The document summarizes key information about the pituitary gland and adrenal glands. It discusses the anatomy and physiology of the pituitary gland and its role in controlling the anterior pituitary via hormones from the hypothalamus. It also discusses specific pituitary tumors like prolactinomas and acromegaly. It then covers the anatomy and physiology of the adrenal glands, including disorders like Cushing's syndrome, Conn's syndrome, adrenal insufficiency, and adrenal tumors. Evaluation and treatment of various pituitary and adrenal pathologies are summarized.
A brief overview of pituitary adenomas, their subtypes, classification, investigation protocols, radiological evaluation, and their medical management.
A brief overview of pituitary adenomas, their subtypes, classification, investigation protocols, radiological evaluation, and their medical management.
Pituitary tumours are abnormal growths that develop in your pituitary gland. Some pituitary tumours cause excessive production of hormones that regulate important functions of your body.
it is a young boy ,suddenly became unconscious, found high blood pressure on clinical exam,. on USG bilateral adrenal mass confirmed on contrast CT scan. Radiological diagnosis was made phaeochromocytoma
Pituitary tumours are abnormal growths that develop in your pituitary gland. Some pituitary tumours cause excessive production of hormones that regulate important functions of your body.
it is a young boy ,suddenly became unconscious, found high blood pressure on clinical exam,. on USG bilateral adrenal mass confirmed on contrast CT scan. Radiological diagnosis was made phaeochromocytoma
A Condition that occurs from exposure to cortisol levels for a long time.the most common cause is the use of steroid drugs,but it can also occur from over production of cortisol by the sdrenal glands.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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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
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
2. Pituitary Gland
Anterior has no direct
blood supply. There is a
portal system with blood
passing through the
posterior pituitary first
Located in the sella turcica
3. Hypothalamus
Releases TRH, CRH, GnRH and dopamine into median eminence
Hypothalamus Posterior Pituitary Anterior Pituitary
Dopamine inhibits prolactin secretion
4. Posterior Pituitary (neurohypohysis)
Axons from the supraoptic and paraventricular nuclei of the hypothalamus to the
posterior pituitary
Secretes 2 hormones
ADH
Release is mostly controlled by the supraoptic nuclei
Regulated by osmolar receptors in the hypothalamus released in response to high osmolarity
Causes increased water absorption in the renal collecting ducts
Oxytocin
Release is mostly controlled by the supraoptic nuclei
Mainly functions in uterine contraction and lactation
*Posterior pituitary does NOT contain cell bodies
5. Anterior Pituitary (adenohypohysis)
Comprises 80% of the pituitary gland mass
Releases ACTH, TSH, GH, LH, FSH, and prolactin
Bi-temporal hemianopia occurs from compression of CN II
by a pituitary mass at the optic chiasm
Bromocriptine can be used to treat all endocrine secreting
pituitary tumors EXCEPT an ACTH secreting tumor
Trans-sphenoid resection is an option, but is
contraindicated with supra-cellar extension (dumbbell-
shaped) and massive lateral extension
6. Prolactinoma
Most common pituitary tumor (most are micro-adenomas)
Symptoms: amenorrhea, galactorrhea, infertility, poor libido, visual problems
Dx: Elevated prolactin (>150), MRI and visual field testing
Tx: Most will not require surgery
Asymptomatic AND micro (≤1cm)= follow with MRI
Symptomatoc OR macro (>1cm)=
Bromocryptine or cabergoline (dopamine agonist)- 85% success (safe with pregnancy)
If failed medical Tx, hemorrhage, significant visual loss, young female wanting pregnancy, or
CSF leak then trans-sphenoid surgery- 85% success (15% recurrence)
7. Acromegaly
Excessive GH, which stimulates secretion of IGF-1
Most are macro-adenomas
Symptoms: jaw enlargement, macroglossia, headaches, HTN, amenorrhea,
DM, giganticism and visual problems
Can have cardiac issues (valvular or cardiomyopathy)
Dx: Elevated IGF-1 (random GH is NOT useful), MRI
Tx: Trans-sphenoid resection is first choice if no invasion to surrounding
tissue
Octreotide and bromocriptine can shrink tumor and improve symptoms
Pegvisomant (GH receptor antagonist)
8. Pituitary Potpourri
Sheehan’s Syndrome
Pituitary insufficiency in mother after delivery
Caused by pituitary ischemia 2/2 hypovolemia/shock following childbirth
Symptoms: Most common initial sign in difficulty with lactation; can also have amenorrhea, adrenal
insufficiency or hypothyroid
Posterior pituitary is usually unaffected 2/2 direct blood supply
Tx- exogenous replacement of deficiency
Craniopharyngioma
Most commonly occur in children 5-10yo and are benign
Calcified cyst near anterior pituitary, remants of Rathke’s pouch (diverticulum arising from the embryonic
buccal cavity, from which the anterior pituitary gland develops)
Symptoms: headaches, growth failure, visual problems, endocrine abnormalities, hydrocephalus
Tx: Surgery if symptomatic (DI is a common post-op complication)
* Keep metastatic disease in mind (women with hx of breast CA and men with hx of lung CA)
9. Adrenal Anatomy
Weighs 4-6 grams
Arterial Supply – Inferior Phrenic, Unnamed Aorta, Renal
A. Branches
Anterior and posterior surface are avascular
Venous Drainage
L Adrenal
Drains from the lower pole into the L Renal V
R Adrenal
Drains the anterior surface of the gland into the posteriolateral
IVC; short
Innervation
Cortex= none
Medulla= splanchnic
10. Adrenal Anatomy
Cortex
Originates from the mesoderm. From the adrenocortical ridge near the gonads during the 5th week
of gestation. Can have adrenal nests in the ovaries, testes or kidneys
3 zones
Glomerulosa (salt)– Aldosterone
Fasciculata (sugar)– Cortisol
Reticularis (sex)– Testosterone/estrogen
Medulla
Originates from the ectoderm from the neural crest
Epinephrine (20%) – Requires PMNT – medulla or zuckerkandl (paraganglia near aortic bifrication)
NorEpi (80%)
11. Physiology
Renin-angiotensin-aldosterone pathway
Decrease Na and volume stimulate renin secretion from the JXA
Renin converts angiotensinogen to angiotensin I
Angiotensin I is converted to angiotensin II by ACE in the lungs
Angiotensin II then causes vasoconstriction and aldosterone secretion
Aldosterone causes sodium retention and potassium excretion in the renal tubules
Cortisol pathway
Hypothalamus releases CRH
CRH stimulates ACTH from the anterior pituitary
ACTH stimulates cortisol synthesis and release from adrenal
Cortisol acts in negative feedback to inhibit CRH/ACTH and also has effects on hepatic gluconeogenesis,
glycogen synthesis, protein catabolism, lipolysis
Also causes hyperglycemia, impaired wound healing, collagen and bone loss
12. Primary Hyperaldosteronism
Conn’s Syndrome
HTN, Hypokalemia, Polyuria, Polydipsia, Muscle Weakness
Adenoma (60%), Bilateral Hyperplasia (40%)
Elevated Aldosterone, Low Renin (Ratio >20:1)
Elevated urine aldosterone following a salt loading test
CT – adenoma vs hyperplasia
If microadenoma (<1cm) or no mass then adrenal venous sampling to distinguish unilateral
adenoma vs B/L hyperplasia
If macroadenoma (>1cm)- resect
Adenoma- Resect (preop with spironolactone to normalize potassium)
18-hydroxycorticosterone elevated (>100)with adenomas and low in hyperplasia
Hyperplasia – Medical Tx – Spironolactone, Ca2+Blockers, Potassium
16. Hypercortisolism
Source
If adrenal suspected CT abdomen (adrenal protocol)
If pituitary suspected MRI sella turcica
If ectopic suspected CT chest (suspected small cell carcinoma)
Adrenalectomy
Unilateral for adenoma or carcinoma
Need perioperative steroid coverage
Bilateral for hyperplasia or in some cases of secondary
hypercortisolism without identification of primary tumor
Will require steroid replacement
*Exogenous steroid use is the MCC of cushingoid appearance
17. Congenital Adrenal Hyperplasia
Deficiency Aldosterone Testosterone
21-Hydroxylase Normal ↑
17-α-Hydroxylase ↑ Normal
11-α-Hydroxylase ↑ ↑
Aldosterone
HTN and hypokalemia
Tertiary
Virilization
18. Adrenal Insufficiency
Primary – Most common is autoimmune
Infection – Histoplasmosis, TB (MC in developing world), Meningococcus (Waterhouse Friderichsen
syndrome)
Secondary-Iatrogenic; Exogenous Corticosteriods, most common
Labs
Elevated ACTH, Hyperkalemmia, Hyponatremia, Hypochloremia, Hypoglycemia, Acidosis
Cosyntropin Stim Test – 250micrograms IV
Cortisol level at 30-60 min if <18 is suggestive of insufficiency
Hydrocortisone will interfere with this; can use dexamethasone
Tx – Glucocorticoids and hydration
Addisonian crisis
Symptoms: hypotension, tachycardia, refractory shock
Treat immediately. Don’t wait for labs
19. Evaluating Adrenal Mass
Functioning or Non Functioning
Majority are non functioning, if functioning resect regardless of size
Blood/Urine levels – VMA, Catecholamines, Metanephrines
Benign or Malignant
Vast Majority are benign
Carcinomas are rare – 50% stage IV at diagnosis
Primary or Secondary
Metastatic lesions from lung, breast, renal cell, melanoma, prostate, colon
20. Adrenal Incidentalomas
Adrenal Mass discovered during imaging for unrelated reason
DDx – Cortical adenoma, carcinoma, pheo, ganglioneuroma, cyast,
hemorrhage, fibrosis
Evaluation
Plasma Cortisol, Estradiol, testosterone, androstenedione
24H urinary cortisol
Low Dose Dexamethasone cortisol suppression test – should suppress pituitary
ACTH yielding decreased levels. No depression means cushing’s
Renin/Aldosterone ratio
Urinary catecholamines, metanephrines, VMA
21. Adrenal Incidentaloma
Benign
Round, smooth, homogenous
Increased fat content
Malignant
Irregular, focal hemorrhage/necrosis
Percutaneous Bx
Contraindicated if surgery indicated
Perform if multiple masses present with primary unknown
Not appropriate for hormonally active large tumor or if pheo is suspected
22. Indication for Surgery
Hyperfunctioning – Conn, Cushing, Pheo
Malignancy – based on CT
Size
Non functioning <cm 4 – Do not operate if benign imaging characteristics (smooth,
homogenous, <10 HU, >60% washout on 15min delay phase)
CT at 3, 6, 12 months, resect if increase in size
Non functioning 4-6cm – Individualize,
<40yo resect, elderly observe
Non Functioning - >6cm – Operate due to increased risk of malignancy unless clearly
benign cyst or myolipoma on imaging
Begin metastatic workup
23. Adrenal Cortical Carcinoma
Rare, aggressive, 60% hyperfunctioning
Women, 40-50yo, Large (90%>6cm)
Left sided more common
Can present with liver mets
Tx – Open Adrenalectomy (concern for tumor spillage), resection en bloc
5 yr survival 20%
No benefit to chemo/rads
If unresectable, consider mitotane (adrenolytic agent that binds mitochondrial
proteins adrenal atrophy and tumor death)
24. Pheochromocytoma
Tumor of adrenal medulla or extra adrenal adrenergic tissue (neuroectodermal origin)
Rule of 10s – 10% familial (MEN II A/B, von Hippel Lindau, Neurofibromatosis), extraadrenal
(secrete NE), multiple, bilateral, pediatric, malignant
Sx- paroxysmal HTN, tachycardia, HTN, palpitations, flushing, sweating
Dx – Initial plasma catecholamines/metaneprhines
24h Urinary catecholamines (dopamine, epi, NE) and metabolites (VMA, metanephrines)
CT abdomen
MRI – bright T2
Pheo Scan – MIBG I131 – concentrates in adrenergic vesicles – identify extra adrenal
Preop – Alpha blockade first – Phenoxybenzamine (7-10d preop), then beta blockade 48 H
prior, hydrate
If beta blockade first yields unopposed alpha yields HTN crisis
Tx: Laparoscopic adrenalectomy
25. MEN
MEN I
Pituitary – Prolactinoma
Initial Tx with bromocriptine; rare surgical excision
Parathyroid – 4 gland hyperplasia (MC manifestation of MEN I)
Pancreas – Neuroendocrine (MC non-functional)
MEN IIA – Autosomal Dominant
Medullary Thyroid Cancer (100%)
Pheochromacytoma
Hyperparathyroid
MEN IIB – Autosomal Dominant
Medullary Thyroid Carcinoma (100%)
Pheochromacytoma
Mucosal Neuroma/Marfanoid Habitus
Genes:
MEN I-
MEN II-
MTC-
MEN I
RET
RET, NTRK1
