHALMOPATHY
HOW WILL MYXEDEMA COMA PRESENT?
AMS, HYPOTHERMIA, AND A CONCOMITANT PRECIPITATING EVENT
NOT ALL WILL PRESENT WITH ALL 3
MORTALITY APPROACHES 100% WITHOUT TREATMENT, AND UP TO 30% WITH OPTIMAL TREATMENT
EXCESS IODINE MAY CAUSE HYPO- OR HYPER- THYROIDISM, T/F
TRUE
EXCESS IODINE MAY INHIBIT THE RELEASE OF THYROID HORMONE OR INDUCE HYPERTHYROIDISM (GOITER, GRAVES DISEASE)
WHAT BENEFIT DOES PROPANOLOL HAVE OVER OTHER BETA BLOCKERS FOR HYPERTHYROID TREATMENTS?
BLOCKS CONVERSION OF T4 TO T3
WHAT ARE 2 OTHER BETA BLOCKERS TO CONSIDER IF YOU'RE CONCERNED ABOUT BETA BLOCKADE DUE TO ASTHMA/COPD OR HEART FAILURE?
WOULD AFIB IN THYROID STORM BE HARD TO TREAT?
GIVE 6 SYMPTOMS OF THYROTOXICOSIS
Constitutional: Weight loss despite hyperphagia, fatigue, generalized weakness
Hypermetabolic: Heat intolerance, cold preference, excessive perspiration
Cardiorespiratory: Palpitations, dyspnea, dyspnea on exertion, chest pains, poor exercise toleran
Gastrointestinal: Nausea, vomiting, diarrhea, dysphagia
Neuropsychiatric: Anxiety, restlessness, hyperkinesis, emotional lability, confusion, insomnia, poor attention
Neuromuscular: Myopathy, myalgias, tremor, proximal muscle weakness (difficulty getting out of a chair or combing hair)
Ophthalmologic: Tearing, irritation, wind sensitivity, diplopia, foreign body sensation
Thyroid gland: Neck fullness, dysphagia, dysphonia
Dermatologic: Flushed feeling, hair loss, pretibial swelling
Reproductive: Oligomenorrhea, amenorrhea, menometrorrhagia, decreased libido, gynecomastia, erectile dysfunction, infertility
GIVE 5 THINGS THAT MAY PRECIPITATE MYXEDEMA COMA...
WHAT ARE THE 3 WAYS MEDICATIONS GIVEN FOR THYROID STORM AFFECT THYROID HORMONE?
REDUCE TH PRODUCTION
REDUCE TH RELEASE
REDUCE CONVERSION OF T4 TO T3
MOST COMMON CARDIAC FINDING IN HYPERTHYROIDISM...
TACHYCARDIA
Vital signs: Tachycardia, widened pulse pressure, bounding pulses, fever
Cardiac: Hyperdynamic precordium, systolic flow murmur, prominent heart sounds, systolic rub (Means-Lerman scratch), tricuspid regurgitation, atrial fibrillation, evidence of heart failure
Ophthalmologic: Widened palpebral fissures (stare), lid lag, globe lag, conjunctival injection, periorbital edema, proptosis, limitation of superior gaze
Neurologic: Fine tremor, hyperreflexia, proximal muscle weakness
Psychiatric: Fidgety, emotionally labile, poor concentration
Dermatologic: Warm, moist, smooth skin; rosy cheeks, blushing face; fine brittle hair; alopecia, flushed facies; palmar erythema; hyperpigmented pretibial plaques, nodules, or induration that is nonpitting; onycholysis (Plummer nails, separation of the distal portion of the fingernail from the nail bed)
Neck: Diffuse symmetric thyroid enlargement, sometimes with a bruit and palpable thrill; thyroid with multiple irregular nodules or a prominent single nodule; tracheal deviation, venous prominence with arm elevation (Pemberton sign)
WHAT ADDITIONAL MEDICATION IS TYPICALLY RECOMMENDED FOR MYXEDEMA COMA IN ADDITION TO TH REPLACEMENT?
HYDROCORTISONE
MYXEDEMA COMA MAY HAVE CONCOMITANT ADRENAL INSUFFICIENCY
WHAT 2 MEDICATIONS CAN BE GIVEN TO REDUCE TH PRODUCTION?
PROPYLTHIOURACIL, METHIMAZOLE
PTU WILL ALSO IMPAIR CONVERSION OF T4 TO T3
IF PREGNANT, PTU PREFERRED IN 1ST TRIMESTER, METHIMAZOLE IS PREFERRED IN 2ND AND 3RD
A NORMAL TSH LEVEL EXCLUDES HYPERTHYROIDISM, T/F
TRUE
IN THYROTOXICOSIS THE TSH IS DEPRESSED OR UNDETECTABLE
ELEVATION OF FREE T4 AND T3 LEVELS IN CONJUNCTION WTH TSH SUPPRESSION IS DIAGNOSTIC
METABOLISM OF SEDATIVES, NARCOTICS AND ANESTHETICS MAY BE SLOWED AND CAUSE PROLONGED EFFECT IN MYXEDEMA COMA, T/F
TRUE
CONSIDER USING LOWER DOSES
WHAT CAN YOU GIVE TO BLOCK THE RELEASE OF STORED TH?
IODINE
MUST WAIT AT LEAST ONE HOUR AFTER GIVING PTU OR METHIMAZOLE OR YOU COULD INCREASE TH SYNTHESIS
MAY GIVE AS POTASSIUM IODIDE OR LUGOL'S SOLUTION
WHAT IS AN ALTERNATIVE TO IODINE, AND IS THE ACTUAL AGENT OF CHOICE FOR IODINE-INDUCED HYPERTHYROIDISM?
NAME 3 DRUGS TO AVOID IN A THYROTOXIC PATIENT...
AMIODARONE, IODINE CONTRAST MEDIA, PSEUDOEPHED, KETAMINE, ALBUTEROL, ASPIRIN
A DIABETIC PRESENTS FOR AMS. YOU CALCULATE A GCS OF 10, THEY ARE HYPOTHERMIC, BRADYCARDIC. YOU FIND THEY ARE IN DKA AND THEIR TSH IS VERY ELEVATED. SHOULD YOU GIVE THEM THYROID REPLACEMENT?
YES
WHAT DRUG CLASS WILL INHIBIT CONVERSION OF T4 TO T3?
CORTICOSTEROIDS
HYDROCORTISONE OR DEXAMETHASONE
YOU CAN PUT SOMEONE INTO THYROID STORM WHEN TREATING FOR MYXEDEMA COMA, T/F
TRUE
INITIAL LOADING DOSE OF THYROID HORMONE IS 200-400 MICROGRAMS. CONSIDER A LOWER DOSE IN SMALL PEOPLE, OLD PEOPLE, HX OF CAD AND ARRHYTHMIAS
WOULD A BETA BLOCKER OR CCB BE PREFERRED FOR AFIB RATE CONTROL IN THYROID STORM?
BETA BLOCKER
CCB MORE PRONE TO HYPOTENSION IN THIS SETTING