The parathyroid glands regulate calcium levels in the blood and bones. There are usually four parathyroid glands located near the thyroid gland. The parathyroid glands secrete parathyroid hormone (PTH) which increases blood calcium levels when low by promoting bone resorption and renal reabsorption of calcium. Primary hyperparathyroidism occurs when one parathyroid gland enlarges and overproduces PTH, commonly caused by a benign tumor in the gland. Surgical removal of the enlarged gland is usually curative for primary hyperparathyroidism.
Short and brief presentation of anatomy, physiology , disorder and management of parathyroid glands.
management of MEN syndrome, hyper and hypoparathyroidism.
disorder of calcium metabolism like tetany,.
surgical steps of parathyroidectomy with indication and complications
Short and brief presentation of anatomy, physiology , disorder and management of parathyroid glands.
management of MEN syndrome, hyper and hypoparathyroidism.
disorder of calcium metabolism like tetany,.
surgical steps of parathyroidectomy with indication and complications
Physiology of Parathyroid glands
Outline :
- Location of Parathyroid glands.
- Who discovered the glands.
- Some info. about it.
- Parathyroid hormone.
- Histology of the gland.
- PTH biosynthesis.
- The calcium-sensing receptors (CaSR)
- Why Calcium is so Important?
- Calcitonin
- vitamin D
-Metabolic bone diseases (Hypercalcaemia and hypocalcaemia)
hyperparathyroidism with detailed discussion of primary Primary hyperparathyroidism, presentation , workup management & surgery & post operative management
Parathyroid hormone by Dr. Amruta Nitin Kumbhar, Asst. Professor Dept. of Phy...Physiology Dept
FUNCTIONAL ANATOMY OF PARATHYROID GLANDS
Histological structure
STRUCTURE, SYNTHESIS AND SECRETION OF PTH
REGULATION OF PTH SECRETION
MECHANISM OF ACTION AND ACTIONS OF PTH
Applied physiology
Physiology of Parathyroid glands
Outline :
- Location of Parathyroid glands.
- Who discovered the glands.
- Some info. about it.
- Parathyroid hormone.
- Histology of the gland.
- PTH biosynthesis.
- The calcium-sensing receptors (CaSR)
- Why Calcium is so Important?
- Calcitonin
- vitamin D
-Metabolic bone diseases (Hypercalcaemia and hypocalcaemia)
hyperparathyroidism with detailed discussion of primary Primary hyperparathyroidism, presentation , workup management & surgery & post operative management
Parathyroid hormone by Dr. Amruta Nitin Kumbhar, Asst. Professor Dept. of Phy...Physiology Dept
FUNCTIONAL ANATOMY OF PARATHYROID GLANDS
Histological structure
STRUCTURE, SYNTHESIS AND SECRETION OF PTH
REGULATION OF PTH SECRETION
MECHANISM OF ACTION AND ACTIONS OF PTH
Applied physiology
Hyperparathyroidism exists in three different forms: primary, secondary and tertiary. Primary hyperparathyroidism (pHPT) is the most frequent pathological condition of the parathyroid glands and one of the most frequent endocrine disorders overall. The most probable location of parathyroid gland is posterior to the thyroid gland. The parathyroid glands produce parathyroid hormone (PTH), which is important for maintaining calcium, phosphate and vitamin D homeostasis, and ultimately bone health.
Primary hyperparathyroidism is characterized by increased production and secretion of parathyroid hormone. This condition causes nephrocalcinosis, urolithiasis, osteoporosis, gastrointestinal disturbances, neuromuscular manifestation and neuropsychiatric disorders. Parathyroidectomy is the only curative treatment for pHPT. pHPT is typically caused by a solitary parathyroid adenoma (80%-90%), hyperplasia (10%) and less frequently parathyroid carcinoma (5%).
Secondary hyperparathyroidism develops as a consequent to a chronic hypocalcemic condition that can be caused by renal failure, gastroinstinal malabsorption, dietary rickets and ingestion of drugs. Secondary hyperparathyroidism is a frequent and serious complication in haemodialysis patients. Tertiary hyperparathyroidism is a condition where parathyroid hyperplasia, secondary to chronic hypocalcemia, becomes autonomous with development of hypercalcemia. Tertiary hyperparathyroidism is used to designate hyperparathyroidism that persists or develops after renal transplantation.
Localization of hyperfunctioning parathyroid tissue (adenomas or hyperplasia) in primary hyperparathyroidism is useful before surgery to help the surgeon localize the lesion, thus shortening the time of the procedure. Parathyroid glands can be imaged with multiple modalities, including scintigraphy, high-resolution ultrasonograhy, thin-section CT and MRI. Parathyroid scintigraphy may also be indicated for localization of hyperfunctioning parathyroid tissue in patients with persistent or
recurrent disease. For this situation scintigraphy is superior to any other radiological modalities, including MRI, CT scan, ultrasonography combined with needle aspiration and also some invasive techniques like arteriography, selective venography and mediastinoscopy.
Hyperparahyroidsm is an endocrinal disorder majorly affecting the parathyroid glands which secrete parathyroid hormone and calcitonin.
A condition characterised by excessive secretion of calcium in blood and Bone resorption and inanbility to metabolise calcium in blood.
After the class the students will be able
Explain the structures and function of Parathyroid gland.
Explain the age affect on parathyroid gland.
Describe the definition, etiology, risk factors, pathophysiology, medical management, surgical management and Nursing management of Hyperparathyroidism.
Describe the definition, etiology, risk factors, pathophysiology, medical management, surgical management and Nursing management of Hypothyroidism.
List down the health education for Hyperparathyroidism and Hypoparathyroidism.
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.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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
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
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
3. Anatomy
There are four parathyroid glands.
All are related to the thyroid glands.
Two upper ( develop from 4th
branchial pouches ) .
two lower glands ( develop from
3rd branchial pouches ).
Each weighs 30 to 50 mg and
measures about 5 mm in dimension.
5. physiology
Factors that affect calcium in the body:
1- PTH (parathyroid hormone)
• PTH is synthesized and secreted by parathyroid glands. It is very sensitive to
serum Ca levels and it aims at keeping serum Ca levels up in the blood.
• Hypocalcemia stimulates PTH secretion.
• Hypercalemia inhibits PTH secretion.
• PTH increases calcium reabsorption in proximal convoluted tubule(PCT) and
increases phosphate clearance.
• It also mobilizes calcium from bones and indirectly increases GI absorption of
calcium by stimulating Vit D production.
6. 2- Vitamin D
• Vitamin D directly enhances GI
calcium absorption.
• Low Vit D levels increase PTH
secretion.
3- Calcitonin:
decreases serum calcium levels
7. Role of CA in body
1-To provide the electrical energy for our nervous
system.
2-To provide the electrical energy for our muscular
system.
3-To provide strength to our skeletal system
Thus, calcium is the most closely regulated element in
our bodies! In fact, calcium is the ONLY element /
mineral that has its own regulatory system (the
parathyroid glands).
8. Primary hyperparathyroidism
• The relation between PTH and Ca is disturbed. Normally, PTH is
secreted or inhibited whenever the balance is disturbed. And it goes
back to normal once this balance is restored.
• High PTH
• Low Phosphorus
• Normal or elevated serum Ca
• Excess PTH secretion leads to increased GI absorption of Ca,
increased urinary excretion of Ca, and bone loss.
9. • Three distinct lesions that can cause PHP:
1- Carcinoma (1%)
2- Adenoma (84%): only one is enlarged.
3- Hyperplasia (15%): all are enlarged.
10. CLINICAL MANIFESTATIONS
• Renal stones and calcinosis
• Bone and joint pains
• Abdominal groans (pancreatitis,
peptic ulcer)
• Psychic moans (mental
disturbance)
Common in women.
Apathy, lack of concentration.
Depression.
• Fatigue overtones
11. INVESTIGATIONS
High serum Calcium sometimes you may find it low, so you have to repeat it again.
High PTH
Low serum Phosphate
High Chloride
x-ray the hand for signs of bone resorption.
12.
13. • Hypercalcemia could be drug-induced e.g. diuretics and Ca supplements.
• Elevated PTH occurs only with PHP, familial hypercalcemic hypocalciurea, or
Vit D deficiency.
• A calcium:creatinine ratio less than 0.05 indicates FHH
• High PTH-rP indicates malignancy.
• Some tumors secrete PTH-rP as paraneoplastic syndrome. The most
common one is bronchial squamous cell carcinoma, others include, breast,
renal, and ovarian cancers.
• Primary bone cancers (multiple myeloma) cause hypercalcemia without
high PTH-rP. Other tumors (lymphoma) that secrete Vit D behave in the same
way.
• Primary bone cancers cause hypercalcemia without high PTH-rP.
14. Management
Patients can be managed medically (in case of hypercalcemia) or
surgically (in case of PHP):
• Hypercalcemia: In case of acute, severe hypercalemia, patients are
managed by large volume infusion. Loop diuretics are used
adjunctively other drugs may be added to decrease bone turnover
e.g. bisphosphate and calcitonin.
15. • Primary hyperparathyroidism: Currently, there is no definitive medical treatment.
• Surgical management: All symptomatic patients should be treated.
• Asymptomatic: do not operate unless there are symptoms. So, it is better to wait.
• For ESRD patients the most effective treatment is renal transplantation.
• Single-gland resection is preferred for adenoma.
• Subtotal resection ( three and half) is preferred for hyperplasia.
16. Post operative management
What is Bone hunger syndrome?
Before operation: high PTH, in addition, bones are resorbed.
After operation: the bones now are free from the high PTH.
Therefore, they will immediately take up calcium from serum which
may lead to severe hypocalcemia to the point that the patient may
have tetany.
To avoid this hungry bone syndrome, patients with advanced bone
diseases are sent to ICU after operations for 24 hours monitoring.
17. Secondary hyperparathyroidism
• The problem here is not in the glands.
• High PTH
• Low Ca levels
• E.g. rickets, malabsorption, Vit D, Renal failure.
• In these cases you should treat the cause.
18. Hypoparathyroidisim
Diagnosis and Causes
1 - Damage to the Parathyroid Glands from Surgery .
2 - Developmental Defects in the Parathyroid Glands.
3 - Autoimmune Hypoparathyroidism .
4 - Defects in the Parathyroid Hormone Molecule.
5 - Defective Regulation of Parathyroid Hormone Secretion.
21. summary
*Parathyroids are NOT related to the thyroid (except they
are neighbors in the neck)
*The thyroid gland controls much of your body's
metabolism, but the parathyroid glands control body
calcium. They have no relationship except they are
neighbors.
22. *All four parathyroid glands do the exact same thing.
*Parathyroid glands control the amount of calcium in your blood
and bones.
*You can easily live with one (or even 1/2) parathyroid gland.
*When parathyroid glands go bad, it is just one gland that goes bad
about 96-98% of the time--it just grows big (develops a benign
tumor) and makes too much hormone.
*There is only ONE way to treat parathyroid problems--Surgery.