Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Hyperaldosteronism is a disorder in which the adrenal gland releases too much of the hormone aldosterone into the blood. Hyperaldosteronism can be primary or secondary.
Congenital Adr Hyperplasia (CAH) can appear at any age from birth to puberty where it can lead to ambiguous genitalia. It is due to absolute or relative deficiency of 17 Hydroxylase or 21 Hydroxylase enzyme.
Hyperaldosteronism is a disorder in which the adrenal gland releases too much of the hormone aldosterone into the blood. Hyperaldosteronism can be primary or secondary.
Addison’s disease important DR. Aijin.A.MohanAijin Mohan
BRIEF DESCRIPTION ABOUT ADDISONS DISEASE FOR DENTAL AND MEDICAL STUDENTS AND FOR GRADUATES AND FOR UNDERGRADUATES WHO FIND IT DIFFICULT TO UNDERSTAND FROM THE MEDICAL PUBLICATONS ABOUT THIS DISEASE AND ITS DIAGNOSIS AND ALSO DIFFERENTIAL DIAGNOSIS.
Adrenal fatigue and Addison's disease are endocrine or hormonal disorders in which the organism does not produce sufficient amounts of adrenal hormones such as cortical and aldosterone. The organism regulates hormone levels through a signaling and feedback system
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Principles of Pathological Investigation and Imaging in Skeletal DisordersPurvi Verma
The current presentation explains about the pathological and pathological investigation required for the skeletal disorders.
The basic requirement for a good prognostic and diagnostic feature which helps in evaluation of any skeletal disorders.
Endocrine disease in dentistry /certified fixed orthodontic courses by Indian...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
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
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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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!
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
6. Lab test
Blood test.: Measuring your blood levels of sodium,
potassium, cortisol and ACTH gives your doctor an initial
indication of whether adrenal insufficiency may be causing
your signs and symptoms. A blood test can also measure
antibodies associated with autoimmune Addison's disease.
ACTH stimulation test. This test involves measuring the level
of cortisol in your blood before and after an injection of
synthetic ACTH. ACTH signals your adrenal glands to produce
cortisol. If your adrenal glands are damaged, the ACTH
stimulation test shows that your output of cortisol in response
to synthetic ACTH is limited or nonexistent.
7. Corticotrophin-releasing hormone (CRH) stimulation test. This test is used
when the ACTH test is abnormal, to help determine the cause of adrenal
insufficiency. CRH is a hormone released by the hypothalamusthat stimulates
ACTH production by the pituitary gland, which in turn stimulates cortisol
production by the adrenal glands. For this test, synthetic CRH is injected
intravenously and blood cortisol and ACTH levels are measured at timed
intervals after the injection, for example, at 30 and 60 minutes. The normal
response is a peak in ACTH levels followed by a peak in cortisol levels.
People with Addison disease (underactive or damaged adrenal glands)
produce a high level of ACTH but no cortisol.
People with secondary adrenal insufficiency have absent or delayed ACTH
responses. If someone has a damaged pituitary, CRH will not stimulate
ACTH secretion and an absent ACTH response indicates the pituitary is the
cause. If ACTH response is delayed, that indicates the hypothalamus is the
cause.
8. Aldosterone. Blood or urine aldosterone levels are measured to
help diagnose Addison disease, to determine whether the adrenal
gland is producing aldosterone. If the level is low, it is another
indication that an individual may have a primary adrenal
insufficiency.
Electrolytes. Electrolytes (sodium, potassium, chloride and carbon
dioxide) are measured to help detect and evaluate the severity of
an existing electrolyte imbalance and to monitor the effectiveness
of treatment. Electrolytes may be affected by many conditions;
with Addison disease, the sodium, chloride, and carbon dioxide
levels are often low, while the potassium level may be very high.
BUN and Creatinine are tests done to monitor kidney function.
Glucose levels may be very low during an adrenal crisis. Glucose
may be ordered in order to help monitor the individual during a
crisis.
9. Occasionally Used Tests
Insulin-induced hypoglycemia test. Occasionally, a doctor will
order this test to learn if pituitary disease (secondary adrenal
insufficiency) is the cause of adrenal insufficiency. Glucose
and cortisol levels are measured at predetermined intervals
after an injection of insulin is used to stress the pituitary
gland. In healthy people, blood glucose levels fall and
cortisol concentrations increase.
In those with adrenal insufficiency, cortisol levels will remain
low and glucose levels will fall, then recover slowly.
10. Renin. Renin activity is elevated in primary
adrenal insufficiency because a lack of
aldosterone causes increased renal sodium
losses. This lowers blood sodium levels and
decreases the amount of fluid in the blood
(which lowers blood volume and pressure),
which in turn stimulates renin production by
the kidney.
21-hydroxylase autoantibodies are
sometimes ordered as part of the diagnostic
process when autoimmune Addison disease
is suspected. The test is considered a good
indicator of autoimmune Addison disease
but is not widely used at this time.
11. Which antibody tests are positive
in Addison’s disease?
There are three known potential adrenal proteins targeted by anticortical antibodies (ACAs):
21-hydroxylase (21-OH)
17-hydroxylase (17-OH)
Cytochrome P-450
Of these, the most commonly used test is for antibodies to 21-OH, since
the other two proteins are also found in non-adrenal tissues, making
them less specific and confirmatory for Addison’s. The test will likely be
called an adrenal (21-OH) antibody test, or something similar. When
positive, there are antibodies in the bloodstream directed against only
adrenal cortex tissue, which confirms the presence of autoimmune
disease.
12. Is it possible to test negative for the
antibodies and still have Addison’s?
Yes. Because Addison’s is not always
autoimmune in nature – it can also be
caused by infection, trauma, cancer and
other etiologies – it is possible to have the
disease without the presence of any
antibodies.
.
13. Genetic test for HLA
Addison’s disease is associated with DRB1*03:01-DQB1*02 (DR17, DQ2)
and DRB1*04-DQB1*03:02 (DR4, DQ8). The most strongly associated
DRB1*04 allele is DRB1*04:04. The major histocompatibility complex
class I related chain – A (MICA) is an additional risk factor. MICA genes
are highly polymorphic with over 70 alleles described.
Autoantibody testing for anti-21-hydroxylase is more diagnostic in
Addison’s disease than genetic testing. Genetic testing does however
contribute to a better understanding of the etiology of the disease.
14. Non lab test
X-rays may be used to look for calcification on the adrenal cortex that
may be due to a tuberculosis infection.
CT (computerized tomography) or MRI (magnetic resonance imaging)
scans are sometimes used to look at the size and shape of the adrenal
glands and the pituitary. The adrenal glands can be enlarged with
infections and cancers. With autoimmune diseases and secondary
adrenal insufficiency, the adrenal glands are often normal or small.
15. treatment
1-hormone replacement is used to
correct the insufficient levels of
steroids.
2-increase in sodium intake
Fludrocortisone
Hydrocortisone
Prednisone
Oral injection
Hydrocortisone oral
Cortisone oral
Dexamethasone oral
16. treatment
All patients with adrenal insufficiency should
receive specific hormone replacement.
Replacement therapy should correct both
glucocorticoid and mineralocorticoid deficiencies.
Hydrocortisone ( cortisol ) is the mainstay of
treatment. Patients are advised to take
glucocorticoids with meals or, if that is impractical,
with milk or an antacid, because the drugs may
increase gastric acidity and exert direct toxic effects
on the gastric mucosa.
17. TREATMENT: Since the replacement dosage
of hydrocortisone does not replace the
mineralocorticoid component of the
adrenal hormones, mineralocorticoid
supplementation is usually needed.
This is accomplished by the administration of
0.05 to 0.1 mg fludrocortisone per day by
mouth. Patients should also be instructed to
maintain an ample intake of sodium (3 to 4 g/d).
18. TREATMENT: In female patients
with adrenal insufficiency,
androgen levels are also low. Thus,
some physicians believe that daily
replacement with 25 to 50 mg of
DHEA orally may improve quality of
life and skeletal density
19. Special Therapeutic Problems: During periods of
intercurrent illness, especially in the setting of
fever, the dose of hydrocortisone should be
doubled. With severe illness it should be
increased to 75 to 150 mg/d..
21. Pharmacological action
Hydrocortisone is the most important human glucocorticoid. It is essential for life and
regulates or supports a variety of important cardiovascular, metabolic, immunologic
and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or
immunosuppressive properties to treat inflammation due to corticosteroid-responsive
dermatoses. Glucocorticoids are a class of steroid hormones characterised by an
ability to bind with the cortisol receptor and trigger a variety of important
cardiovascular, metabolic, immunologic and homeostatic effects.
22. Mechanism of action:
1. Hydrocortisone binds to the cytosolic glucocorticoid receptor.
2. the receptor the newly formed receptor-ligand complex
translocate itself into the cell nucleus, where it binds to many
glucocorticoid response elements (GRE) in the promoter region
of the target genes.
3. The DNA bound receptor then interacts with basic transcription
factors, causing the increase in expression of specific target
genes. The anti-inflammatory actions of corticosteroids are
thought to involve lipocortins, phospholipase A2 inhibitory
proteins which, through inhibition arachidonic acid, control the
biosynthesis of prostaglandins and leukotriene.
23. Prednisone
Prednisone is a glucocorticoid. Glucocorticoids are
adrenocortical steroids, both naturally occurring
and synthetic, which are readily absorbed from
the gastrointestinal tract. The molecular formula
for prednisone is C21H26O5. Chemically, it is
17,21-dihydroxypregna-1, 4-diene-3,11, 20-trione
and has the following structural formula:
24. CLINICAL PHARMACOLOGY
Glucocorticoids, such as prednisone, cause profound
and varied metabolic effects. In addition, they modify
the body’s immune response to diverse stimuli.
25. fludrocortisone
Fludrocortisone (also called 9α-fluorocortisol or 9α-fluorohydrocortisone) is a synthetic
corticosteroid with moderate glucocorticoid potency and much greater mineralocorticoid
potency.
. Fludrocortisone has been used in the treatment of cerebral salt wasting.[1] It is used
primarily to replace the missing hormone aldosterone in various forms of adrenal
insufficiency such as Addison's disease and the classic salt wasting (21-hydroxylase
deficiency) form of congenital adrenal hyperplasia. Due to its effects on increasing Na+
levels, and therefore blood volume.
26. Fludrocortisone is available in 0.1 mg tablets. Typical daily doses for mineralocorticoid
replacement are between 0.05 mg - 0.2 mg. Renin plasma, sodium, and potassium is
checked through blood tests in order to verify that the correct dosage is reached.
27. Chemically, fludrocortisone is
identical to cortisol except for the
substitution of fluorine in place of
one hydrogen. Fluorine is a good
bioisostere for hydrogen because it
is similar in size. The major
difference is in its electronegativity.
28. Dexamethasone
Dexamethasone is a potent synthetic member of
the glucocorticoid class of steroid drugs that has
anti-inflammatory and immunosuppressant
effects. It is 25 times more potent than cortisol in
its glucocorticoid effect, while having minimal
mineralocorticoid effect.
29. A Classic Case of Addison's
Disease
A 23-year-old female presented to the Emergency Department complaining of
nausea and vomiting for one week. She also reported 8 months of progressively
worsening fatigue. The patient was previously very active as a ballet student, but
for the past 8 months she stopped participating in ballet because of lack of
energy. She was now living with her mother and sleeping or watching television
most of the day. One week prior to admission, she developed nausea and had
several episodes of vomiting which provoked her visit to the Emergency
Department. She also reported a poor appetite for months and had lost 5 to 10
pounds. In addition, she endorsed poor concentration, dry skin and "darkening
"of the skin in several areas. She repeatedly denied purposefully restricting food
intake or binging and purging behaviors. There was no abdominal pain, diarrhea,
fevers, dysuria or headache.
30. Past medical history was significant for hypothyroidism diagnosed several
months prior. The patient was prescribed levothyroxine and subsequently
Amour Thyroid but had stopped taking them a month prior because "they
made her feel ill." Her only current medication was progesterone to regulate
her menstrual cycle. There was no family history of autoimmune or endocrine
disorders. Initial examination was remarkable for a blood pressure of 93/50
mmHg and heart rate of 104 beats/min. There were significant orthostatic
changes. The patient was a thin, nontoxic appearing Caucasian female in no
distress. She was alert, oriented and cooperative. Her examination was
otherwise unremarkable except for mild skin hyperpigmentation over the
knuckles, elbows and knees. The thyroid, abdominal, and neurological
examinations were normal.
31. Laboratory testing revealed a normal complete blood count. A basic
metabolic panel showed a sodium of 111 mmol/L (normal range 135-145),
potassium 4.5 mmol/L, chloride 78 mmol/L, bicarbonate 23 mmol/L, glucose
85 mg/dL and creatinine 0.7 mg/dL. Further testing showed serum osmolality
at 234 mosm/kg (normal range 275-295), urine osmolality of 162 mosm/kg,
and urine sodium less than 20 mmol/L consistent with severe hypovolemic
hyponatremia.
32. A random cortisol level was less than 0.2 μg/dL and a subsequent cortisol
level following the administration of 250 mcg of Cosyntropin (Cosynstropin
stimulation testing) remained less than 0.2 μg/dL.
The plasma adrenocorticotropic hormone (ACTH) level was elevated at 882
pg/dL (normal range 5-27) and adrenal antibody testing (antibodies against
the enzyme 21-hydroxylase) was positive with a 1:40 titer (normal<1:10).
Further endocrine testing showed an elevated thyroid-stimulating hormone
level of 29.2 μIU/mL (normal 0.3-4.7), and a thyroid peroxidase
autoantibody level greater than 600 IU/ml (normal<20). Estradiol, folliclestimulating hormone, luteinizing hormone, and prolactin levels were all
within normal limits.