THYROID/PARATHYROID—–DANIEL TODD, MD FROM THE 4TH AND 5TH BRANCHIAL ARCH(MESODERM) FOLLICULAR CELLS FROM THE 1ST AND 2ND BRANCHIAL ARCHES—-CAN FORM NEOPLASM IN BOT C-CELLS (PARAFOLLICULAR CELLS)–FROM THE ULTIMOBRANCHIAL BODY—-NEURAL CREST CELL ORIGIN—-NEUROENDOCRINE—CANNOT FORM MEDULLARY CA IN THE BOT 80% HAVE SOME PYRAMIDAL LOBE 1/3000 HAVE SOME LINGUAL THYROID FIBROUS CAPSULE—-MIDDLE LAYER OF DCF LYMPHATIC DRAINAGE—–PRETRACHEALCRICOTHYROID (DELPHIAN)/ORACLE OF DELPHI/ LN—THYROID CA UNTIL PROVEN OTHERWISE—–DEEP CERVICAL LN_S—–ANY THYROID LAT TO IJV=METS HYPOTHYROIDISM—-1/2 CAN PRESENT WITH HORSENESS_–CONSIDER FOR DEPRESSION , HYPERLIPIDEMIA, DEMENTIA, FATIQUE, SNHL BEST SCREENING TEST IS A TSH—COST EFFECTIVE SO NOT TRY TO TEST THYROID STATUS IN HOSPITALIZED PTS, PTS ON STEROIDS, AMIODARONE, LITHIUM, PROPRANOL, ASA, DILANTIN, OR DA (FES04 CAUSES DECREASED ABSORBTION) I131 CAN CAUSE STERILITY ASCHER_S=AUTO D—-NONTOXIC GOITER, DOUBLE LIP DEFORMINTY, BLEPHAROCHALASIA PENDRED_S=AUTO R—-GOITER(PERCHLORATE +)–FAULTY IODINATION OF TYROSINE, SNHL, HYPOTHYROID CHECK A TSH PRIOR TO AN IODINE SCAN TO AVOID JOD -BASDOW PHENOM (MONTHS OF THYROTOXICOSIS) AND FUTURE INABILITY TO GIVE RAI DIFFUSE GOITER—GRAVES, HASHIMOTOS, LYMPHOMA, ANAPLASTIC CA—ALL TOUGH SURGERIES THYROGEN=TSH ANALOGUE—WILL MAKE WELL DIFF THYROID CA GROW THYROID NODULE MORE PAPERS ABOUT WELL DIFFERENTIATED THYROID CARCINOMA THAN THERE ARE DEATHS FROM IT! 4-5% POP HAS A PALPABLE NODULE—-30% HAVE A SONOGRAPHICALLY EVIDENT NODULE TYPE OF THYROID ENLARGEMENT–SMOOTH AND DIFFUSE VS NODULAR(SINGULAR VS MULTIPLE) 1-2% INCIDENCE OF MALIGNANCY IN MULTI NODULAR GOITER (FNA A DOMINANT NODULE IN MULTINODULAR Dz) UP TO A 10% INCIDENCE OF CA IN A CYSTIC LESION 1/200 NODULES MAY BE CARCINOMA LARGE CYSTS WITH CLEAR WATERY FLUID—-THINK PARATHYROID CYST (PEMBERTON_S MANUEVER FOR SUBSTERNAL Dz) PRESSURE ON ADJACENT STRUCTURES–DYSPHAGIA, ODYOPHAGIA, STRIDOR FROM CHONDROMALACIA OF THE TRACHEAL ARCHES, HOARSENESS FROM TVC EDEMA, SUP. (VENA CAVA) MEDIASTINAL SYNDROME INFILTRATION OF ADJACENT STRUCTURES—TVC PARALYSIS, TRACHEAL FIXATION, HEMOPTYSIS, HORNER_S SYNDROME, CN PAULSEY, BRACHIAL PLEXUS INVOLVEMENT EVIDENCE OF REGIONAL AND DISTANT METS–LAD (CRICOTHYROID NODE=DELPHIAN NODE) EVIDENCE OF ENDOCRINE DYSFUNCTION 80% OF PTS WITH WELL DIFF THYROID CA PRESENT WITH A NODULE 70% OF THYROID CA ARE FEMALE IF PT UNDER 20_MORE LIKELY TO BE A CA 4% OF POP HAS A THYROID NODULE(6% FEMALES, 1-2% MALES)—OF THESE OVERALL 5-30% HARBOR A MALIGNANCY LOW DOSE RT (OFTEN A 5-30 YEAR LATENCY) FOR TINEA CAPITUS, LYMPHOID HYPERPLASIA, AND THYMIC ENLARGEMENT—-REALLY QUIT THIS PRACTICE IN 1955 TN99 SCAN—COLD NODULE MORE LIKELY (20%) THAN HOT (10%) TO BE CA 95% OF ALL NODULES WILL BE COLD—PROBABLY VERY LITTLE UTILITY IN NUC MED SCAN PT UNDER 20 OR OLDER 60 -MORE LIKELY TO HAVE A CA C COLLIOD CYST A ADENOMA(40% of cold nodules)—TRUELY A CLONAL NEOPLASM T THYROIDITIS (ACUTE, LYMPHOCYTIC, GRANULOMATOUS) C CA H HEMATOMA P A PARATHYROID ABSCESS L LYMPHOMA(ALMOST ALWAYS ARISES IN AREA OF PREVIOUS AUTOIMMUNE THYROIDITIS)!!!—-FNA SUGGESTIVE OF LYMPHOMA —DO AN AUTOIMMUNE W/U M MET CA HISTORY, FH, RADIATION EXPOSURE, PE CHILD GETS CT OF THE NECK, CXR AND TSH TO START FNA= GOLD STANDARD IN THE ADULT FNA (FIRST POPULARIZED BY HAYS MARTIN IN 1930) WITH 22 GAUGE?(SOME USE UP TO A 25) NEEDLE TO A 3-10 ML SYRINGE—LOOSEN UP THE PLUNGER—CONSIDER USING A BUTTERFLY NEEDLE—CLEAN SKIN WITH ALCOHOL WIPE—GENERALLY NO ANESTHETIC NEEDED–FIX MASS AGAINST SOMTHING BETWEEN FINGERS–TELL PT NOT TO SWALLOW–INSERT NEEDLE INTO MASS WHILE KEEPING THE NEEDLE IN THE MASS—APPLY NEG PRESSURE—MAKE 3 TO 6 PASSES THROUGH THE MASS— RELEASE THE NEGATIVE PRESSURE SO AS NOT TO SEED THE SKIN AND SUB Q TISSUE GENTLY PUSH THE ASPIRATED MATERIAL ON THE SLIDE—CYTOSPRAY OR DIP QUICKLY IN 95% ETOH CAN CONSIDER USING US GUIDANCE—–ESPECIALLY FOR A SECOND TRY
PUSH ASPIRATED MATERIAL ON TO A SLIDE USING A NEW SYRINGE AND FIX WITH CYTOSPRAY–? ONE CASE OF TUMOR SEEDING? A NON DIAGNOSTIC FNA IS AS IF YOU DROPPED IT ON THE FLOOR—MUST REPEAT IT 2% FALSE NEGATIVE 10% FALSE POSITIVE—-CAN OPERATE SOLEY ON THE FNA RESULT IF A DIFFINITIVE MALIGNANCY IS REPORTED A LOT OF INCONCLUSIVES—HURTHLE CELLS COULD BE HASHIMOTOS, HURTHLE CELL ADENOMA, OR HURTHLE CELL CA THE DX OF FOLLICULAR CA IS BASED ON PATHOLOGIC EVIDENCE OF INVASION—NOT CELLULAR CHANGES SEEN ON FNA CAN CONSIDER A US OR CT GUIDED “CORE” BIOPSY—-THE PRESENCE OF FOLLICULAR CELLS ON FNA COULD REPRESENT FOLLICULAR ADENOMA, FOLLICULAR ADENOCA, OR PAPILLARY CA CXR,CBC, SMAC (CALCIUM AND PHOSPHOROUS AND MG++), TSH—-PARATHYROID DZ OFTEN CORRELATES WITH THYROID DZ—CT WITH CONTRAST IS A VERY USEFUL STUDY BUT WILL DELAY AND RADIOACTIVE TREATMENTS—-CAN ALSO LEAD TO JOD BASDOW PHENOM RADIONUCLEOTIDE SCINTIGRAPHY, US–USEFUL IN CHILDREN AND PREGNANT PTS, CT, MRI TFT_S (TSH), THYROGLOBULIN, TCT(WITH PENTAGASTRIN OR CALCIUM STIM) ANTIMICROSOMAL ANTIBODIES(PEROXIDASE AB)—–A GOOD IDEA TO TEST FOR A LOT “THE GREAT MIMICKER” RET PROTO-ONCOGENE FOR MEDULLARY THYROID CA (CAN DO WITH A BLOOD TEST) SHOULD TEST ALL FAMILY MEMBERS FOR POSSIBLE MEN IIA AND B SYNDROME THYROID CA RELATIVELY RARE MOST COMMON ENDOCRINE TUMOR WELL DIFF CA = PAPILLARY AND FOLLICULAR = >85% OF THYROID CA Rx=CONTROVERSY ABOUNDS WELL CIRCUMSCRIBED, ISOLATED, LESS THAN 1-1.5 CM, IN A PT 20-40, WITH NO Hx OF RT–HEMITHYROIDECTOMY AND ISTHMUTHECTOMY—THE LEAST SURGERY TO EVER DO—–ALWAYS ID RLN AND PARATHYROIDS—STAY DEEP TO THE SURGICAL CAPSULE USE FROZENS—BUT INFORM PTS THEY MAY NEED FURTHER SURGERY BASED ON PERMANENTS SO NOT DO ANYTHING DANGEROUS BASED ON FROZENS ALONE ALL OTHERS–TOTAL THYROIDECTOMY, B TYPE III (TOTALLY FUNCTIONAL)SELECTIVE NECK DISSECTIONS(WITH LEVEL I PRESERVATION) OR SELECTIVE ANT COMPARTMENT / LEVEL VI (CENTRAL COMPARTMENT) NECK DISSECTIONS, WITH RAI Rx POST OP NODE PICKING/PLUCKING PROCEDURE— LEVEL II,III,AND IV—-CONTRAINDICATED BECAUSE OF A HIGHER INIDENCE OF LOCAL/REGIONAL RECURRENCE IN A VIOLATED/SCARRED BED PAPILLARY(FINGER LIKE PROJECTIONS) (62%) AGE 30-40 90% 5 YEAR SURVIVAL FEMALE 3:1 PREDISPOSING FACTORS: LOW DOSE RT(ACNE-ADENOTONSILLITIS-CHERNOBLE), IODINE EXCESS, HASHIMOTOS THYROIDITIS, GARDNER’S SYNDROME (COLONIC POLYPOSIS, FRONTAL SINUS OSTEOMAS), COWDENS DZ(FAMILIAL GOITER, SKIN HAMARTOMAS, PAPILLARY CA) 50% B–HIGH CONCENTRATION OF INTRATHYROID LYMPHATICS ACCOUNTS FOR MULTICENTRICITY OF MONOCLONAL TUMOR, 30% LAD—NOT A WORSE Px, 5% DISTANT METS(PRIMARILY LUNG AND BONE) PSAMOMMA BODIES= (ALSO SEE WITH MENINGIOMAS) CALCIFIC DEPOSITS, MAY SEE ON X-RAY—-CALCIFICATION WITH CYSTIC THYROID MASS), INTRANUCLEAR VACUOLES WITH CLEARING OUT OF THE NUCLEAR CHROMATIN = ORPHAN ANNIE EYES (BIG SCLERA WITH NO PUPILS), GROUND GLASS APPEARANCE, OVER ALL FRAUNDY APPEARANCE—-THESE PSUEDOINCLUSIONS ARE PATHOGNEUMONIC OF THE Dz_CAN MAKE DX ON FNA PRIMARILY MET VIA LYMPHATICS REGIONAL METS—NOT WORSE PX IN KIDS—SLIGHTLY WORSE PX IN ADULTS <1.5 CM = OCCULT = BETTER Px EXTENT BEYOND THE CAPSULE = SLIGHTLY WORSE Px TALL CELL AND DIFFUSE SCLEROSING VARIANTS DO WORSE (AGGRESSIVE) FOLLICULAR VARIANT—-BEHAVES LIKE FOLLICULAR CA MAY BE HURTHLE CELL VARIANT—BEHAVES LIKE PAPILLARY CA FOLLICULAR(10-18%) PREDISPOSING FACTORS: IODINE DEFICIENCY FEMALE 3:1, MEAN AGE 40-50 60% TEN YEAR SURVIVAL TEND TO MET HEMATOGENOUSLY-FAMOUS FOR DISTANT METS (REGIONAL METS ARE RARE)—-LUNG AND BONE (AND LIVER , BRAIN, BLADDER, AND SKIN) HALLMARK IS ANGIOINVASION, CAPSULAR INVASION–CORRESPONDS TO Px—-MUST HAVE THIS MACROSTRUCTURE TO MAKE Dx—-CAN NOT Dx ON FNA—ALSO DIFFICULT TO MAKE DX ON FROZENS —-IF YOU DO HAVE TO GO BACK—-DO IT EARLY—WITHIN 1 WEEK TO LESSEN ANY POSSIBLE SCARRING. DIFFERENTIATE FURTHER TO: CLEAR CELL (BETTER PROGNOSIS)–NOT EOSINOPHILIC– VERY SENSITIVE TO I 131
HURTHLE CELL _ OXYPHILIC VARIANT OF FOLLICULAR—5% OF ALL THYROID NEOPLASMS (WORSE PROGNOSIS)–NOT AS RESPONSIVE TO RAI— OLDER PTS—-MEAN AGE 62 FEMALE PREPONDERANCE CELL SIZE IS LARGER —GRANULAR EOSINOPHILIC (OXYPHILIC) CYTOPLASM_VERY DISTINCT HISTO APPEARANCE HURTHLE CELLS APPEAR IN HASHIMOTOS, HURTHLE CELL ADENOMA, AND HURTHLE CELL CA—-MUST DEMONSTRATE > 75 % HURTHLE CELLS IN AN ENCAPSULATED FOLLICULAR NEOPLASM—-CONSIDER INTRAOP FROZENS USUALLY PRESENT AS A SOLITARY NODULE 50% REGIONAL LAD METS MEDULLARY(2-10%) NO PREDISPOSING FACTORS OTHER THAN HEREDITY—C-CELL HYPERPLASIA MAY WALL BE A PREMALIGNANT CONDITION A BAD Dz TO GET—METS ARE OFTEN SMALL ROCK HARD AND IMPOSSIBLE TO CLEAR—LOCALLY CAN ACT LIKE REIDELS STRUMA PARAFOLLICULAR OR C-CELLS OF THE THYROID—A DIFFERENT CELL LINE—–DOES NOT TAKE UP IODINE—RAI OBSOLETE APUD CELLS OF NEURAL CREST ORIGIN (ULTIMOBRANCHIAL BODY)- IMPOSSIBLE TO HAVE THIS ENTITY IN THE LINGUAL THYROID SECRETES TCT (TONES THE BONES) 32 AA SEQUENCE WHICH ANTOGONIZES OSTEOCLASTIC ACTIVITY, PROMOTES BONE ABSORPTION OF CA++, AND PROMOTES URINARY EXCRETION OF CA++—CAN ALSO LEAD TO WATERY DIARRHEA AND FLUSHING AS A PARANEOPLASTIC SYNDROME OF HYPERCALCITONINEMIA SECRETE TCT—-TONES THE BONES IN FISH AND ASTRONAUTS(WEIGHTLESS ENVIRONMENT) ASK ABOUT SX CONSISTENT WITH PHEO (PALPITATIONS, HTN, TREMULOUS) AND HYPER PTH—-BONES, STONES, ABD GROANS ECT..—ASK ABOUT MUCOSAL NEUROMAS OF GI TRACT OR OC ROUND/POLYGONAL TO SPINDLE SHAPED CELLS—_CARCINOID LIKE_ ECS OR REGIONAL METS PORTENDS A MUCH WORSE Px SHOULD DO AN ELS (ELECTIVE NECK DISSECTION) FOR THE N0 NECK IF THE PRIMARY IS > 2 CM OR PALPABLE HISTOPATH: AMYLOID STROMA—(LIKE ACINIC CELL CA OF THE SALIVARY GLANDS)–ROUND TO POLYGONAL TO SPINDLE SHAPED CELLS ARRANGED IN NESTS AND SHEETS SEPARATED BY FIBROVASCULAR AMYLOID STROMA--+CONGO RED—BRILLIANT–FILM DOES NOT CAPTURE WHAT THE MICROSCOPE CAN—+ BIREFERINGENCE (ABLE TO POLARIZE LIGHT), +IMMUNOPEROXIDASE STAIN, + CALCITONIN IMMUNOHISTOCHEMICAL STAIN Dx–PENTAGASTRIN STIM TEST TO MEASURE CA++ LEVELS (ALSO PENDRED_S(AUTO R)) INDIUM OCTREOTIDE(SOMATOSTATIN) SCAN, PARATHYROID HORMONE LEVELS SEND BLOOD TO MAYO FOR MEN (RET PROTO ONCOGENE) ANALYSIS TCT LEVELS–REALLY SHOULD FALL TO ZERO IN ABOUT 3 WEEKS, CXR, RAI SCAN, CA++, THYROID PROFILE TEST FOR CATECHOLAMINE SECRETING TUMORS_ HOT GUANO SCAN–24 HOUR URINE FOR VMA, EPI, NOREPI, METANEPHRINE, NORMETANEPHRINE CEA LEVELS, ACTH LEVELS, PROSTAGLANDIN LEVELS CT SCAN OF THE NECK CHEST AND ADRENALS ENDOCRINOLOGY CONSULT 80-90% SPORADIC–USUALLY UNILAT–ACTUALLY WORSE Px -50% SURVIVAL AT 5 YEARS PEAK = 4TH – 6TH DECADE 1/3 PRESENT WITH INTRACTABLE DIARRHEA—HIGH TCT, PROSTAGLANDINS, SEROTONIN, VIP–GUT HYPER MOTILITY NON-MEN FAMILIAL TYPE IS UP TO 25% OF SPORATIC—-GOOD PX 10-20% FAMILIAL(FAMILIAL MEDULLARY THYROID CA) OR PART OF A MEN SYNDROME–ACTUALLY BETTER Px–OFTEN BILATERAL INITIALLY SCREEN THE PT FOR A GERM CELL MUTATION–IF THAT IS + THEN: SHOULD SCREEN FAMILY MEMBERS FOR THE RET PROTO-ONCOGENE—LOCUS ON CHROMOSOME #10 MEN I (WERMER_S SYNDROME)-—-ASSOC WITH NON-MEDULLARY THYROID CA, MULTI-GLAND PARATHYROID HYPERPLASIA AND HYPERPARATHYROIDISM, PANCREATIC ISLET CELL TUMORS, AND PITUITARY TUMORS MEN IIA (SIPPLES SYNDROME)--AUTO D–RARE—BETTER Px—80% SURVIVAL AT 5 YEARS BILAT PHEOS–BEWARE OF CATECHOLAMINES!—OLD 10% RULE (10% BILAT, EXTRA-ADRENAL, MALIGNANT DOES NO APPLY) BILAT MEDULLARY CA—USUALLY C-CELL HYPERPLASIA PARATHYROID HYPERPLASIA –HYPERPARATHYROIDISM MEN IIB–RAREST--WORSE Px—SURVIVAL 50% AT 2 YEARS——MORE COMMON IN CHILDREN/ADOLESCENCE-(YOUNGER AGE)– 3RD DECADE AUTO D OR SPORADIC BILAT PHEOCHROMOCYTOMAS BILAT MEDULLARY CA ASSOC MUCOSAL NEUROMAS OF THE ANT. TONGUE, CONJUNCTIVA, TARSUS, LIPS, BUCCAL MUCOSA GANGLIONEUROMAS OF THE BOWEL—MEGACOLON MARFANOID HABITUS–LONG EXTREMITIES, HIGH ARCHES, KYPHOSCOLIOSIS
RARELY HAVE PARATHYROID HYPERPLASIA Rx= TOTAL THYROIDECTOMY, CENTRAL NECK DISSECTION, AND IPSI FUNCTIONAL ND—–SOME CENTERS DO B FUNCTIONAL NECKS AND PARATHYROID REIMPLANTATION (BRACHIORADIALIS IF PART OF THE MEN SYNDROME) RAI–USUALLY NOT OF MUCH BENEFIT UNLESS A MEDULLOFOLLICULAR VARIANT (CELLS DO NOT TAKE UP I-) EXT BEAM RT POST OP—PROBABLY A GOOD IDEA—MAY WAIT UNTIL Dz REAPPEARS FOLLOW AS A ROUTINE H&N PT—GET TCT AND CXR Q 6 MONTHS ANAPLASTIC (<10%) SUBDIVIDED INTO SPINDLE CELL, GIANT CELL, AND SMALL(SQUAMOID) CELL TYPES SMALL CELL HAS BETTER Px = MORE RADIOSENSITIVE –PREVIOUSLY MAY HAVE BEEN MISDIAGNOSED LYMPHOMAS BEFORE THE ADVENT OF IMMUNOHISTOCHEMICAL STAINING—–LYMPHOMA IS RUBBERY AND INDOLENT WHEREAS ANAPLASTIC IS ROCK HARD HASHIMOTOS (ANTIMICROSOMAL Abs) OR SMALL CELL LYMPHOCYTIC CA MAY BE PRECURSOR PRIMARILY 7TH DECADE PRIMARILY PRESENT AS A RAPIDLY GROWING ROCK HARD NECK MASS REGIONAL LAD MET 90% PULM METS 50% TRACHEAL INVASION 25% Dx: FNA AND A CXR—NOTHING MORE—-AVOID A TRACH!—-YOU ARE NOT DOING THESE PTS ANY FAVORS AVG SURVIVAL = 4-6 MONTHS <10% 3 YEAR SURVIVAL ? 0% 5 YEAR SURVIVAL Rx SOME SAY EXT BEAM RT ONLY IF LESION < 5 CM WITH NO DISTANT METS THEN TRY FOR CURATIVE SURGERY! COMBINATION SURGERY, RT(HYPERFRACTIONATION), CHEMO(CISPLATIN/ADRIAMYCIN) IF POSSIBLE—-TRY TO ACHIEVE LOCAL/REGIONAL CONTROL AND THINK PALLIATION! THYROID LYMPHOMA 20% OF PTS DEVELOP THIS IN A PRE-EXISTING MASS—USUALL B-CELL EITHER HASHIMOTOS OR MULTINODULAR GOITER CAN BE MISTAKEN FOR ANAPLASTIC—BUT FAR MORE INDOLENT AND RUBBERY Dx: FNA Px: BEST IS ANN ARBOR STAGING—NEED BONE MARROW AND STAGING CT SCANS Rx: 6 CYCLES OF CHOP AND POSSIBLE EXT BEAM RT PROGNOSIS MAYO CLINIC—PRESERVE THE STRAPS A–AGE G–GRADE (PLOIDY) E–EXTENT, INVASION (ECS) S–SIZE, >1.5 CM IS WORSE S–SEX–FEMALES TEND TO DO BETTER LAHEY CLINIC–CUT THE STRAPS A-AGE M-METS E-ECS S-SIZE THYROIDITIS THE VAST MAJORITY ARE FEMALE INCIDENCE IS PROPORTIONAL TO THE DURATION ACUTE RAPID ONSET, FLUCTUANT RARE, BACTERIAL, HEMATOGENOUS, SL, (POSSIBLY FROM LOCAL TRAUMA)––PALPATION THYROIDITIS—KARATE RELATED PRIMARILY S.a, SECODARILY STREP CAN FOLLOW A URTI 90% OF PEDS CASES DUE TO A LEFT PIRIFORM SINUS TRACT (3RD POUCH DEFECT) SUDDEN ONSET, PAIN, DYSPHAGIA, FEVER, CHILLS, TOXIC, FLUCTUANT, ERYTHEMA, TENDER Dx: CLINICAL, MIGHT DO A MOD BARIUM SWALLOW TO R/O INT. FISTULA FROM PIRIFORM Rx: I&D, G.S. C&S, IV ABX, LOCAL HEAT SUBACUTE GRANULOMATOUS (de QUERVAIN_S) GRANULOMATOUS, GIANT CELL, PSEUSOTUBERCULOUS, CREEPING THYROIDITIS POST VIRAL—TYPICALLY LASTS 2-5 MONTHS
ASSOC WITH HLA SUBTYPE BW35 PAINFUL, HARD, NODULAR VIRAL, PAINFUL, TENDER FEMALE 5-6:1 AGE 20-50 MAY BE UNILATERAL—-CAN THEN PROGRESS TO BILATERAL HIGH ESR, NO LEUKOCYTOSIS, ANTIBODY COUNTS DOWN FEVER, MALAISE, PHARYNGITIS, MYALGIAS <10% PERSISTENT GOITER, HYPERREFLEXIC AND TACHY, Dx: HIGH T3 AND T4, HIGH ESR–> 80, LOW I131 (RAIU) UPTAKE <1% PTS INITIALLY HYPERTHYROID AND THEN DEPLETE STORES AND BECOME HYPOTHYROID AND FINALLY EUTHYROID Bx:FNA–MULTINUCLEATED GIANT CELLS, HISTIOCYTES, AND GRANULOMAS (TUBERCULOID APPEARANCE) Rx: ASA, NSAIDS, AND T4(SYNTHROID)— STEROIDS IN PHARMICOLOGIC DOSES (PRED 40 MG PO Q D) LYMPHOCYTIC (PAINLESS) PAINLESS RARE–MAY BE AN EARLY AND UNUSUAL FORM OF HASHIMOTOS (HLA DR5) INCREASED TSH TRANSIENTLY PRIMARILY POST PARTUM NON-SPECIFIC–USUALLY NOT SUCH A HIGH ESR LYMPHHOID INFILTRATE WITH NO GERMINAL CENTERS OR OXYPHILIC EPITHELIAL CHANGES (VS HASHIMOTOS) Rx: SUPPORTIVE AND SYNTHROID REPLACEMENT CHRONIC REIDEL_S (STRUMA), INVASIVE FIBROUS, LIGNEOUS/STONEY, WOODY THYROIDITIS, FIBROSCLEROSIS OF THE THYROID RARE DIFF Dx IS A FIBROUS VARIANT OF HASHIMOTOS IDIOPATHIC, INSIDIOUS FIBROSING THYROIDITIS OFTEN HYPOTHYROID PAINLESS FIBROSING SCLEROTIC HYPERPLASIA AND INVASIVE FIBROSIS–GLAND IS ADHERENT TO SURROUNDING STRUCTURES BUT NOT TO SKIN OFTEN WITH A LYPHOCYTIC INFILTRATE MAY BE ASSOC. WITH RETROPERITONEAL FIBROSIS, ORBITAL PSEUDOTUMOR, AND MEDIASTINAL FIBROSIS–CAN BE LUMPED TOGETHER AND CALLED TUMEFACTIVE FIBROINFLAMMATORY Dz OF THE NECK—-EXACERBATED BY METHYLSERGIDE _WOODY FIBROSIS_—RELATIVELY AVASCULAR—LOOKS LIKE A BAR OF IVORY SOAP LOCALLY AGGRESSIVE CAN RESULT IN LOCAL (TRACHEAL) COMPRESSION Bx: FIBROINFLAMMATORY TISSUE Rx: SURGICAL — DECOMPRESSION—ISTHMUSECTOMY–THERE IS NO SUCCESSFUL MEDICAL THERAPY—-STEROIDS OCCASIONALLY WORK WELL DECANNULATION OR TRACH AVOIDANCE IS THE KEY_ HASHIMOTO_S AUTOIMMUNE THYROIDITIS = STRUMA LYMPHOMATOSUM/ CHRONIC LYMPHOCYTIC THYROIDITIS BY FAR THE MOST COMMON TYPE OF THYROIDITIS BY FAR THE MOST COMMON CAUSE OF HYPOTHYROIDISM IN THE US IN THE US IODINE ACTS LIKE A TOXIN IN THOSE WITH THYROID AUTO ANTIBODIES BOTH A CELL MEDIATED AND HUMORAL IMMUNE PROBLEM A CLOSE RELATIONSHIP WITH GRAVES (SOME INHERITANCE) USUALLY BILAT—DESCRIBED AS BOSSILATING-DISTINCTLY PALPABLE UPPER LOBES AND ISTHMUS (AND OFTEN PYRAMIDAL LOBE)—POSSIBLY A REACTIVE DEPLPHIAN NODE AS WELL—FIRM/RUBBERY–LUMPY-BUMPY—“PEBBLY” FEEL LYMPHO-PLASMA CELL INFILTRATE WITH GERMINAL CENTERS (VS SUBACUTE LYMPHOCYTIC) HLA-DR5 (VS GRAVES HLA-DR3) SLOWLY PROGRESSIVE PAINLESS MAY INITIALLY BE THYROTOXIC(ANTI TSH RECEPTOR AB—HASHITOXICOSIS)—-THEN USUALLY _BURN OUT_ TO BE HYPOTHYROID(ANTI TSH AB)–HOARSENESS, HYPERLIPIDEMIA, SNHL, DEMENTIA, DEPRESSION, WT LOSS OR GAIN FEMALE 10:1 AGE 40-60 Dx: HIGH ANTI-MICROSOMAL= (TPO-THYROID PEROXIDASE) AB—THE PRIMARY MODE OF MAKING THE Dx—-AN ENZYME IN THE EARLY SYNTHESIS OF THYROXINE, ANTI-THYROGLOBULIN AB, ANTI-NUCLEAR(THYROID) AB, MILD INCREASE IN ESR Bx: INTACT CAPSULE WITH LOSS OF FOLLICLES, LYMPHOPLASMA CELL INFILTRATE WITH GERMINAL CENTERS ASKANSZY CELLS, OXYPHILLIC(REGENERATIVE) HURTHLE CELLS Rx: REPLACEMENT (SYNTHROID)
ALSO SHOULD PROVIDE SURVEILLANCE– HIGHER? INCIDENCE OF WELL DIFF EPITHELIAL NEOPLASMS (PRIMARILY PAPILLARY) AND LYMPHOMA (NHL)—FNA IN THIS SETTING CAN ALTER YOUR THERAPY FROM SURGERY TO RT/CHEMO CAVEATE—-MAY CHECK FOR ANTI MICROSOMAL AB IN SSNHL IF YOU HAVE A MALIGNANT LYMPHOMA IN THE THYROID—-YOU WILL HAVE SURROUNDING HASHIMOTOS THYROIDITIS! GRAVES DISEASE=DIFFUSE TOXIC GOITER-EXOPHTHALMIC GOITER, BASEDOW_S Dz, PARRY_S Dz HLA-DR3 AUTOIMMUNE–LATS/TSI DIFFUSE EPITHELIAL HYPERPLASIA 35% SPONT REGRESSION PRETIBIAL MYXEDEMA—POLYSACH OFTEN PRESENT WITH ANXIETY, PALPITATIONS OR A FIB RETROBULBAR INFILTRATE—EXOPHTHALMOS—LID LAG/LOGOPHTHALMOS–AM EYE IRRITABILITY FEMALE 9:1 AGES 20-50 GRAVES DYSTHYROID ORBITOPATHY OGURA—CWL INF AND MEDIAL WALL RESECTION (LEAVE A BONEY STRUT BETWEEN THE DECOMPRESSIONS) KENNEDY–ENDOSCOPICALLY DOING THE SAME PROCEDURE NOW CAN DO A BALANCED DECOMPRESSION WITH A LAT WALL COMPONENT 30% INCIDENCE OF NEW ONSET STRABISMUS TOXIC MULTINODULAR GOITER–PLUMMER_S Dz PRIMARILY THE ELDERLY—MAY PESENT WITH DIARRHEA OR A FIB MULTINODULAR GOITER—GENERALLY NOT GOING TO SHRINK UP WITH SUPPRESSION DO A FNA AND SOME LAB WORK—MAYBE AN US AND FNA OF THE DOMINANT NODULE ENDEMIC GOITER / IODINE DEFIECEINCY TOXIC ADENOMA=SOLITARY TOXIC NODULE CHRONIC INFECTIOUS THYROIDITIS ECHINOCOCCUS, ACTINOMYCOSIS, TB, SYPHILIS(GUMMAS) VERY RARE—Dx WITH FNA CATECHOLAMINE SECRETING TUMOR EXTRACTION- IF PT WITH A THYROID NODULE IS EUTHYROID AND HAS LABILE SEVERE HTN MUST CONSIDER SIPPLE_S (MEN II) CHECK PRE-OP FOR BREAK DOWN PRODUCTS VMA– END ORGAN BLOCKADE REGITINE(PHENTOLAMINE) /PHENOXYBENZAMINE (ALPHA-ADRENERGIC BLOCKADE)–10 MG PO Q 12 HOURS _ TOO MUCH –POSTURAL HYPOTN + BETA BLOCKADE POST OP SODIUM NITROPRUSSIDE NO HYPERPYREXIA DISCONTINUE THE PROCEDURE FOR FURTHER W/U THYROTOXIC CRISIS=THYROID STORM + FEVER/HYPERPYREXIA (DIFFERING FROM THYROTOXICOSIS) USUALLY HAPPENS IN PTS WITH DIFFUSE TOXIC GOITER (GRAVE_S Dz) WITH UNDERLYING STRESS–SUCH AS SURGERY OR INFXN 10% MORTALITY TEMP > 101 PROFUSE SWEATING TACHY ANGINA DYSRYTHMIAS-CHF N/V DELERIUM,APATHY,STUPOR Rx: INHIBITION OF HORMONE SYNTHESIS (PTU 200 MG PO Q 4 HOURS) INHIBITION OF THYROXINE RELEASE (SSKI 5 DROPS Q 6 HOURS) SODIUM IODINE B- BLOCKADE (INDERAL) COOLING BLANKET–ICE PACKS IVF O2
STEROIDS-HYDROCORTISONE PLASMAPHORESIS SALICYLATES ARE CONTRAINDICATED AS THEY PROPAGATE THE FORMATION OF T3 FROM T4 (MORE POTENT) MALIGNANT HYPERTHERMIA DESCRIBED IN 1960 SUSPECT EVERYONE-HIGH IN PEDS PTS—ASSOC WITH EYE SQUINTS PROLONGED NUCHAL RIDGIDITY IS THE 1ST SIGN ABNL IN THE SARCOPLASMIC RETICULUM HYPERMETABOLIC (HYPERPYREXIC) STATE CAUSED BY TRIGGERING SUBSTANCES–SUCCINYL CHOLINE AND VOLATILE GASES Dx: VASTAS LATERALIS Bx CAFFEINE-HALOTHANE CONTRACTURE TEST EARLY SIGNS OF HYPERMETABOLIC STATE TACHY, MET ACIDOSIS, HYPOXEMIA, HIGH END TIDAL CO2, SKIN MOTTLING, UNSTABLE BP, MASSETER STIFFNESS(RIDGIDITY),WHOLE BODY RIDGIDITY, HTN—–HYPERPYREXIA (BY THE TIME TEMP RISES IT IS TOO LATE!)—-PYREXIA > 43 DEGREES—DIC—MSOF—-DEATH MORTALITY > 10 % EVEN WHEN TREATED STOP THE OPERATION–ABORT STOP ALL TRIGGERING AGENTS (CHANGE THE ANESTHESIA MACHINE AND RUBBER TUBING) 100% O2 HYPERVENTILATE DANTROLENE 5 MG/KG IMMEDIATELY–INHIBITS CA RELEASE FROM THE SARCOPLASMIC RETICULUM SODIUM BICARB 1MEQ/KG GLUCOSE 0.5GM/KG; INSULIN 0.15 U/KG COLD IVF COOLING BLANKET—COOL AIR—COOL, COOL, COOL LASIX—-PREVENT ATN FROM MYOGLOBINURIA TREAT TACHY–DYSRYTHMIAS (PROCAINAMIDE/PROCARDIA) HYPOKALEMIC PERIODIC PARALYSIS CAN OCCUR WITH EITHER HYPER OR HYPOTHYROIDISM ANATOMY: RLN (6TH ARCH)—-LOOPS AROUND THE AORTIC ARCH JUST PAST THE LIGAMENTUM ARTERIOSUM ON THE LEFT——LOOPS AROUND THE SUBCLAVIAN ARTERY ON THE RIGHT (ANOMALOUS R SUBCLAVIAN WHICH ORIGINATES FROM THE DECENDING AORTA INSTEAD OF THE INOMINANT(BRACHIOCEPHALIC TRUNK)—-FOLLOWS A RETROTRACHEAL (USUALLY RETROESOPHAGEAL) COURSE INTO THE R ARM)—CAN GIVE YOU BAYFORD_S SYNDROME OF INTERMITTENT DYSPHAGIA LUSORIA, WEIGHT LOSS AND A NON-RECURRENT R LARYNGEAL NERVE(0.6% INCIDENCE—SEEN IT)—CAN THEORETICALLY HAVE A LEFT NON-RECURRENT INF LARYNGEAL NERVE BUT YOU MUST HAVE BOTH SITUS INVERSUS AND A RETROESOPHAGEAL SUBCLAVIAN—-CONSIDER PRE OP CXR EXTEROCEPTIVE (GVA) TO SUBGLOTTIC MUCOSA ANTERTIOR (ADDUCTOR) BRANCH (SVE) TO MAJORITY OF INTRINSIC LARYNGEAL MUSCULATURE POSTERIOR (ABDUCTOR) BRANCH (SVE) TO PCA—MORE SUSCEPTIBLE TO INURY—FEWER AND MORE TENUOUS THAN THE ADDUCTOR FIBERS SEMON_S LAW—–VOICE WILL BE GOOD AND AIRWAY WILL BE MORE OF A PROBLEM THAN ASPIRATION—-_THE ACTION OF THE POSTERIOR BRANCH OF THE RLN (ABDUCTION) TO THE PCA WILL BE LOST FIRST AND RETURN LAST FOLLOWING INJURY_—-IN THYROID SURGERY HAVE SEMON_S LAW WORKING AGAINST YOU BUT THE ANT BRANCH MAY BE MORE AT RICK IN YOUR SURGICAL FIELD SVE TO CRICOPHARYNGEUS ALONG WITH THE PHARYNGEAL PLEXUS RELATIONSHIP OF THE RLN TO THE LAT/POST SUSPENSORY LIGAMENT OF BERRY IS THE MOST IMPORTANT—-MUCH MORE IMPORTANT THAN THE RELATIONSHIP OF THE NERVE TO THE INF THYROID ARTERY (OFF TCT) —-THIS RELATIONSHIP IS QUITE VARIABLE LORE SAYS THE NERVE CAN PASS OVER BERRY_S LIG IN 0.25% OF CASES—THIS IS CONTROVERSIAL UNILATERAL TVC PARALYSIS——SUBTLE Sx—-OFTEN MISSED—IN REALITY PROBABLY MUCH MORE PREVALENT—–NONE OF THE GENERAL SURGEONS EVER LOOK L>R—–SOME SOURCES SAY R>L (SHORTER, MORE EASILY STRETCHED L—OFTEN ASSOC WITH CV OR PULM DEFECT R—OFTEN ISOLATED FINDING THYROIDECTOMY—-OPERATE FOR TVC PARALYSIS, MALIGNACY ON FNA, SYMPTOMATIC GOITER REFRACTORY TO SUPPRESSION, RET PROTO ONCOGENE POSITIVITY, SINGLE NODULE IN A CHILD, YOUNG MALE, RAPID GROWTH OF A NODULE—ESPECIALLY IN THE ELDERLY, PT ANXIETY——WHICH OPERATION IS CONTROVERSIAL 1ST= MIKULICZ 1885-FOR GOITER (GOITER=THYROCELE) KOCHER NOBEL LAUREATE 1909 EVEN WITH EXCELLENT SURGICAL TECHNIQUE–YOU WILL GET SOME ALTERATION OF VOICE GET PREOP THYROID PROFILE, CA++, AND ALBUMIN-(OR IONIZED CA) NOW GET IONIZED CA++—-DO NOT FORGET ABOUT MG++ AND VIT D—-CHRONIC HYPOCA++ USUALLY DUE TO THESE FACTORS NL THYROID = 15-25 G
SUBTOTAL REFERS TO LEAVING A WEDGE OF THYROID TISSUE (1-2G) IN THE TE GROOVE=OFFERS NO ADVANTAGE OVER TOTAL AS THE RLN CAN BE DAMAGED AND THE REMNANT CAN RE GROW—ONLY POSSIBLE INDICATION IS PTS WHO WILL BE NON-COMPLIANT WITH SYNTHROID(THOUGHT TO PROTECT PARATHYROIDS AND RLN) DO NOT ROUTINELY NEED ABX USUALLY DO NOT NEED TO WORRY ABOUT INTUBATION WITH THESE GOITER PTS ONE STUDY SHOWED DECREASED NEUROPRAXIA OF RLN WITH INTRA OP STEROIDS FROM 10 TO 3% USED TO PRE OP WITH LUGOL_S OR IODINE TO INCREASE FIRMNESS AND DECREASE VASCULARITY HOWEVER A HIGH IODINE LOAD (CONTRAST MEDIA) WITH A PREVIOUS GOITER (ESPECICIALLY ENDEMIC GOITER) CAN LEAD TO THYROTOXICOSIS (JOD-BOSDOW PHENOMENON)—INABILITY TO TREAT WITH RAI POSITION PT(OCCIPUT AT EDGE OF TABLE) SHOULDER ROLL POSITION PT, TUCK ARMS MAY TAPE CHIN UP AND CHEST DOWN INJECT 10 CC LIDO WITH EPI OLIVER BEAHRS PUTS THEM IN A BIT OF REVERSE TRENDELENBERG FOR HEMOSTASIS MAY USE STRING TO CREATE INCISION LINE (RSTL) ALWAYS KEEP CENTERED–EVEN FOR A LOBECTOMY–OFF CENTER LOOKS BAD BEST TO MAKE A BIT OF A LOW INCISION—-PLAN WITH PT SITTING UP IN THE MOST HIDDEN RSTL BIG GOITERS WILL DISTORT THE ANATOMY INJECT/PREP/DRAPE CROSS HATCH INCISION SKIN INCISION TO LAND 1-2 FINGER BREADTHS ABOVE THE CLAVICLE, EXTENDING 10 CM IN LENGTH–MEASURE IT 10 BLADE- RAISE SUB PLATYSMAL FLAPS SUP FLAP LARGER–UP TO HYOID BONE INF FLAP TO STERNAL NOTCH-PROBABLY DON_T HARDLY EVEN NEED AN INF FLAP SWEEP MIDLINE WITH DRY SPONGE USE 2 GELPIES (PARAMEDIAN) FOR RETRACTION—OR JUST SUTURE IT UP TAKE ALL ANT. JUGULAR VEINS JAMISON/MAYOS AND DEBAKEYS TO DISSECT DOWN ONTO AND CLEAN OFF STRAP MUSCLES, ID MIDLINE AND DISSECT ALONG IT CLEAN S.C.M. FROM STRAPS LATERALLY HELPS TO DIVIDE THE ISTHMUS WITH THE HOT KNIFE—-THEN OVERSEW WITH A LOCKING STITCH IF YOU ONLY NEED TO DO A LOBECTOMY ID CAROTID SHEATH STRUCTURES (ESPECIALLY IJV) DIVIDE STRAPS BY PASSING KELLY CLAMP BENEATH OUTER STRAPS AND ACROSS FROM THE MIDLINE OUT. INNER STRAPS ARE DIVIDED IN SAME WAY. CLAMPS STAY ON UNTIL THE END. DEEP STRAPS OFTEN ADHERENT TO SUP THYROID GLAND—–LAHEY CLINIC METHOD DIVIDE STRAPS SUP TO CRICOID TO AVOID DENERVATING THEM FROM THE ANSA-USE BOVIE RAISE STRAPS OFF THYROID CAPSULE WITH BOVIE ON CUT SOME KEEP THE STRAPS INTACT AND JUST RETRACT THEM WITH A GREEN RETRACTOR–OR ARMY NAVY CAN RETRACT ON THE THYROID QUITE A BIT WITH A LAP OR SPONGE DO NOT BE AFRAID TO PICK UP AND TURN THE PTS HEAD FOR YOUR EXPOSURE SOME SAY TO WORK FROM THE SIDE OF THE PATHOLOGY—BE FLEXIBLE—WHAT IS GOOD FOR THE SURGEON IS GOOD FOR THE PATIENT FIRST ID THE RLN AT THE THORACIC INLET—WILL OFTEN FIND THE INF THYROID ARTERY CROSSING OVER THE RLN DOWN IN THE T-E GROOVE—IS MEDIAL TO THE LYMPHOFATTY TISSUE HERE REVISION CASES AND RIGHT SIDES ARE MORE PRONE TO INJURY—-A VERY UNFORGIVING NERVE THE RIGHT RLN IS USUALLY MORE ANT AND VARIABLE IN ITS LOCATION BENEATH THE DEEPER FAT WILL LIE THE INF. THYROID ARTERY (OFF THE TCT)–COMES OUT FROM BEHIND THE COMMON CAROTID LOOK FOR POSSIBLE MULTIPLE BRANCHES—EARLY BIFURCATION INTO ANT AND POST BRANCHES! INF.. THYROID A. CONG.ABSENT 2-5% NO MATTER WHAT —ALWAYS FIND THE NERVE BEFORE BIGINNING DISSECTION—MAY WANT TO CONSIDER A NERVE STIMULATOR/SENSOR ETT USE A KITNER—THE RELATIONSHIP BETWEEN THE NERVE AND THE LAT SUSP LIG IS QUITE COMMON THE INF THYROID ARTERY IS PRETTLY EASY TO FIND STARTING LATERALLY, PEEL LOBE OF THE THYROID UP FROM LATERAL TISSUES. FIRST FIND MIDDLE THYROID VEIN AND DIVIDE IT. STAY RIGHT ON THE CAPSULE, AND KEEP THE TIPS OF YOUR CLAMPS POINTED TOWARD THE SPECIMEN SUP. THYROID ARTERY THE 1ST BR. OF THE ECA 5-10% OF PATIENTS HAVE UNPAIRED THYROIDEA IMA OFF BCT, CC, OR AA. THIS RUNS SUPERFICIAL AND PERPENDICULAR TO THE RLN(70% INTIMATELY ASSOC WITH EACH OTHER) 0.6% INCIDENCE OF NON-RECURRENT LARYNGEAL NERVES (R>L)-BAYFORD_S SYNDROME (DYSPHAGIA LUSORIA)–SEEN IT THE RLN SHOULD BE ABOUT 1 CM LAT TO THE TE GROOVE FOLLOW THE RLN TO WHERE IT ENTERS THE LARYNX NEAR THE INF CORNU OF THE THYROID CARTILAGE (KILLIAN-JAMISON AREA)–ALMOST ALWAYS POST TO THE LAT SUSP. LIG OF BERRY(1888)—CAN ALSO BE TEATHERED WITHIN IT—GET IT OUT BEFOR YOU GO CUTTING THIS OR BURNING IT CLEAN OFF THE TOP OF THE NERVE WITH A FINE TIPPED MOSQUITO OR MCABE_S
THE NERVE MAY BIFURCATE—ANT/MEDIAL (ADDUCTOR) BRANCH AND MORE TENUOUS(SEMON_S LAW) POST/LATERAL (ABDUCTOR) BRANCH TO THE PCA USE A KITNER FREELY THE INF. THYROID ARTERY SHOULD BE LIGATED DISTAL TO THE PARATHYROIDS—TRY TO SEE THEM CONTINUE TO PEEL THE THYROID BY DIVIDING BERRY_S (LAT. SUSPENSORY) LIGAMENT WITH JAMISON SCISSORS–CUTTING TOWARD BUT NOT ENTERING THE TRACHEAL WALL–DIVIDE BERRY_S LIGAMENT SHARPLY TO AVOID RLN TRACTION–RLN ALWAYS RUNS DEEP TO THIS LIGAMENT? TAKE GREAT CARE NOT TO DISRUPT THE SLN EITHER (AMALITA GALIKERTZI)-INT BR ENTERS LARYNX AT THYROHYOID MEMBRANE (WHERE AN EXT. LARYNGOCELE CAN ARISE)—EXT BRANCH LIE ON THE CRICOTHYROID—EASILY VISIBLE MAY BE INTIMATELY ASSOC. WITH THE SUP. THYROID VESSELS—DOING A METICULOUS DISSECTION ON THE GLAND—HAVING IDENTIFIED THE RLN—YOU SHOULD NOT HAVE A PROBLEM WITH THE SLN DO THIS PART OF THE DISSECTION LAST—INF AND ANT TRACTION WILL GIVE YOU EXCELLENT VISUALIZATION OF THE EXT BR OF THE SLN TAN-OVAL SHAPED WEIGH ABOUT 35MG, ADENOMATOUS GLANDS SINK IN NS (NL GLANDS AND FAT FLOAT) ID ALL 4 PARATHYROIDS AND PRESERVE AT LEAST 2 75% OF SUP. PARATHYROIDS LIE BEHIND BODY OF SUP. POLE OF THYROID 2% OF PTG’S ARE INTRATHYROIDAL CAREFULLY EXAMINE THE SPECIMEN EX VIVO AS WELL AS THE DISSECTED BED FOR DVASCULARIZED PTG’S—REIMPLANT THEM—NEVER TOO LATE PULL ANTERO-MEDIALLY ON THE GLAND AND CLAMP ACROSS THE ISTHMUS (80% POSSESS SOME PYRAMIDAL LOBE)–STICK TIE WITH A 3-0 SILK ISTHMUS AT 2ND TO 4TH TRACHEAL ARCHES BOVIE THYROID=ACRID SMELL PROBABLY WAIT FOR FROZEN—-CONSIDER A SELECTIVE ANT NECK DISSECTION FOR MALIGNANCIES IRRIGATE WITH SALINE PLACE A #10 J.P. TO SUCTION, SOME ADVOCATE A PENROSE AS BEING KINDER TO THE NERVE CAN BRING THE DRAIN OUT THROUGH THE INCISION OR THROUGH A SEPARATE INCISION REAPPROXIMATE STRAPS BY ASSISTANT HOLDING CLAMPS TOGETHER USE 2-3 SEPARATE 3-0 VICRYL/BIOSYN STITCHES IN A HORIZ. MATTRESS FASHION IN EACH STRAP MUSCLE CLOSE PLATYSMA WITH 3-0 VICRYL, AND SKIN WITH 5-0 NYLON CLOSE SKIN WITH A RUNNING INTRACUTICULAR 4-0 BIOSYN POST OP CONSIDER POST OP CXR TO R/O PNEUMO MUST BE ACUTELY AWARE OF HEMATOMA-AIRWAY GET AN IONIZED CALCIUM IN RECOVERY FOR BASELINE GIVE 10 MG DECADRON IV INTRAOPERATIVELY AND Q 8 HOURS X 3—HELPS WITH PERINEURONAL EDEMA GIVE MULTIVITAMIN (INCLUDING VIT A) PUT 1 G MGSO4 IN 1ST BAG OF IVF_S OSCAL WITH D 5OO MG PO QD AND MG-GLUCONATE 500MG P.O. QD PUT IMMEDIATELY ON TUMS EX—2 TABS PO BID AND MG-GLUCONATE 1 TAB PO BID CHECK CALCIUMS Q AM—-CAN PROBABLY D/C AND FOLLOW ON AN OUTPT BASIS COMPARISON OF THE 1ST AND 2ND POST OP CALCIUM ARE PREDICTIVE OF SIG HYPOCALCEMIA CRITICAL TIME IS 24-96 HOURS, USUALLY IF NO PROBLEMS BY 72 HOURS –PT WILL NOT HAVE PROBLEMS AFTER A TOTAL FOR NON MALIGNANT PATHOLOGY—START ON 50 MICROGRAMS Q D—-RECHECK THYROID PROFILE IN 1 MONTH CONSIDER POST OP LABS (NL ALBUMIN=4) POST OP ALBUMIN IS OFTEN LOW DUE TO DILUTION SECONDARY TO INTRAOPERATIVE RELEASE OF ADH—–IONIZED CA++ AND SMAC GET CA++,ALB Q 6 HOURS (10% INCIDENCE TEMP HYPO CA++)–NOW GET IONIZED CA, SHOULD BE > 1.06 MUST ALSO CHECK MG++ Q 12 HOURS AS IT IS REQUIRED FOR THE SECRETION OF PTH AND THE PTH ACTION ON THE END ORGAN Sx: PERIORAL PERISTHESIAS, HYPERACTIVE DTR_S, ABD. CRAMPS, Q-T PROLONGATION—–LARYNGOSPASM SIGNS: TROUSSEAUS(MORE SENSITIVE AND SPECIFIC), CHEVOSTEKS, ESCHERICH_S(ORAL COMMISURE TINEL_S), ROSENBACH_S(FINE BLEPHOROTREMOR WITH EYES CLOSED) IF CA > 7.0 -7.5 OR SYMPTOMATIC THEN: 10 CC 10% IV CA GLUCONATE (1 AMPULE = 1 GRAM) IN OVER 30 MIN (CACL IS TOO BIOACTIVE–CAN CAUSE DYSRHYTHMIAS) THEN: ZITSCH GIVE 2 G IV IN 200 CC NS OVER 30-60 MINUTES 1-5 G PER LITER NS IN AT 50CC/HOUR UNTIL CA > 8.0 THEN: 1-3 G P.O Q D (TUMS EX = 750 MG) GIVE 2 PO BID RARELY NEED TO GIVE VIT D—CALCITRIOL 0.5 – 2.0 MCG PO Q D (CAUTION—WILL JUMP UP CA VERY FAST) PRIOR TO SCAN OR RAI STOP SYNTHROID 5 WKS PRIOR (T1/2 IS ABOUT 1 WEEK), THEN USE CYTOMEL(T1/2 IS ABOUT 1 DAY) FOR 3 WEEKS (OR NOTHING)–LIOTHYRONINE (T3) 25 MICROGM Q D ALSO LOW IODINE DIET– THEN
NOTHING FOR 2 WEEKS—WANT TSH>40-50—TSH WILL SLOWLY CLIMB TO ABOUT 10 AND THEN SHOOT UP—-FOR A STICKY DISSECTION IT MAY BE DIFFICULT TO GET THE TSH UP OVER 30-40—-THEN RAI –50-150 mCi GIVEN AT ABOUT 6 WEEKS POST OP–PROBABLY GIVE ABOUT 100 (INPT DOSE) VS 30 (OUTPT DOSE) AND AVOID WASTING TIME ON A DIAGNOSTIC SCAN—-MAKE THE THERAPEUTIC SCAN YOUR DIAGNOSTIC ONE NEED 2 NEGATIVE SCANS ABOUT 9 MONTHS APART–TOTAL DOSE NOT TO EXCEED 300-400 mCi—-THIS IS HARD ON THE PT AS THEY ARE MISERABLE WHEN SEVERELY HYPOTHYROID—-RISK OF HEMATOGENOUS MALIGNANCY DOES NOT BEGIN UNTIL > 900 mCi NEED ALSO TO CHECK A YEARLY THYROGLOBULIN (ESPECIALLY JUST BEFORE EACH SCAN)—FALSE NEG BY DEDIFFERENTIATION OF TUMOR CELLS—OR HIGH AB COUNTS SERUM THYROGLOBULIN MADE EXCLUSIVELY BY THYROID TISSUE–A VALUE > 10 ng/ml = RECURRENCE GET YEARLY CXR MAY GET HIGH RESOLUTION ULTRASOUND TO DETECT RECURRENCE AS WELL MYXEDEMA COMA—–LACTIC ACIDOSIS, LOW K+, AND NA+ FOR NONCANCER PTS WITH TOTAL THYROIDECTOMIES—EMPIRICALLY START ON 125 MCG SYNTHROID QD AND REFER TO ENDOCRINOLOGIST FOR F/U OTHER ENTITIES: LINGUAL THYROID ECTOPIC THYROID—ANYWHERE FROM CIRCUMVALLATE PAPILLA TO EPIGLOTTIS MUST BE POST TO CIRCUMVALLATE PAPILLA AND TUBERCULUM IMPAR IS A FAILURE OF DESCENT (?ARRESTING MATERNAL ANTIBODIES) 4TH WEEK–FORAMEN CECUM LINGUALE DESCENDS DOWN PRIOR TO FORMATION OF THE BOT OR HYOID BONE TGDC LINED WITH EPITHELIUM TOWARDS THE END OF DESCENT IT IS JOINED BY THE LATERAL FOURTH POUCH NEUROECTODERMAL C-CELLS (PARAFOLLICULAR CELLS) FROM THE ULTIMOBRANCHIAL BODY——CAN FORM MEDULLARY CA INCIDENCE = 1/100,000 FEMALE 4.7:1 33% CLINICALLY HYPOTHYROID 70-100% HAVE LINGUAL THYROID AS ONLY FUNCTIONING THYROID TISSUE VERY RARELY UNDERGO MALIGNANT DEGENERATION—-27 CASES (APPEARS TO HAVE THE SAME INCIDENCE AS THYROID IN THE NL LOCATION CAVEATE—-CANNOT HAVE MEDULLARY THYROID CA HERE AS THE C-CELLS (PARAFOLLICULAR CELLS) MIGRATE IN FROM THE ULTIMOBRANCHIAL BODY OFTEN WILL PRESENT WITH A MASS EFFECT —- DYSPHAGIA, DYSPHONIA, DYSPNEA, EVEN STRIDOR—–RARELY MAY HEMORRAGE—RED VASCULAR APPEARING SMOOTH MIDLINE BOT MASS OFTEN PRESENT AT A TIME OF STRESS WHEN HIGH TSH LEVELS PROMOTE GLANDULAR HYPERPLASIA Dx: ALWAYS PALPATE FOR NL THYROID GLAND LAB: TSH, T3, T4, THYROGLOBULIN CT WITH NO CONTRAST—NL THRYROID NATURALLY HAS ACCUMULATED I- FIRST STEP—-TN99 SCAN—-DIAGNOSTIC—-AVOIDS THE NEED FOR Bx Rx: SYNTHROID SUPPRESSION—-LOWERS TSH—DECREASES GLANDULAR HYPERPLASIA—-DECREASES SYMPTOMS IF THIS FAILS—REPEAT IMAGING STUDIES——SURGERY—-CAN USUALLY SUPPRES THEM THROUGH PUBERTY AND THEN THEY ARE ABLE TO GET ALONG WITHOUT TOO MANY SYMPTOMS IF NOT A SURGICAL CANDIDATE CONSIDER I131 (RAI) THYROGLOSSAL DUCT CYST (TGDC) UP TO 7 % OF ALL COMERS A CAN HAVE SOME RESIDUAL NOTED POST MORTEM PRIMARY MIDLINE NECK MASS IN PEDIATRICS (>DERMOID), 3 X MORE COMMON THAN A BRANCHIAL CLEFT ABNL, MIDLINE CERVICAL DEFECT INCIDENCE OF CA = RARE—–ALWAYS PAPILLARY NORMALLY THE THYROGLOSSAL DUCT DISSAPPEARS AT 9 WEEKS GESTATION PRIMARILY AT THE HYIOD BONE(HYOID BONE = 2ND ARCH CARTILAGE/REICHERTS—ALMOST ALWAYS INVOLVED) > INFRAHYOID(65%) > SUPRAHYOID(25%) > SUPRASTERNAL (8-9%) > BOT(1-2%) 1-5 CM MOVES WITH DEGLUTITION AND TONGUE PROTRUSION (RETAINED FIBROUS THYROGLOSSAL DUCT TRACT)=PATHOGNEUMONIC 2/3 PRESENT BEFORE AGE 10 90% IN THE MIDLINE, IF NOT DIRECTLY IN MIDLINE L > R LINED WITH EITHER RESP OR SQUAMOUS EPITHELIUM WITH ISLANDS OF LYMPHOID AND THYROID TISSUE ALMOST ALWAYS HAVE A PATENT PROXIMAL THYROGLOSSAL DUCT (TO THE FORAMEN CECUM) Dx: US–PROBABLY THE BEST, CT, MRI—PROBABLY SHOULD GET PRE OP TN99 THYROID SCAN AS THIS MAY BE THE ONLY FUNCTIONING THYROID TISSUE—THIS MAY NOT ALTER YOUR TREATMENT AND MANY SOURCES SAY NOT TO BOTHER—–BUT IT WOULD AT LEAST CLUE YOU IN TO THE NEED FOR FUTURE REPLACEMENT
Rx: OBSERVATION (RARELY ASSOC. WITH A NEOPLASM) IF Hx OF RT—-THEN SHOULD REMOVE—–+/- POST OP RAI EXCISION VIA SISTRUNK (1926) PROCEDURE—-EXT APPROACH—REMOVE MID HYOID—-<4-5 % RECURRENCE 5 CM HORIZONTAL INCISION OVER THE CYST RAISE SUP AND INF SUBPLATYSMAL FLAP—-GELPIES DIVIDE (INFRAHYOID) STRAPS BOVIE RIGHT DOWN ON THE HYOID—CAN TAKE ALL MUSCLES OFF THE CENTRAL HYOID BEWARE OF 12 LATERALLY—ALSO SLN EXT BR. DISSECT OUT CYST—USE MARTINS ON STRAPS BONE CUTTERS ON HYOID FOLLOW CYST UP TO BOT AND DOWN TO PYRAMIDAL LOBE CLOSE OVER A #10 JP MIDLINE CERVICAL DEFECT A FAILURE OF BRANCHIAL ARCHES TO FUSE IN THE MIDLINE RARE OFTEN MISTAKEN FOR A TGDC PARATHYROIDS 1ST OBSERVED—OWEN 1852, NAMED BY A SWEDISH MEDICAL STUDENT—-1878-SANDSTROM IN UPSULLA 1890—GLEY DISCOVERS THAT PARATHYROIDECTOMY LEADS TO TETANY 1891–VON RECKLINGHAUSEN DESCRIBES OSTEITIS FIBROSA CYSTICA—-BROWN GIANT CELL TUMORS AND WIDESPREAD MARROW FIBROSIS AND BONE CYSTS—-AT THIS TIME THE ASSOC PARATHYROID ADENOMA WAS THOUGHT TO BE COMPENSATORY—NOT THE CAUSE 1909—MACCULLUM RECOGNIZED THE LINK WITH CALCIUM HEMOSTASIS 1925—COLLIP PROVED THAT BIOLOGICALLY ACTIVE EXTRACTS LED TO HYPERCA++ 1925—DR FELIX MANDL—AFTER TRYING TO INJECT ANIMAL AND CADAVERIC PTH AND —FINALLY EXPLORED THE NECK OF A PT (ALBERT) WITH VON RECKLINGHAUSEN_S Dz AND REMOVED AN ADENOMA—CURING THE PT 1927—-DR EDWARD CHURCHILL SPLITS THE STERNUM OF CAPT. CHARLES MARTELL AND FINALLY FINDS THE ECTOPIC PARATHYROID ADENOMA—DIED POST OF—FLORID VON RECKLINGHAUSENS 1928—FIRST SUCCESSFUL PARATHYROIDECTOMY IN THE US IN ST LOUIS MO DESCEND INDEPENDANTLY EMBRYOLOGICALLY—FROM THE ULTIMOBRANCHIAL BODY POSITION IS MUCH MORE VARIABLE THAN THE THYROID INF PTG POSITION IS THE MOST VARIABLE—-SUP ARE REALLY JUXTA-CRICOIDAL—-HOWEVER CAN BE INTRATHYROIDAL PRIMARY BLOOD SUPPLY IS THE INF THYROID ARTERY!!!(OFF TCT)—SO DON_T HURT IT ALSO SOME BLOOD SUPPLY FROM SUP THYROID A (ECA) 10% POP HAVE MORE OR LESS THAN 4 PTG (UP TO 6) 15% ABBERENT LOCATION–USUALLY INF 30-40MG EACH—–5-6MM IN DIAM—TAN/YELLOW—LENTIL BEAN SHAPE SUP—4TH POUCH DERIVATIVE INF– 3RD POUCH DERIVATIVE COMPOSED OF CHIEF (PRINCIPLE) CELLS AND CLEAR (OXIPHILIC) CELLS CHIEF CELLS–ONLY PARYNCHYMAL CELLS OF THE PARATHYROIDS–POLYGONAL—ARRANGED IN CORDS AND SHEETS, LOW STROMAL FAT—SLIGHTLY ACIDOPHILIC, CONTAIN SECRETORY GRANULES CONTANING THE PTH POLYPEPTIDES CLEAR CELLS—PALE VACUOLATEDOXYPHILIC, LARGER CELLS–FUNCTION UNKNOWN CALCIUM METABOLISM 99% IN BONE 1% CIRCULATING—-40-47% PPB(85%ALBUMIN), 6-10% COMLEXED TO ANIONS, 47-50% IONIZED—–NOW ABLE TO MEASURE THIS DIRECTLY—-OTHERWISE CALCULATE 0.8 MEQ FOR EACH DROP OF 1 GM ALBUMIN MG EFFECTS THE SECRETION AND END ORGAN EFFECT OF PTH QUESTIONABLE ROLE OF ZINC AS A COFACTOR—-MAY WANT TO CHECK THIS HALF OF ALL WOMEN OVER AGE 50 EXPERIENCE A FRACTURE DUE TO OSTEOPOROSIS 1/5 OF ALL HIP FRACTURE PATIENTS DIE WITHIN THE YEAR HYPOCA++ POST OPERATIVELY, ACUTE PANCREATITIS, MALABSORBTION, MALNUTRITION Q-T PROLONGATION IRRITABLE, TETANIC, PERIORAL HYPERESTHESIAS PSUEDOHYPERPARATHYROIDISM/SECONDARY HPT—LOW CA++ AND HIGH PTH USUALLY DO TO RENAL FAILURE (RARELY DUE TO MALNUTRITION, MALABSORBTION, OR LACK OF SUN EXPOSURE) AND SUBSEQUENT VIT D3 DEFEIFEINCY—–GET HYPERPHOSPHATEMIA AND HYPOCA++-–GET REACTIVE HPT—SUBSEQUENT OSTEITIS FIBROSA CYSTICA, BONE PAIN, ECT… PROBABLY DO SERIAL BONE DENSIOMETRY (US OF THE CALCANEUS OR BETTER A DEXA SCAN) AND RENAL FUNCTIONS RECOMMEND ADEQUATE HYDRATION CONSIDER ORAL PHOSPHATE THERAPY CONSIDER ESTROGEN REPLACEMENT THERAPY—–FOSAMAX, ACTONEL, DIDRONEL SELECTIVE ESTROGEN RECEPTOR MODULATION—-EVISTA CALCITONIN NASAL SPRAY
CUT BACK ON CAFFIENE AND ALCOHOLCUT OUT SMOKINGAVOID STERIODSAVOID EXCESS THYROXINEBE AWARE OF ANTICONVOLSANTS DO NOT FORGET ABOUT MAGNESIUM!!! ZINC MAY BE IMPORTANT LIFT WEIGHTS, RAILINGS ON STAIRWAYS, GOOD SHOES, STRONGER GLASSES HYPERCA++ (>11.5) GET IRMA PTH, CR CLEARANCE, 24 HOUR URINE CA, BONE DENSIOMETRY PREGANT PTS AT RISK FOR NEONATAL TETANY! 45% HYPERPARATHYROIDISM—(HIGH PTH LEVELS)–81% ADENMOMA, 15% HYPERPLASIA, 4% CA 45% MALIGNANCY—(LOW PTH LEVELS)—LYMPHOMA/LEUKEMIA—VIT D, SCCA—PTH LIKE SUBSTANCE, BREAST CA—-OSTEOCLAST+, PROSTATE CA—-OSTEOBLAST+, MM—OAF(OSTEOCLAST+), RCC—-PTH, LUNG CA—-THIS TYPE OF HYPER CALCEMIA IS BEST TREATED WITH MITHROMYCIN!!!—?ETIDRONATE (HYDRATION WITH SALINE? 10%—–OTHER–SARCOID(VITAMINOGENIC), TB, FUNGAL INFXN, IMMOBILIZATION, MILK ALKALI SYNDROME(EXCESS VIT D), LITHIUM, PAGETS, VIT A OR VIT D TOXICITY, THIAZIDES—MUST CONSIDER THIAZIDE DIURETICS FAMILIAL HPT HYPERPTH—–HAVE LOW PO4 HIGH CA++ AND HIGH URINARY PO4 AND CA PTH INCREASES THE CA ABSORBTION FROM THE GUT AND STIMULATES INCREASE PO4 WASTING FROM THE KIDNEYS FEMALE 2:1 PTS ARE USUALLY FOUND TODAY INCIDENTALLY ON A LABORATORY SCREENING TEST WORK WITH AN ENDOCRINOLOGIST BE SLOW TO OPERATE—-10 YEAR STUDY IN NEJM BY SILVERBERG SHOWED NO SIG PROGRESSION OF DZ. BEST TEST IS THE PTH(IRMA) ASSAY—-MUST R/O SECONDARY HPT USUALLY DO TO RENAL FAILURE, OR MALABSORBTION LABS: SERUM CA IS HIGH—–3 READINGS ABOVE 10.6 PO4 (PHOSPHATE) IS LOW CHLORIDE IS HIGH ALK PHOS IS HIGH URINE CA AND PO4 IS HIGH—-24 HOUR URINE TO ASSES RENAL FUNCTION CXR IS NL SUBPERIOSTEAL RESORBTION ON HAND X-RAY—DISTAL RADIUS IS MOST SPECIFIC IF CONSIDERING OBS—-REPEAT SERUM CALCIUM AND PTH 3-6 MONTHS PROBABLY DO SERIAL BONE DENSIOMETRY (US OF THE CALCANEUS OR BETTER A DEXA SCAN) AND RENAL FUNCTIONS RECOMMEND ADEQUATE HYDRATION CONSIDER ORAL PHOSPHATE THERAPY CONSIDER ESTROGEN REPLACEMENT THERAPY CUT BACK ON CAFFIENE CUT OUT SMOKING AVOID STERIODS AVOID EXCESS THYROXINE THESE THINGS MAY ACTUALLY INCREASE PTH AND THUS BONE LOSS—-SURGERY IS GENERALLY RECOMMENDED AS IT IS USUALLY SUCCESSFUL WITH LOW MORBIDITY AND PERMANENTLY CURES THE PROBLEM. THIS IS IN CONTRAST TO PTS WITH FHH (FAMILIAL HYPOCALCIURIC HYPERCALCEMIA/ FHH(AUTO D)–HIGH SERUM CA AND HIGH NL PTH BUT LOW URINE CA++—MUST DO A 24 HOUR URINE CA++ AS THESE PTS WILL NOT BENEFIT FROM A PARATHYROIDECTOMY X-RAY SHOWS SUBPERIOSTEAL RESORBTION OF DISTAL PHALANGES AND DISTAL 1/3 OF CLAVICLES INITIALLY BONES-—PSEUDOGOUT—VERTEBRAL OSTEOPENIA–LATER RECKLINGHAUSEN_S OSTEITIS FIBROSA CYSTICA-=-BONE CYSTS AND BROWN TUMORS (OSTEOCLAST TUMORS) AND BONE PAIN STONES—NEPHROCALCINOSIS(85% RADIO-OPAUE)(MADE WORSE BY LOOPS)—LASIX–LEADS–TO LITHIASIS, POLYDIPSIA AND POLYURIA—5-10% OF PTS WITH INCIDENTAL CA RENAL STONES HAVE HPT ABD GROANS—CONSTIPATION, NAUSEA, ANOREXIA, ULCERS, PANCREATITIS FATIGUE MOANS—LISTLESS, WEAKNESS PSYCHIC OVERTONES–LETHARGY, DEPRESSION, OBTUNDATION, PSYCHOSIS—-MEMORY LOSS PRURITIS, POLYURIA, POLYDIPSIA Dx: Hx (FAMILIAL?), PE, CXR, CBC, SMAC (HIGH CA++ AND LOW PO4--AND NL ALBUMIN-——SERUM CL- IS > 102 IN 80% OF CASES DUE TO THE INCREASES RENAL WASTING OF HCO3 (HYPERCHLOREMIC METABOLIC ACIDOSIS), HIGH PTH ASSAY, RENAL FUNCTION TESTS, 24 HOUR HIGH URINE FOR CA AND PO4 Rx: NECK EXPLORATION AND PARATHYROIDECTOMY—–NO LOCALIZATION PROCEDURES NECESSARY INTITIALLY?—-MAY NEED TO LOOK FROM HYOID TO MEDIASTINUM (THYMECTOMY)
RECENT STUDIES ON PREOP SESTEMIBI SCAN PROVE THAT LOCALIZATION IS COST EFFECTIVE—-INJECT SESTEMIBI IV—-SCAN IN 15 MINUTES—-SEE THYROID—-WAIT FOR THYROID WASH OUT—-RESCAN IN 1:45 MINUTES (2 HR FROM INJECTION)—SEE PARATHYROID ADENOMA—-THEN HAVE 2 HOURS TO DO GAMMA PROBE GUIDED SURGERY INTRAOP ASSAY OF PTH JUST PRIOR TO AND AFTER ADENOMA REMOVAL—SEE A >50% DROP IN SUCCESSFUL EXIRPTATION—-MAY THEN CLOSE ON PERMANENT HISTOPATH—-SEE LOW AMOUNTS OF _OIL RED O_ LIPOPHILIC STAIN IN ADENOMAS AND HIGH AMOUNTS IN OTHER ATROPHIED GLANDS LOCALIZATION STUDIES ARE ALWAYS NECESSARY ON RE-EXPLORATION ALSO CONSIDER US OR MRI (US IS TECH DEP) Rx: SUBTOTAL PARATHYROIDECTOMY—-LEAVE _ TO 1/4 OF ONE VIABLE GLAND (REMOVE 3 _ GLANDS) _HUNGRY BONE SYNDROME—POST OP SURGERY FOR HYPERPARATHYROIDISM—GET TRANSIENT SEVER HYPOCA++ 80% PTS HAVE 4 GLANDS 5% HAVE 5 15% HAVE 3 INF PTG MORE LIKELY TO BE HETEROTOPIC—-PRIMARY PLACE IS IN THE THYMUS 2% ECTOPY IS INTRATHYROIDAL PRIMARY SITE FOR SUP PTG ECTOPY IS RETROESOPHAGEAL 27% OF PATIENTS WILL HAVE PERSISTENT HYPER PTH AFTER CURATIVE PARATHYROID ADENOMA REMOVAL—USUALLY TRANSIENT AND MORE COMMON IN PTS WITH MUSCULOSKELETAL SYMPTOMS AND BLACKS—-MOST LIKELY A SECONDARY RESPONSE TO BONE REMINERALIZATION. MEN I – WERMER_S SYNDROME (BOTH MEN I AND II HAVE PARATHYROID HYPERPLASIA) PARATHYROID GLAND HYPERPLASIA PITUITARY TUMOR (USUALLY PROLACTINOMA) PANCREATIC ISLET CELLTUMORS—-THINK OF ZES–GASTRINOMA–PUDz THESE ARE OFTEN SEQUENTIAL PARATHYROID CARCINOMA RARE(0.5-4% OF HPT)—-VERY VERY HIGH PTH OFTEN PRESENT AS A PALPABLE NECK MASS–CAN PRESENT WITH PULM METS HAVE A DENSE DESMOPLASTIC RXN _MATTING_ SURROUNDING THEM INTRAOPERATIVELY Rx: WLE—SKELETINIZE ALL THE VITAL STRUCTURES SURROUNDING THEM AND DO AN IPSI THYROID LOBECTOMY AND ISTHMUSECTOMY LOCAL RECURRENCE=30% DISTANT METS=30% PARATHYROID CYST OFTEN PRESENT WITH MASS EFFECT—-TRACHEAL DEVIATION, SOB, DYSPHAGIA UNILOCULAR, SOLITARY, TENSE MEAN = 4 CM CONTAIN NONCOLLOID WATERY CLEAR FLUID HORMONALLY INACTIVE PRIMARILY INF POLE (3RD PHARYNGEAL POUCH)