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Diagnosis and Treatment of Pituitary Tumors PowerPoint Presentation

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Description : Check out this medical presentation on Carney Complex, which is titled "Diagnosis and Treatment of Pituitary Tumors", to know about pituitary tumors and their treatment.

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Published on : May 13, 2021 | Views : 2836 | Downloads : 6

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Slide 1-

Diagnosis and Treatment of Pituitary Tumors Kevin O. Lillehei, M.D. Professor of Neurosurgery Chairmen, Dept of Neurosurgery University of Colorado Health Sciences Center
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Pituitary Hormones Critical Roles in Growth, Reproduction, Metabolism and Stress Response
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Pituitary Gland Regulation Schneider HJ. Hypopituitarism. 2007 Lancet 369:1461-1470 Complex Integration Of Signals: Higher CNS Centers Thalamus Limbic System RAS Retina Nutritional Status Hormone Cross-Talk
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Assessment of Pituitary Hormones Evaluation-Signs/Symptoms, Physical Exam and Biochemical Evaluation EXCESS DEFICIENCY GH Acromegaly GH Deficiency PRL Hypogonadism Failed Lactation FSH/LH Rarely Clinically Evident Hypogonadism ACTH Cushing’s Disease Adrenal Insufficiency TSH Hyperthyroidism Hypothyroidism ADH SIADH Diabetes Insipidus
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DIAGRAMMATIC REPRESENTATION OF PITUITARY GLAND
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Sagittal post-contrast, T1-weighted MRI, demonstrating normal adult anterior and posterior pituitary gland and sellar region anatomy. Courtesy R.Bert
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Normal Pituitary Pituitary Mamillary Body Optic chiasm Infundibulum Tuber cinereum
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Pituitary Pathology Pituitary Adenomas (10-15% of intracranial tumors) Rathke’s Cleft cyst Craniopharyngiomas Mesenchymal/stromal tumors (i.e., meningiomas,chordomas) Germ Cell Tumors (i.e., Germinomas, Teratomas) Neuronal/paraneuronal tumors (i.e., Gangliocytomas, Neuroblastoma) Miscellaneous-Inflammatory/infiltrative disease, aneurysm, metastatic disease Pituitary carcinomas (<0.1%)
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Pituitary Adenoma Clinically-apparent disease: prevalence~1:3,000-10,000 Pituitary adenoma distribution: Sporadic, monoclonal disease (>95%) Familial, genetic mutations (5%) Multiple Endocrine Neoplasm 1 (MEN1), Familial isolated pituitary adenoma (AIP), Multiple Endocrine Neoplasm 4 (p27Kip1/CDKN1B), Carney Complex (PRKAR1A) Generally younger age of onset (<30 yrs.), and larger/more aggressive pituitary tumors
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University of Colorado Series (Lillehei) : 1986 – 2017 1,964 Transsphenoidal Procedures 1,016 (52%) Non-Secretors (Gonadothroph / Null) 214 (11%) ACTH (Cushing’s) 175 (9%) Rathke’s Cleft Cysts 165 (8%) Prolactinomas 141 (7%) GH (Acromegaly/Gigantism) 59 (3%) Plurihormonal (GH/PRL) 6 (0.3%) TSH 178 (9%) “Other”
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PITUITARY ADENOMAS: Clinical Presentation Hormone hypersecretion Acromegaly Cushing’s Disease Amenorrhea / Galactorrhea Symptoms from mass effect Headaches Vision loss Pituitary gland dysfunction
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Surgery is generally the first line of treatment for all pituitary tumors except for tumors that secrete prolactin. Tumors that secrete both prolactin and growth hormone generally are candidates for surgical intervention
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Prolactinomas-The Basics Most Common Functional Pituitary adenoma (30-40%) Female:Male Prevalence-10:1, median age of diagnosis-34 yrs. Microadenomas Macroadenomas Impairs GnRH pulse generator
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Prolactinoma Diagnosis Random PRL level (gender-based normative ranges) Levels usually correlate with tumor size >100-150 ng/dl with microadenomas >200-250 ng/dl with macroadenomas Pituitary MRI (with/without contrast)
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Prolactinoma Treatment : MEDICATIONS, surgery, radiation Treatment: medications, surgery , rarely XRT
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Dopamine Agonists Bromocriptine (Parlodel) 2.5 mg tab. “Start low and go slow” Common Side Effects: GI upset, Nasal Congestion, Orthostatic Dizzyness. Preferred only if planned pregnancy Cabergoline (Dostinex) 0.5 mg tab Greater efficacy and better tolerated than bromocriptine 1st Line agent in most cases
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WHY? Pre Treatment Post Treatment
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Pre Treatment Post Treatment
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Problems of GH Excess GIGANTISM-Growth hormone excess before puberty (before closure of the growth plates). ACROMEGALY-GH excess after puberty (after completion of linear growth).
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Excess growth hormone secretion results in pituitary gigantism; man at left is 5' 7” and patient at right is 8‘ 5” tall. Inset: note comparison in these two men’s hand sizes ('acral megaly' = acromegaly).
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Clinical Presentation of Acromegaly
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Growth Hormone Excess Diagnosis Clinical Features of GH excess (old pictures are helpful), AND Elevated IGF-1 level (age and gender matched)-best screening test. Integrated 24 h secretion. Long-half life. Conversely, GH levels fluctuate widely over 24 hrs and normal values can overlap with GH-secreting tumors. OGTT-GH test for equivocal cases, or post-op assessment of cure. Pituitary MRI-macroadenomas are detected in >80% of acromegaly. Molitch M. Clinical Manifestations of Acromegaly. Endocrinol Metab Clin North America. 1992;21:597-614
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Acromegaly Treatment A multi-modal and disciplinary approach a dedicated team of: Neurosurgeons, Endocrinologists, Neuropathologists, Radiologists and Radiation/Oncologists. Treatment Approach Surgery Medical Therapies Somatostatin Analogs Growth Hormone Receptor Antagonist Radiation Therapies
Slide 24-

Holdaway, IM, et al. J Clin Endocrinol Metab. 2004;89:667-674. Copyright © 2004 The Endocrine Society. Mortality Rates in Acromegaly 1 0.8 0.6 0.4 0.2 0 Probability 0 5 10 15 20 25 30 Time (years) GH <1 ng/mL Controls GH <2 ng/mL GH <5 ng/mL GH >5 ng/mL A large difference in mortality rates is seen with a small change in the control of GH (large shift between GH <1 and <2 ng/mL).
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Cushings Disease Incidence: 2-3 cases per 1 million/year. ~10-15% of Functional Pituitary adenomas Female, Middle-aged predominance 50% of MRI’s are normal
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The Complications of Chronic Cortisol Excess Changes in Carbohydrate, Protein and Fat Metabolism Peripheral Wasting of Fat/Muscle Central obesity, Moon facies, fat pads Osteoporosis Diabetes Hypertriglyceridemia Changes in Sex Hormones Amenorrhea/Infertility Excess hair growth (♀) Impotence Salt and Water Retention HTN and Edema Impaired Immunity Neurocognitive Changes
Slide 27-

Cortisol Excess (Hypercortisolism) Newell-Price, J et. al., Endocr. Rev. 1998 19:647-672 70-75% 25-30%
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Screening Tests for Cushing’s Syndrome Disrupted Circadian Rhythm Midnight Salivary or Serum Cortisol Increased Filtered Cortisol Load 24 hr Urine Free Cortisol Attenuated Negative Feedback Low Dose (1 mg) Dexamethasone Suppression test (11-12 p.m.) Raff 2004 Curr Opin Endocrin Diabetes 11:271-5 Normal Subject Mild Cushing’s Severe Cushing’s Clock Time Cortisol (nmol/L)
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Inferior Petrosal Venous Sinus Sampling (IPSS) Sample both Sides for ACTH If ACTH >2-3 times higher than ACTH in peripheral vein Then ACTH source is the Pituitary
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Specific Signs of Cushing’s Syndrome Plethoric/moon facies Wide (>1 cm), violaceous striae (abdominal, axillary) Spontaneous Ecchymoses Proximal Muscle Weakness Early/Atypical Osteoporosis (atraumatic rib fx)
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with permission
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Sx of mass effect: Headache Vision loss Pituitary hormone dysfunction Cranial Nerve Abn.
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Surgery
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Approaches
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Transnasal Microscopic Approach
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Transnasal Microscopic Approach
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The Set-up Transnasal Endoscopic Approach
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Transnasal Endoscopic Approach
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Thank you
Slide 43-

Ontogeny and primary transcription factors for pituitary cell type lineage (Adapted from Asa SL. Practical pituitary pathology: what does the pathologist need to know? Arch Pathol Lab Med 2008, 132: 1231–1240)
Slide 44-

Pituitary Adenoma SRS 18 Gy tumor <8 Gy optic chiasm Radiation therapy: critical need for expert Neuro-oncologist: Dr. Laurie Gaspar and colleagues
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Radiotherapy Conventional Multi-fractional 40 years experience Stereotactic Single fraction Less radiation to surrounding tissues Limited experience Gamma knife LINAC Proton beam Gamma knife LINAC Proton beam
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Anatomy Sellar & Parasellar Rhoton
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Anatomy Sellar & Parasellar Rhoton
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Anatomy Optic Nerve & Chiasm Rhoton
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Anatomy Cavernous Sinus Rhoton
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Anatomy: Cavernous Sinus
Slide 51-

A, Child at age 9 years prior to development of an ACTH-secreting pituitary adenoma. B, Same child as in Figure 29.27A, now at age 11 years with severe Cushing’s disease, photographed just prior to surgical removal of his corticotroph adenoma. Note plethora and truncal obesity. A B