This document discusses the diagnosis and management of parathyroid disease. It reviews calcium homeostasis and parathyroid hormone secretion and regulation. It covers the etiology and pathogenesis of hyperparathyroidism including parathyroid adenomas. The document discusses parathyroid anatomy and histopathology, including the normal parathyroid gland. It also reviews the clinical features of primary hyperparathyroidism and its symptoms affecting the kidneys, skeletal system, and other areas. The goal is to understand the diagnosis and treatment of hyperparathyroidism through surgical and medical management.
Nuclear medicine application in parathyroid diordersRamin Sadeghi
A brief explanation of nuclear medicine application in parathyroid disorders including diagnosis and minimally invasive radioguided parathyroid surgery including parathyroid adenoma, carcinoma, hyperplasia, etc.
Nuclear medicine application in parathyroid diordersRamin Sadeghi
A brief explanation of nuclear medicine application in parathyroid disorders including diagnosis and minimally invasive radioguided parathyroid surgery including parathyroid adenoma, carcinoma, hyperplasia, etc.
This is a clinical case presentation of Nodular Thyroid in a 40 year old woman. Detailed Anatomy, Physiology of Neck region including thyroid with their pahophysiology. Possible investigations and modalities of treatment have also been discussed in this presentation.
This is a clinical case presentation of Nodular Thyroid in a 40 year old woman. Detailed Anatomy, Physiology of Neck region including thyroid with their pahophysiology. Possible investigations and modalities of treatment have also been discussed in this presentation.
hyperparathyroidism with detailed discussion of primary Primary hyperparathyroidism, presentation , workup management & surgery & post operative management
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...
Parathyroid goda
1. Diagnosis andDiagnosis and
Management ofManagement of
Parathyroid DiseaseParathyroid Disease
BYBY
PROF/ GOUDA ELLABBANPROF/ GOUDA ELLABBAN
FOM/SCUFOM/SCU
ellabbang@yahoo.comellabbang@yahoo.com
2. ObjectivesObjectives
Review calcium homeostasisReview calcium homeostasis
Understand parathyroid anatomy andUnderstand parathyroid anatomy and
histopathologyhistopathology
Review embryo-anatomic relationships inReview embryo-anatomic relationships in
the central neckthe central neck
Recognize the clinical features, diagnosisRecognize the clinical features, diagnosis
and surgical/medical management ofand surgical/medical management of
hyperparathyroidismhyperparathyroidism
Understand the molecular basis ofUnderstand the molecular basis of
localization studieslocalization studies
3. CALCIUM HOMEOSTASIS ANDCALCIUM HOMEOSTASIS AND
PARATHYROID HORMONEPARATHYROID HORMONE
SECRETION AND REGULATIONSECRETION AND REGULATION
Parathyroid hormone (PTH) containsParathyroid hormone (PTH) contains
84 amino acids84 amino acids
Degradation into amino(N) andDegradation into amino(N) and
carboxyl(C)-terminal fragments.carboxyl(C)-terminal fragments.
The N-terminal fragment biologicallyThe N-terminal fragment biologically
active and rapidly clearedactive and rapidly cleared
C-terminal fragment is biologically inertC-terminal fragment is biologically inert
and cleared by the kidneyand cleared by the kidney
4. Continued….Continued….
PTH release governed by serum ionizedPTH release governed by serum ionized
calcium levels.calcium levels.
PTH secreted in response to decrease inPTH secreted in response to decrease in
serum-ionized calcium and inhibited by anserum-ionized calcium and inhibited by an
increase serum-ionized calcium.increase serum-ionized calcium.
Target end organs: kidneys, skeletalTarget end organs: kidneys, skeletal
system, and intestine.system, and intestine.
PTH binding to receptor sites results inPTH binding to receptor sites results in
cAMP 2cAMP 2ndnd
messenger system activation.messenger system activation.
Half-life PTH few minutes.Half-life PTH few minutes.
6. Etiology and PathogenesisEtiology and Pathogenesis
of Hyperparathyroidismof Hyperparathyroidism
Parathyroid adenomas (PA) consideredParathyroid adenomas (PA) considered
monoclonal or oligoclonal neoplasms.monoclonal or oligoclonal neoplasms.
Propagation through clonal expansion ofPropagation through clonal expansion of
cells with altered sensitivity to calcium.cells with altered sensitivity to calcium.
PRAD1 implicated in only some PA.PRAD1 implicated in only some PA.
Another mechanism involves alternation inAnother mechanism involves alternation in
tumor suppressor gene expression.tumor suppressor gene expression.
9. Parathyroid Anatomy andParathyroid Anatomy and
Histopathology: TheHistopathology: The
Normal Parathyroid GlandNormal Parathyroid Gland
Supernumerary fifth parathyroid foundSupernumerary fifth parathyroid found
between 0.7%-5.8% patientsbetween 0.7%-5.8% patients
55thth
glands found in the mediastinumglands found in the mediastinum
(thymus or related to the aortic arch),(thymus or related to the aortic arch),
thyrothymic tractthyrothymic tract
10. Parathyroid GlandParathyroid Gland
LocationLocation
80% of superior parathyroid glands found at80% of superior parathyroid glands found at
the cricothyroid junction ~1 cm cranial tothe cricothyroid junction ~1 cm cranial to
juxtaposition of RLN & ITA.juxtaposition of RLN & ITA.
Inferior parathyroid glands (IPG) variable inInferior parathyroid glands (IPG) variable in
location.location.
61% of (IPG) near the lower pole of the61% of (IPG) near the lower pole of the
thyroid gland and 26% in thyrothymicthyroid gland and 26% in thyrothymic
ligament.ligament.
Incidence of intrathyroidal parathyroidIncidence of intrathyroidal parathyroid
glands ~0.5% to 3%.glands ~0.5% to 3%.
12. MorphologicMorphologic
Characteristics ofCharacteristics of
Parathyroid GlandsParathyroid Glands
Shape-oval, bean, or teardropShape-oval, bean, or teardrop
appearance or flat shape whenappearance or flat shape when
juxtaposed to thyroid gland.juxtaposed to thyroid gland.
Color-yellowish brown to reddishColor-yellowish brown to reddish
brown in normal parathyroid glandsbrown in normal parathyroid glands
and lighter gray tone in pathologicaland lighter gray tone in pathological
states.states.
13. Vascular Anatomy of theVascular Anatomy of the
Parathyroid GlandsParathyroid Glands
Normal parathyroid glands most commonlyNormal parathyroid glands most commonly
are supplied by a single dominant arteryare supplied by a single dominant artery
(80%).(80%).
The length of the dominant artery supplyingThe length of the dominant artery supplying
glands vary from 1 to 40 mm.glands vary from 1 to 40 mm.
ITA is dominant blood supply to bothITA is dominant blood supply to both
superior & inferior parathyroid glands mostsuperior & inferior parathyroid glands most
of the time.of the time.
14. Histopathology of theHistopathology of the
Parathyroid GlandsParathyroid Glands
Parathyroid gland composed of chief cells,Parathyroid gland composed of chief cells,
oxyphilic cells and intermediate cellsoxyphilic cells and intermediate cells
Solitary parathyroid adenoma ~80%-85% ofSolitary parathyroid adenoma ~80%-85% of
patients with primary hyperparathyroidismpatients with primary hyperparathyroidism
Variations in parathyroid adenoma includesVariations in parathyroid adenoma includes
other subtypes (oncocytic adenoma,other subtypes (oncocytic adenoma,
lipoadenoma, large clear cell adenoma,lipoadenoma, large clear cell adenoma,
water-clear cell adenoma, and atypicalwater-clear cell adenoma, and atypical
adenoma).adenoma).
15. Continued….Continued….
Primary parathyroid hyperplasia-proliferationPrimary parathyroid hyperplasia-proliferation
of parenchymal cells with increase in weightof parenchymal cells with increase in weight
in multiple glands with absence of stimulusin multiple glands with absence of stimulus
for parathyroid hormone secretion.for parathyroid hormone secretion.
Two types of parathyroid hyperplasia areTwo types of parathyroid hyperplasia are
seen: the common chief cell hyperplasiaseen: the common chief cell hyperplasia
and the rare water cell or clear celland the rare water cell or clear cell
hyperplasia.hyperplasia.
16. Continued….Continued….
Parathyroid carcinoma (PC) ~0.1% to 5.0% casesParathyroid carcinoma (PC) ~0.1% to 5.0% cases
of primary hyperparathyroidism.of primary hyperparathyroidism.
PC tend to be large tumors, (30% to 50% palpablePC tend to be large tumors, (30% to 50% palpable
presentation).presentation).
May measure up to 6 cm in diameter, mean ~3 cm.May measure up to 6 cm in diameter, mean ~3 cm.
Lesion adheres to surrounding tissues including softLesion adheres to surrounding tissues including soft
tissues of the neck (thyroid gland, strap muscles,tissues of the neck (thyroid gland, strap muscles,
trachea & recurrent laryngeal nerve).trachea & recurrent laryngeal nerve).
Regional metastasis rare.Regional metastasis rare.
Pulmonary metastasis most common distantPulmonary metastasis most common distant
metastasis site.metastasis site.
17. Continued….Continued….
PC tends to be an indolent tumor.PC tends to be an indolent tumor.
Multiple recurrences after resectionMultiple recurrences after resection
common and may occur over a 15- tocommon and may occur over a 15- to
20-year period.20-year period.
Death results from from effects ofDeath results from from effects of
excessive PTH secretion andexcessive PTH secretion and
uncontrolled hypercalcemia ratheruncontrolled hypercalcemia rather
than growth of the tumor mass.than growth of the tumor mass.
18. Clinical features PrimaryClinical features Primary
Hyperparathyroidism (PH)Hyperparathyroidism (PH)
Incidence 27 cases annually perIncidence 27 cases annually per
100,000100,000
Prevalence PH general populationPrevalence PH general population
0.1%-0.3%0.1%-0.3%
Prevalence women >60 years morePrevalence women >60 years more
than 1%than 1%
19. CALCIUM HOMEOSTASIS ANDCALCIUM HOMEOSTASIS AND
PARATHYROID HORMONEPARATHYROID HORMONE
SECRETION AND REGULATIONSECRETION AND REGULATION
20. Continued….Continued….
Osteitis fibrosis cysticaOsteitis fibrosis cystica
NephrolithiasisNephrolithiasis
Hypercalcemic crisisHypercalcemic crisis
Osteitis fibrosis occurs ~1% of patientsOsteitis fibrosis occurs ~1% of patients
Renal stones ~10%-20% of patients have renalRenal stones ~10%-20% of patients have renal
stones.stones.
Nonspecific symptoms: malaise, fatigue,Nonspecific symptoms: malaise, fatigue,
depression, sleep disturbance, weight loss,depression, sleep disturbance, weight loss,
abdominal pains, constipation, vagueabdominal pains, constipation, vague
musculoskeletal pains in the extremities, andmusculoskeletal pains in the extremities, and
muscular weaknessmuscular weakness
21. Continued….Continued….
Kidney/Urinary Tract:Kidney/Urinary Tract: 4% with nephrolithiasis4% with nephrolithiasis
and nephrocalcinosis (stone composition, calciumand nephrocalcinosis (stone composition, calcium
oxylate or calcium phosphate). Sx of urolithiasis:oxylate or calcium phosphate). Sx of urolithiasis:
renal colic, hematuria, pyuria.renal colic, hematuria, pyuria.
Skeletal System:Skeletal System:
1.1. Osteitis fibrosis cystica (rare)Osteitis fibrosis cystica (rare)
2.2. Subperiosteal erosion of the distal phalangesSubperiosteal erosion of the distal phalanges
3.3. Bone wasting and softeningBone wasting and softening
4.4. Chondrocalcinosis as a result of bone demineralizationChondrocalcinosis as a result of bone demineralization
5.5. Bone painBone pain
6.6. Pathologic fracturePathologic fracture
7.7. Cystic bone changesCystic bone changes
8.8. Bone loss: cortical bone sites sparing trabecular boneBone loss: cortical bone sites sparing trabecular bone
22. Continued….Continued….
NeuromuscularNeuromuscular ::
1.1. Muscle weakness, (proximal extremity muscle groupsMuscle weakness, (proximal extremity muscle groups
with fatigue and malaise)with fatigue and malaise)
2.2. Neuromuscular syndrome improves in 80%-90% ofNeuromuscular syndrome improves in 80%-90% of
patients.patients.
Neurologic:Neurologic:
1.1. Depression, nervousness, and cognitive dysfunctionDepression, nervousness, and cognitive dysfunction
2.2. Deafness, dysphagia, and dysosmiaDeafness, dysphagia, and dysosmia
3.3. Many psychiatric symptoms improve afterMany psychiatric symptoms improve after
parathyroidectomy. Fifty percent of patients withparathyroidectomy. Fifty percent of patients with
depression or anxiety, or both will improve after surgery.depression or anxiety, or both will improve after surgery.
23. Continued….Continued….
CardiovascularCardiovascular
1.1. Hypertension (50% of patients)Hypertension (50% of patients)
2.2. Parathyroidectomy results in a reduction in BP inParathyroidectomy results in a reduction in BP in
minority of patients.minority of patients.
Hypercalcemic syndromeHypercalcemic syndrome
1.1. polydipsia and polyuria, anorexia, vomiting, constipation,polydipsia and polyuria, anorexia, vomiting, constipation,
muscle weakness and fatigue, mental status changes.muscle weakness and fatigue, mental status changes.
2.2. Metastatic calcifications at the corneal/scleral junction,Metastatic calcifications at the corneal/scleral junction,
so-called band keratopathyso-called band keratopathy
3.3. Shortened Q-T interval on electrocardiogram, ectopicShortened Q-T interval on electrocardiogram, ectopic
calcium deposits, and pruritus.calcium deposits, and pruritus.
25. Continued….Continued….
Diagnosis:Diagnosis:
1.1. Elevated serum CaElevated serum Ca
2.2. Elevated PTH (suppressed in PTH-rp inducedElevated PTH (suppressed in PTH-rp induced
hypercalcemia)hypercalcemia)
3.3. Other:Other:
AlbuminAlbumin
PhosphorousPhosphorous
BUN/CrBUN/Cr
24-hour urine Ca (r/o FHH)24-hour urine Ca (r/o FHH)
Bone Mineral DensityBone Mineral Density
26. Localization StudiesLocalization Studies
Noninvasive preoperative methods Noninvasive preoperative methods
1.1. Ultrasonography Ultrasonography
2.2. Radioiodine or technetium thyroid scan Radioiodine or technetium thyroid scan
3.3. Thallium-technetium scintigraphy Thallium-technetium scintigraphy
4.4. Technetium-99m sestamibi scintigraphy Technetium-99m sestamibi scintigraphy
5.5. Computed tomography scan Computed tomography scan
6.6. Magnetic resonance imagingMagnetic resonance imaging
Invasive preoperative methods Invasive preoperative methods
1.1. Fine-needle aspiration Fine-needle aspiration
2.2. Selective arteriography or digital subtraction angiography Selective arteriography or digital subtraction angiography
3.3. Selective venous sampling for parathyroid hormone assay Selective venous sampling for parathyroid hormone assay
4.4. Arterial injection of selenium-ethionineArterial injection of selenium-ethionine
Intraoperative MethodsIntraoperative Methods
1.1. Intraoperative ultrasonography Intraoperative ultrasonography
2.2. Toluidine blue or methylene blue Toluidine blue or methylene blue
3.3. Urinary adenosine monophosphate Urinary adenosine monophosphate
4.4. Quick parathyroid hormone intraoperativeQuick parathyroid hormone intraoperative
27. Sestamibi-Technetium 99mSestamibi-Technetium 99m
ScintographyScintography
Sestamibi taken up mitochondria of parathyroid cells greaterSestamibi taken up mitochondria of parathyroid cells greater
than surrounding parenchyma.than surrounding parenchyma.
Inject 20 to 25 millicuries of technetium-99m sestamibi.Inject 20 to 25 millicuries of technetium-99m sestamibi.
Images obtained at 10-15 minutes then 2-3 hours after theImages obtained at 10-15 minutes then 2-3 hours after the
injection.injection.
Late phase preferable for detecting parathyroid adenomas, asLate phase preferable for detecting parathyroid adenomas, as
thyroid nodules clear uptake faster than do parathyroidthyroid nodules clear uptake faster than do parathyroid
neoplasms.neoplasms.
Sensitivity (solitary adenoma) ~100%, Specificity ~90%.Sensitivity (solitary adenoma) ~100%, Specificity ~90%.
False-positive:False-positive:
1.1. Solid thyroid nodules (adenomas)Solid thyroid nodules (adenomas)
2.2. Hurthle cell carcinomaHurthle cell carcinoma
3.3. Malignant thyroid lymph node metastasesMalignant thyroid lymph node metastases
4.4. No false-positive with cystic lesions of the thyroid glandNo false-positive with cystic lesions of the thyroid gland
32. Case 1Case 1
65 y.o. male with history of a left65 y.o. male with history of a left
thyroid mass underwent, FNA atypicalthyroid mass underwent, FNA atypical
follicular lesion. Patient underwent L.follicular lesion. Patient underwent L.
thyroid lobectomy with final diagnosisthyroid lobectomy with final diagnosis
of follicular adenoma. Patient hadof follicular adenoma. Patient had
been noted in past to havebeen noted in past to have
asymptomatic hypercalcemia. PTHasymptomatic hypercalcemia. PTH
126, 24-hour urine calcium 380mg,126, 24-hour urine calcium 380mg,
Ionized Ca 1.4Ionized Ca 1.4
35. Continued….Continued….
664 mg right superior parathyroid664 mg right superior parathyroid
gland identifiedgland identified
PTH decreased from 126 to 15PTH decreased from 126 to 15
36. Surgical ManagementSurgical Management
Clinical indicators for surgery*Clinical indicators for surgery*
1.1. Serum calcium is >1.0 mg/dL above the upper limitSerum calcium is >1.0 mg/dL above the upper limit
of normal.of normal.
2.2. Creatinine clearance is reduced >30% for age inCreatinine clearance is reduced >30% for age in
the absence of another cause.the absence of another cause.
3.3. Twenty-four hour urinary calcium is >400 mg/dL.Twenty-four hour urinary calcium is >400 mg/dL.
4.4. Patients are younger than 50 years of age.Patients are younger than 50 years of age.
5.5. Bone mineral density measurement at the lumbarBone mineral density measurement at the lumbar
spine, hip, or distal radius is reduced >2.5 standardspine, hip, or distal radius is reduced >2.5 standard
deviations (by T score).deviations (by T score).
6.6. Patients request surgery, or patients are unsuitablePatients request surgery, or patients are unsuitable
for long-term surveillance.for long-term surveillance.
*Consensus conference held by the National Institutes of Health in 2002
37. Continued….Continued….
AdenomaAdenoma
1.1. Directed unilateral cervicalDirected unilateral cervical
exploration.exploration.
2.2. Curative in >95% of patientsCurative in >95% of patients
3.3. Preoperative localization withPreoperative localization with
technetium-99m sestamibi + IOPTHtechnetium-99m sestamibi + IOPTH
38. Continued….Continued….
MEN 1MEN 1
1.1. Subtotal vs. total with autotransplantation.Subtotal vs. total with autotransplantation.
Men 2a-Men 2a-
1.1. 100% cure rate with no recurrences100% cure rate with no recurrences
whether total parathyroidectomy,whether total parathyroidectomy,
subtotal parathyroidectomy, or excisionsubtotal parathyroidectomy, or excision
of enlarged glands performed.of enlarged glands performed.
2.2. R/O pheochromocytoma prior to OR tripR/O pheochromocytoma prior to OR trip
(hypertensive crisis).(hypertensive crisis).
39. Continued….Continued….
Non-MEN familialNon-MEN familial
hyperparathyroidism (NMFH).hyperparathyroidism (NMFH).
1.1. Subtotal or total (autotransplant) withSubtotal or total (autotransplant) with
bilateral cervical thymectomy.bilateral cervical thymectomy.
Familial neonatalFamilial neonatal
hyperparathyroidism.hyperparathyroidism.
1.1. Total (autotransplant) + bilateralTotal (autotransplant) + bilateral
transcervical thymectomytranscervical thymectomy
40. Continued….Continued….
Renal failure-inducedRenal failure-induced
hyperparathyroidism.hyperparathyroidism.
1.1. Subtotal vs. total parathyroidectomy (autotransplant)Subtotal vs. total parathyroidectomy (autotransplant)
with or without cryopreservation.with or without cryopreservation.
Parathyroid CarcinomaParathyroid Carcinoma
1.1. en bloc resection of the tumor and areas of potentialen bloc resection of the tumor and areas of potential
local invasion and/or regional metastasis (ipsilaterallocal invasion and/or regional metastasis (ipsilateral
central neck contents including the thyroid lobe andcentral neck contents including the thyroid lobe and
tracheoesophageal soft tissues, lymphatics, andtracheoesophageal soft tissues, lymphatics, and
resection of soft tissues within the superior anteriorresection of soft tissues within the superior anterior
mediastinum)mediastinum)
2.2. RLN, esophageal wall, or strap muscles may requireRLN, esophageal wall, or strap muscles may require
sacrifice if the tumor adheres to them.sacrifice if the tumor adheres to them.
3.3. Not enough data to recommend for or againstNot enough data to recommend for or against
chemotherapy or RT.chemotherapy or RT.
41. Continued….Continued….
MIRPMIRP
1.1. Preoperative administration of technetium 99m sestamibiPreoperative administration of technetium 99m sestamibi
before operation + intraoperative hand-held gamma probe.before operation + intraoperative hand-held gamma probe.
2.2. Advantages:Advantages:
1.1. Improved patient comfort postoperatively.Improved patient comfort postoperatively.
2.2. Performance of ambulatory procedures.Performance of ambulatory procedures.
3.3. Reduced cost.Reduced cost.
4.4. Avoidance of general anesthetic.Avoidance of general anesthetic.
3.3. Disadvantages:Disadvantages:
1.1. Potential for conversion to bilateral dissection in event of failedPotential for conversion to bilateral dissection in event of failed
exploration.exploration.
2.2. Patient anxiety when conversion needed (general anesthesia).Patient anxiety when conversion needed (general anesthesia).
42. ConclusionConclusion
No substitute for strong foundationNo substitute for strong foundation
surgical embryology, anatomy, andsurgical embryology, anatomy, and
technique for approaching parathyroidtechnique for approaching parathyroid
disease.disease.
43. BibliographyBibliography
Cummings Otolaryngology Head andCummings Otolaryngology Head and
Neck Surgery. 2005.Neck Surgery. 2005.
Rosen F., Pou A.,Rosen F., Pou A., ParathyroidParathyroid
Disease. March 2002Disease. March 2002. UTMB site. UTMB site
http://www.mrcophth.com/corneacommonchttp://www.mrcophth.com/corneacommonc
(Image-Band Keratopathy)(Image-Band Keratopathy)