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36 Cards in this Set
- Front
- Back
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4 CAUSES OF THYROTOXICOSIS W/O HIGH RADIOACTIVE IODINE UPTAKE
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1. SUBACUTE GRANULOMATOUS THYROIDITIS-"PAINFUL" (DEQUERVAIN'S)
2. SUBACUTE LYMPHOCYTIC THYROIDITIS-"PAINLESS" 3. LEVOTHYROXINE OVERDOSE 4. IODINE INDUCED |
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CLINICAL FEATURES OF AROMATASE DEFICIENCY
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AMBIGOUS GENITALIA (F)
CLITOROMEGALY PUBERTAL FAILURE (SEXUAL INFANTILISM) HIGH LEVELS OF TESTOSTERONE/ANDROSTENEDIONE/FSH/LH MOTHER CAN PRESENT WITH VIRILIZATION THAT ENDS WITH DELIVERY |
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4 CRITERIA FOR PARATHYROIDECTOMY IN ASX PT?
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- < 50 YO
- CA+ > BY 1 OVER LIMIT - RENAL IMPAIRMENT - DEXA < 2.5 |
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7 YO P/W ADVANCED SEXUAL CHARACTERISTICS. FSH/LH ARE HIGH. MLDX? IF LOW FSH/LH, DX?
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EARLY ACTIVATION OF HPAx ( CENTRAL PRECOCIOUS PUBERTY)
LOW FSH/LH SUGGESTS PERIPHERAL CAUSES (INCREASED HORMONE RELEASE BY GLAND) |
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15 YO F W/ DELAYED PUBERTY AND STREAK GONADS. DX? MNGT? HOW TO DIFFERENTIATE FROM TURNER'S?
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XY GONADAL DYSGENESIS.
GONADECTOMY STAT. - XY HAS NO UTERUS ON U/S |
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15 YO F PRESENTS W/ AMENORRHEA AND NORMAL SEXUAL CHARACTERISTICS. UTERUS IS ABSENT AND THERE ARE INGUINAL MASSES. DX? MGNT? DIFFERENCE FROM MULLERIAN DYSGENESIS?
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ANDROGEN INSENSITIVITY SYNDROME.
WAIT FOR BREAST DEVELOPMENT TO REMOVE TESTIS (LOW RISK OF MALIGNANCY). - NO AXILLARY HAIR. |
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MOST COMMON CAUSE OF CONGENITAL HYPOTHYROIDISM IN USA?
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THYROID DYSGENESIS
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ELECTROLYTE DISORDER IN A PT W/ ALKALOSIS. WHY?
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HYPOCALCEMIA.
HIGH PH FAVORS ALBUMIN-CA++ BINDING THEREFORE DECREASING IONIZED CA++ LEVELS |
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BESIDES TFTS AND PREGNANCY TESTS, WHAT OTHER PHYSIOLOGIC TESTS SHOULD BE DONE TO R/O CAUSES OF HYPERPROLACTINEMIA?
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BUN/CR
LFTS * LIVER AND RENAL DZ RAISE PROLACTIN |
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BEST INITIAL TX FOR GRAVES EXOPHTHALMOS?
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STEROIDS
* RADIATION IF NO RESPONSE |
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PT P/W A THYROID NODULE. TFTS ARE WNL. NEXT STEP?
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BX ANY NODULE AS/W NORMAL TFTS
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PT W/ A THYROID NODULE CAUSING HYPERTHYROIDISM IS AT RISK OF WHAT CODITION IF LEFT UNTREATED?
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BONE LOSS FROM INCREASED OSTEOCLASTIC ACTIVITY 2/2 THYROID HORMONE STIMULATION
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FINDING OF BX OF PT ABUSING THYROID HORMONES?
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FOLLICULAR ATROPHY
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WHATS THE COMPLICATION IN A CHILD WITH PRECOCIOUS PUBERTY? TX?
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SHORT STATURE 2/2 PREMATURE FUSION OF EPIPHISEAL PLATE.
TX: GNRH AGONIST |
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WHICH IS THE MOST RELIABLE MARKER OF RECOVERY FROM DKA?
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ANION GAP.
*URINE KETONES TAKE LONGER TO DISAPPEAR |
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MENTION 3 VIRUSES CAN CAUSE B-CELL DESTRUCTION LEADING TO IDDM.
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RUBELLA
COCKSAKIE MUMPS |
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F PT P/W SIGNS OF VIRILIZATION AND REPORTS NORMAL PERIODS. DX? WHATS ELEVATED?
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CAH
17-HDP |
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WHY OBESE, POSTMENOPAUSAL WOMEN HAVE LESS VASOMOTOR SX THAN THIN WOMEN?
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PRESENCE OF AROMATASE IN PERIPHERAL FAT RESUMES THE CONVERSION OF ANDROGENS INTO ESTROGENS AFTER OVARIAN FAILURE
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PT P/W HYPOTENSION, HYPERPIGMENTATION OF THE AXILLA AND FATIGUE. LABS SHOW LOW NA+, HIGH K+ AND BUN. BEST INITIAL TEST? DDX (4) AND HOW R/O? TX OF CHOICE?
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COSYNTROPIN STIMULATION TEST (HIGH CORTISOL S/P TEST R/O DZ).
1 CANCER (LUNG) 2 ADRENOLEUKODYSTROPHY (LONG CHAIN FATTY ACID LEVELS) 3 HEMOCHROMATOSIS (TRANSFERRIN LEVELS LOW) 4 TB AND PHEO (CXR/CT SHOW CALCIFICATIONS) TOC: HYDROCORTISONE |
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PT P/W S/S OF HYPERTHYROIDISM. A NODULE IS NOTED WHICH TAKES UP RADIOACTIVE IODINE THOUGH THERE'S NO UPTAKE IN REST OF THE GLAND. DX?
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TOXIC ADENOMA
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PT P/W WEAKNESS, POLYURIA AND HA. BP IS 116/140. LABS SHOW NORMAL NA+, LOW K+ AND METABOLIC ALKALOSIS. URINE K+ IS HIGH. DX? MGT?
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PRIMARY HYPERALDOSTERONISM.
SX OR SPIRONOLACTONE. |
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PT ON CHRONIC STEROID TX UNDERGOES SX AND BECOMES HYPOTENSIVE W N/V AND WEAKNESS. DX? INITIAL STEP IN MGT? SKIN CHANGES ASS/W THIS CONDITION? FIRST DX TEST?
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ADRENAL INSUFFICIENCY.
IVF AND HYDROCORTISONE (DONT DELAY TX 2/2 GETTING DX RIGHT). VITILIGO/ALOPECIA AREATA. ACTH CHALLENGE TEST (IN CHRONIC INSUFFICIENCY DO AM CORTISOL FIRST). |
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DEFINITION OF PRIMARY AMENORRHEA
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NO MENSES W NORMAL SEX CHARACTERISTICS BY 16 YO OR LACK OF SEX CHARACTERISTICS BY 13 YO
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PT P/W SX/SI OF CUSHING'S SYNDROME. WHATS THE WORK UP?
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1- LOW DOSE DEXAMETHASONE..LOW AM CORTISOL?--> R/O CUSHING'S.
2- HIGH AM CORTISOL--> DO 24 HR URINE CORTISOL...STILL HIGH?---> DO HIGH DOSE DEXAMETHASONE...IF CORTISOL IS SUPRESSED, IT'S CUSHING'S DZ...CORTISOL STILL HIGH?---> DO ACTH LEVEL...LOW ACTH---> ADRENAL TUMOR...HIGH ACTH---> LUNG CA |
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3 MAIN DIFFERENCES BTN 1* AND 2* HYPERALDOSTERONISM?
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- 1* ALD---> NO EDEMA, HTN AND LOW RENIN...
- 2* + EDEMA, HOTN AND HIGH RENIN |
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HOW CAN A PT W/ ADDISONS DEVELOPS ACIDOSIS?
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LOW ALDO---> NA+ EXCRETION / K+ AND H+ REABSORPTION---> NONANION GAP ACIDOSIS
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WORK UP TO DX ACROMEGALY? TX?
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1- IGF MIGHT BE ENOUGH
*CAN ALSO GIVE GLUCOSE AND MEASURE GH 2 HOURS LATER: NORMAL RESPONSE CONSISTS IN DECREASE OF GH, HIGH GH IS SUGGESTIVE OF ACROMEGALY. 2- MRI ONLY FOR LOCALIZATION OF ADENOMA AFTER HORMONAL DISORDER DX. TX: OCTREOTIDE FIRST LINE, DOPAMINE AGONIST AND SX |
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PT P/W "WORST HA EVER!", WEAKNESS IN HIS RIGHT ARM AND LEG AND PERIPHERAL BLINDNESS. MENINGEAL SIGNS ARE NOTED AS WELL AS HOTN. DX? WHAT INDICATES EMERGENT SX? TEST OF CHOICE?
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1- PITUITARY APOPLEXY
2- VISION LOSS, EOM PALSY INDICATES CAVERNOUS COMPRESSION. 3- MRI IS BETTER BC CAN IDENTIFY NECROSIS BUT CT PREFERRED IN UNSTABLE PTS |
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MENTION 3 CAUSES OF NEPHROGENIC DIABETES INSIPIDUS
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1- DRUGS (LITHIUM, DEMECLOCYCLINE, COLCHICINE)
2- HYPERCALCEMIA 3- SICKLE CELL DZ |
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WORK UP OF DIABETES INSIPIDUS?
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1- RESTRICT WATER
2- SERUM OSM > URINE OSM SUGGESTIVE 3. GIVE ADH..RISE IN URINE OSM IS DX FOR CDI VS SAME IN NDI |
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TX FOR NDI
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- DIURETICS
- NSAIDS |
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MEDICATION TO CONTROL ACROMEGALY SX IF OCTREOTIDE IS UNSUCCESFUL?
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PEGVISOMANT: GH ANTAGONIST
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TEST OF CHOICE IF YOU SUSPECT EXTRA-ADRENAL PHEOCHROMOCYTOMAS?
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MIBG SCAN
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PT P/W A NECK LUMP. TSH IS LOW AND T4 IS HIGH. NEXT STEP?
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RAI SCAN.
HOT NODULE DOESNT NEED FNB JUST TX AS HYPERTHYROIDISM |
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PT P/W NECK LUMP. TSH AND T4 ARE WNL. NEXT STEPS?
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U/S THEN BX
*U/S DETECTS CYSTIC VS SOLID NODULE. NO FNB IF CYSTIC AS THERE'S NO MALIGNANCY RISK |
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CAUSE OF CARPAL TUNNEL SYNDROME A/W MATRIX SUBSTANCE ACCUMULATION?
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HYPOTHYROIDISM
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