The document discusses the hypothalamic-pituitary-adrenal (HPA) axis and adrenal gland function. It describes:
- The zones of the adrenal cortex that produce glucocorticoids, mineralocorticoids, and androgens under control of the HPA axis.
- Diseases like Cushing's syndrome caused by excess cortisol and primary hyperaldosteronism caused by excess aldosterone.
- Investigations used to diagnose HPA axis and adrenal disorders and their treatment options which may include drugs, surgery, or radiotherapy depending on the underlying cause.
Art Therapy For Mind Healing
Art therapy is a form of psychotherapy that promotes creative self-expression on a symbolic level,
through the creative use of art media that leads to the safe expression of emotions and internal
conflicts.
Art Therapy For Mind Healing
Art therapy is a form of psychotherapy that promotes creative self-expression on a symbolic level,
through the creative use of art media that leads to the safe expression of emotions and internal
conflicts.
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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!
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
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.
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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
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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 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
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.
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.
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
- 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
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
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.
Couples presenting to the infertility clinic- Do they really have infertility...
Endocrinilogy.pptx
1.
2. HYPOTHALAMO–PITUITARY–
ADRENAL AXIS
• The human adrenals weight 8–10 g
• Comprise an outer cortex and inner medulla.
• The cortex has three zones:
Zona glomerulosa, which secretes aldosterone under the control of the renin–
angiotensin system
Zona fasciculate and Zona reticularis, which produce glucocorticoids, cortisol, and sex
steroids and androgens under feedback control of the hypothalamic–pituitary–adrenal
(HPA) axis.
• The inner medulla synthesizes, stores and secretes catecholamines
3.
4. The adrenal cortex
• The steroids produced by the adrenal cortex are grouped into three
classes, based on their predominant physiological effects:
Glucocorticoids,
Mineralocorticoids
Androgens.
5.
6. Glucocorticoids
• These are named after
their effects on
carbohydrate
metabolism.
• They act on intracellular
corticosteroid receptors
and combine with
coactivating proteins to
bind the ‘glucocorticoid
response element’ (GRE)
in specific regions of DNA
to cause gene
transcription.
7. Mineralocorticoids
• The predominant effect of mineralocorticoids is on the extracellular
balance of sodium and potassium in the distal tubule of the kidney.
• Aldosterone, produced solely in the zona glomerulosa, is the
predominant mineralocorticoid in humans (about 50%);
corticosterone makes a small contribution to overall
mineralocorticoid activity.
• Mineralocorticoids act on type 1 corticosteroid receptors, while
glucocorticoids act on type 2 receptors, both having a very similar
structure.
8. Androgen
• Although secreted in considerable quantities, most androgens have
relatively weak intrinsic androgenic activity until metabolized
peripherally to testosterone or dihydrotestosterone.
• Dihydrotestosterone is metabolized from testosterone by 5α-
reductase and is a potent androgen receptor agonist.
• The androgen receptor has been well characterized and mutations
within this gene may cause androgen insensitivity syndromes.
9. Control of the hypothalamic–pituitary–adrenal
axis.
Pituitary adrenocorticotrophic hormone (ACTH) is
secreted in response to hypothalamic
corticotrophin-releasing hormone (CRH), triggered
by circadian rhythm, stress and other factors, and
stimulates secretion of cortisol from the adrenal.
Cortisol has multiple actions in peripheral tissues
and exerts negative feedback on the pituitary and
hypothalamus.
10. • Glucocorticoid production by the adrenal is under hypothalamic pituitary
control.
• Corticotrophin-releasing hormone (CRH) is secreted in the hypothalamus in
response to circadian rhythm, stress and other stimuli.
• CRH travels down the portal system to stimulate adrenocorticotrophin
(ACTH) release from the anterior pituitary.
• Hypothalamic vasopressin (antidiuretic hormone, ADH) also stimulates
ACTH secretion and acts synergistically.
• ACTH is derived from the prohormone pro-opiomelanocortin (POMC),
which undergoes processing within the pituitary to produce ACTH and a
number of other peptides, including beta-lipotrophin and beta-endorphin.
• Many of these peptides, including ACTH, contain melanocyte-stimulating
hormone (MSH)-like sequences, which cause pigmentation when levels of
ACTH are markedly raised as in Addison’s disease.
11. • Circulating ACTH stimulates cortisol production in the adrenal.
• The secreted cortisol (or any other synthetic corticosteroid
administered to the patient) causes negative feedback on the
hypothalamus and pituitary to inhibit further CRH/ACTH release.
• The set-point of this system varies through the day according to the
circadianrhythm, and is usually overridden by severe stress.
• Unlike cortisol, mineralocorticoids and sex steroids do not cause
negative feedback on the CRH/ACTH axis.
• Following adrenalectomy or other adrenal damage (e.g. Addison’s
disease), cortisol secretion is absent or reduced; ACTH levels will
therefore rise.
• Mineralocorticoid secretion is mainly controlled by the renin–
angiotensin system
12. Investigation of glucocorticoid abnormalities
• Basal levels
Cortisol has a circadian rhythm and increases in response to stress.
When taking a blood sample, remember:
Sampling time should be recorded.
Basal cortisol levels should be taken between 8am and 10am, near
the peak of the circadian variation, if investigating for deficiency
Stress should be minimized
Appropriate reference ranges (for time and assay method) should be
used.
13. • ACTH Level
The measurement of ACTH levels are only really required once
an abnormality in cortisol levels has been identified.
A plasma sample is required and has to be transported on ice to the lab
immediately.
Suppression tests are used if excess cortisol is suspected, and
stimulation tests are used if cortisol deficiency is suspected.
14. • Suppression tests
Administration of a synthetic glucocorticoid (dexamethasone) to a
normal subject produces suppression of CRH and ACTH levels, and
thus of endogenous cortisol secretion (dexamethasone is not measured
by most cortisol assays).
Three forms of the test, used in the diagnosis and differential diagnosis
of Cushing’s syndrome, are available
15. • ACTH stimulation tests
Synthetic ACTH (tetracosactide, which consists of the first 24 amino
acids of human ACTH) is given to stimulate adrenal cortisol production
16. Cushing’s syndrome
• Cushing’s syndrome describes the
clinical state of increased free
circulating glucocorticoid.
• It is most often iatrogenic following
the therapeutic administration of
synthetic steroids.
• The next most common cause is
excess endogenous secretion of
ACTH from a pituitary adenoma,
when it is called Cushing’s disease
17. • Increased circulating ACTH from the pituitary (65% of cases), known as
Cushing’s disease, or from an ‘ectopic’, non-pituitary, ACTH-producing
tumour elsewhere in the body (10%) with consequent glucocorticoid
excess (‘ACTH-dependent’ Cushing’s).
• A primary excess of endogenous cortisol secretion (25%) by an adrenal
tumour or, more rarely, by bilateral primary pigmented nodular hyperplasia
(PPNH) with suppression of ACTH (‘non-ACTH- dependent’ Cushing’s).
• Rare cases are due to aberrant expression of receptors for other hormones
(e.g. glucose-dependent insulinotrophic peptide (GIP), LH or
catecholamines) in adrenal cortical cells.
• Germline changes in protein kinase A (PKA) can also result in adrenal
hyperplasia and adenomas.
18.
19. • Pigmentation occurs only with ACTH-dependent causes (most
frequently in ectopic ACTH syndrome).
• A cushingoid appearance can also be caused by excess alcohol
consumption (pseudo-Cushing’s syndrome); the pathophysiology is
poorly understood.
• Impaired glucose tolerance or frank diabetes is common, especially
with ectopic ACTH.
• Hypokalaemia due to the mineralocorticoid activity of cortisol is
common with ectopic ACTH secretion.
• Hypertension is common in all causes of Cushing’s syndrome.
20. Investigations
• There are two phases to investigation.
Confirmation
48-h low-dose dexamethasone test
24-hour urinary free cortisol measurements.
Circadian rhythm
Other tests: insulin stress test, desmopressin stimulation test and
corticotrophin releasing hormone (CRH)
Differential diagnosis of the cause
21.
22. Exclude Differencial
• Adrenal CT or MRI scan. Adrenal adenomas and carcinomas causing
Cushing’s syndrome are relatively large and always detectable by CT.
Carcinomas are distinguished by their large size and irregular outline, and
signs of infiltration or metastases. Bilateral adrenal hyperplasia may be
seen in ACTH-dependent causes or in ACTH-independent nodular
hyperplasia.
• If plasma ACTH levels are normal or high on two or more occasions, this is
a reliable indicator of ACTH-dependent disease and pituitary imaging
should be planned in the first instance and biochemical tests to distinguish
between pituitary and ectopic sources of ACTH.
• Pituitary MRI. A pituitary adenoma may be seen but the adenoma is often
small and not visible in a significant proportion of cases.
23. • High-dose dexamethasone suppression test . Failure of significant
plasma cortisol suppression suggests an ectopic source of ACTH (or an
adrenal tumour).
• CRH test. An exaggerated ACTH and cortisol response to exogenous
CRH suggests pituitary-dependent Cushing’s disease, as ectopic
sources rarely respond.
• Chest X-ray. A carcinoma of the bronchus or a bronchial carcinoid is
sought. Carcinoid lesions may be very small; if ectopic ACTH is
suspected, whole-lung, mediastinal and abdominal CT scanning
should be performed.
24. Management
• Untreated Cushing’s syndrome has a very poor prognosis, with death
from venous thromboembolism, hypertension, myocardial infarction,
infection and heart failure.
• Whatever the underlying cause, cortisol hypersecretion should be
controlled prior to surgery or radiotherapy.
• Considerable morbidity and mortality are otherwise associated with
operating on unprepared patients, especially when abdominal
surgery is required.
25. Drugs
The usual drug is metyrapone, an 11β-hydroxylase
blocker,
which is given in doses of 750 mg to 4 g daily in 3–4 divided doses.
Ketoconazole (200 mg three times daily) is also used and is synergistic
with metyrapone. Plasma cortisol should be monitored, aiming
to reduce the mean level during the day to 150–300 nmol/L,
equivalent to normal production rates. Aminoglutethimide, trilostane
(which reversibly inhibits 3-hydroxysteroid
dehydrogenase/
5–5,4 isomers) and etomidate infusion (in severe cases) are
occasionally used.
26. Choice of further treatment depends upon the cause.
• Trans-sphenoidal removal of the tumour is the treatment of choice.
Selective adenomectomy nearly always leaves the patient ACTH-
deficient immediately postoperatively, and this is a good prognostic
sign. Overall, pituitary surgery results in remission in 75–80% of cases,
but results vary considerably and an experienced surgeon is essential.
• External pituitary irradiation alone is slow-acting, only effective in
50–60% even after prolonged follow-up, and mainly used after failed
pituitary surgery. Children respond much better to radiotherapy, 80%
being cured. Stereotactic radiotherapy can be useful in selected cases.
27. • Medical therapy to reduce ACTH (e.g. bromocriptine, cabergoline and
cyproheptadine) is rarely effective. The somatostatin analogue
pasireotide may provide medical control of Cushing’s in some
patients, but is associated with hyperglycaemia as a common side-
effect. Aggressive corticotroph adenomas may respond to
temozolomide chemotherapy.
• Bilateral adrenalectomy is an effective last resort if other measures
fail to control the disease (see ‘Nelson’s syndrome’ later). This can be
performed laparoscopically.
28.
29. Addison’s disease
• There is destruction of the entire adrenal cortex.
• Glucocorticoid, mineralocorticoid and sex steroid production are
therefore all reduced.
• This differs from hypothalamic–pituitary disease, in which
mineralocorticoid secretion remains largely intact, being
predominantly stimulated by angiotensin II. Adrenal sex steroid
production is also largely independent of pituitary action.
• In Addison’s disease, reduced cortisol levels lead, through feedback,
to increased CRH and ACTH production, the latter being directly
responsible for the hyperpigmentation.
30.
31. • These symptoms may be the prelude to an addisonian crisis with
severe hypotension and dehydration precipitated by intercurrent
illness, accident or operation.
• Pigmentation (dull, slaty, grey–brown) is the predominant sign in over
90% of cases.
• Postural systolic hypotension, due to hypovolaemia and sodium loss,
is present in 80–90% of cases, even if supine blood pressure is
normal.
• Mineralocorticoid deficiency is the cause of the hypotension.
32.
33. Investigation
• Single cortisol measurements are of little value, although a random
cortisol below 100 nmol/L during the day is highly suggestive, and a
random cortisol higher than 550 nmol/L makes the diagnosis unlikely.
• The short ACTH stimulation test (short synacthen test) should be
performed. Note that an absent or impaired cortisol response
confirms the presence of hypoadrenalism but does not differentiate
Addison’s disease from ACTH deficiency or iatrogenic suppression by
steroid medication. The long ACTH test is no longer used because of
the availability of accurate ACTH assays.
34. • A 09:00-hours plasma ACTH level is measured, a high level (>80 ng/L) with
low cortisol confirming primary adrenal insufficiency.
• Adrenal antibodies are present in approximately 90% of cases of
autoimmune adrenalitis.
• Chest and abdominal X-rays or cross-sectional imaging of the abdomen (CT
or MRI) may show evidence of tuberculosis and/or calcified adrenals.
• Plasma renin activity is high due to low serum aldosterone.
• Serum creatinine and electrolytes classically show hyponatraemia,
hyperkalaemia and a high urea, but they can be normal.
• Blood glucose may be low, with hypoglycaemia.
• Hypercalcaemia and anaemia (after rehydration) are sometimes seen.
37. Adequacy of glucocorticoid dose is judged by:
• clinical wellbeing and restoration of normal, but not
excessive, weight; ideally aiming for a low dose, for
example, total dose of hydrocortisone between 15 and 25
mg split in two or three divided doses throughout the day.
• Measuring cortisol levels during the day while on
replacement hydrocortisone (cortisol levels cannot be
used for synthetic steroids) is not recommended as an
assessment of dose adequacy.
Adequacy of fludrocortisone replacement is assessed by:
• Restoration of serum electrolytes to normal
• No evidence of hypertension or postural hypotension (it
should not fall >10 mmHg systolic after 2 minutes’
standing)
• Suppression of plasma renin activity to high normal.
Replacement therapy
38. Patient advice
All patients requiring replacement steroids should:
• know how to increase steroid replacement by doubling the dose for
intercurrent illness
• carry a ‘steroid card’
• wear a MedicAlert bracelet (or similar), which gives details of their
condition so that emergency replacement therapy can be given if
found unconscious
• keep an (up-to-date) ampoule of hydrocortisone at home in case oral
therapy is impossible, for administration by self, family, ambulance or
doctor.
39. Secondary hypoadrenalism
• This may arise from:
hypothalamic–pituitary disease (inadequate ACTH production) or
long-term steroid therapy leading to ACTH suppression.
• Most people with hypothalamic–pituitary disease have panhypopituitarism
and need T4 replacement, as well as cortisol; in this case, hydrocortisone
must be started before T4.
• Long-term corticosteroid medication for non-endocrine disease is the most
common cause of secondary hypoadrenalism.
• The hypothalamic–pituitary axis and the adrenal may both be suppressed
and the patient may have vague symptoms of feeling unwell. ACTH levels
are low in secondary hypoadrenalism.
• Weaning off steroids is often a long and difficult process.
40.
41. Primary hyperaldosteronism
• Increased mineralocorticoid secretion from the adrenal cortex, termed
primary hyperaldosteronism, accounts for 5–10% of all hypertension.
• Other endocrine causes of hypertension should also be considered if there
is clinical suspicion.
• It is impracticable to screen all hypertensive patients for secondary
endocrine causes. The highest chances of detecting such causes are in
patients:
• under 35 years, especially those without a family history of hypertension
• with accelerated (malignant) hypertension
• with hypokalaemia
• resistant to conventional antihypertensive therapy (e.g. more than three drugs) or
• with unusual symptoms (e.g. sweating attacks or weakness).
42.
43. • Primary hyperaldosteronism
is characterized by excess aldosterone production leading to sodium
retention, potassium loss and the combination of hypokalaemia and
hypertension.
• secondary hyperaldosteronism,
which arises when there is excess renin (and hence angiotensin II)
stimulation of the zona glomerulosa. Common causes of secondary
hyperaldosteronism are accelerated hypertension and renal artery
stenosis, when the patient will also be hypertensive.
Causes associated with normotension include congestive cardiac
failure and cirrhosis, where excess aldosterone production
contributes to sodium retention.
44. Adrenal adenomas (Conn’s syndrome)
Originally accounted for 60% of cases of primary hyperaldosteronism
but represented a rare cause of hypertension.
The use of the aldosterone: renin ratio in the routine investigation of
hypertension now suggests that hyperaldosteronism due to bilateral
adrenal hyperplasia(idiopathic hyperaldosteronism) is much more
common than the classical Conn’s adenoma.
45. Clinical features
• The usual presentation is simply
Hypertension
hypokalaemia(<3.5 mmol/L) is frequently not present.
The few symptoms are non-specific;
• rarely, muscle weakness
• nocturia
• tetany
• Hypertension may be severe and associated with renal, cardiac and retinal
damage.
• Adenomas, often very small, are more common in young females, while bilateral
hyperplasia rarely occurs before the age of 40 years and is more common in
males.
46. investigation
• Plasma aldosterone : renin ratio (ARR) (high) is now most frequently used
as a screening test for the condition, but raised ARR alone does not confirm
the diagnosis.
• Suppressed plasma renin activity 0.9% saline infusion (2 L over 4 h) or
fludrocortisone administration. Between 30% and 50% of people with a
raised ARR on screening will suppress normally, excluding the diagnosis.
• Elevated plasma aldesteron
• Hypokalaemia is often present but a normal potassium does not exclude
the diagnosis.
• Urinary potassium loss greater than 30 mmol daily.
47. Treatment
• An adenoma can be removed surgically, usually laparoscopically;
blood pressure falls in 70% of patients.
• Those with hyperplasia should be treated with the aldosterone
antagonist, spironolactone (100–400 mg daily); frequent side-effects
include nausea, rashes and gynaecomastia.
• The pure aldosterone receptor antagonist, eplerenone, is a useful
• Amiloride and calcium-channel blockers are moderately effective in
controlling hypertension but do not correct the hyperaldosteronism.
48. The adrenal medulla
• The adrenal medulla is the innermost part of the adrenal gland,
consisting of cells that secrete the major catecholamines,
noradrenaline (norepinephrine) and adrenaline (epinephrine), which
produce the sympathetic nervous response.
• The catecholamines are interconverted in the adrenal medulla, and
an increase in levels of their metabolites in the urine is a marker of
abnormal hypersecretion.
49.
50. Phaeochromocytoma and paraganglioma
• These are very rare tumours of the sympathetic nervous system (less than
1 in 1000 cases of hypertension)
• secrete catecholamines, noradrenaline (norepinephrine), adrenaline
(epinephrine) and their metabolites.
90% arise in the adrenal medulla (phaeochromocytomas)
10% occur elsewhere in the sympathetic chain (paragangliomas).
• Some are associated with MEN 2 , von Hippel–Lindau’s (VHL) syndromeand
neurofibromatosis.
• Most tumours release both noradrenaline (norepinephrine) and adrenaline
(epinephrine), but large tumours and extra-adrenal tumours produce almost
entirely noradrenaline.
51. • Paragangliomas typically occur in the head and neck but are also
found in the thorax, pelvis and bladder.
• They are more closely associated with other genetic associations than
phaeochromocytoma.
• The association of paraganglioma, bilateral adrenal
phaeochromocytomas, positive family history or young age at
presentation is seen in multiple endocrine neoplasms.
• Mutations in the succinate dehydrogenase (SDHD) gene have been
shown to be strongly associated with the development of
paraganglioma.
52.
53. Investigations
• Measurement of urinary catecholamines and metabolites. (most sensitive
and specific)
• 24 hour urine collection of catecholamines metabolites / VMA
• Resting plasma catecholamine (increased)
• CT abdomen- localized tumor
• Plasma chromogranin A (a storage vesicle protein) is raised.
• Clonidine suppression test may be appropriate but should only be
performed in specialist centres
• Genetic testing for MEN2, VHL, SDHB and SDHD mutations should be
performed in all people with confirmed phaeochromocytoma or
paraganglioma
54.
55. Management
• Tumours should be removed if possible; 5-year survival is about 95% for
non-malignant tumours.
• Medical preoperative and perioperative treatment is vital and includes
complete alpha-and beta-blockade with phenoxybenzamine (20–80 mg
daily in divided doses), then propranolol (120–240 mg daily)
• intravenous hydration to re-expand the contracted plasma volume.
• When operation is not possible, combined alpha-and beta-blockade can be
used long term.
• Radionucleotide treatment with MIBG has been employed but has had
limited success in malignant phaeochromocytoma.
56.
57. Questions
1. Regarding Cushing syndrome
a) Pigmentation supports adrenal tumour as a cause
b) Presence of hypo K+ favours ectopic ACTH tumour
c) Lesion is usually seen on pituitary imaging
d) May have increased predisposition for fractures
e) May have proximal muscle weakness
FTFTT
58. ACTH INDEPENDENT ACTH DEPENDENT
Exogenous glucocorticoid
Adrenal adenoma
Adrenal hyperplasia
Adrenal carcinoma
Pituitary adenoma
Ectopic ACTH secretion
Lung cancer
Carcinoid tumor
Other cancer
59. 2. Features of Conn's disease;
a) Hypertension
b) Hyponatraemia
c) Hyperkalaemia
d) Facial flushing
e) Abdominal mass can be seen
TFFTF
60.
61. 3. In Conn's syndrome
a) Peripheral oedema is usually present
b) Proximal myopathy is due to hypokalemia
c) Polyuria and polydipsia is characteristic
d) DM is often present
e) High Renin hypertension
FTTFF
62.
63.
64.
65. 4. Addison's disease
a) May present with tetani due to hypo Ca2+
b) Pigmentation of palmer increases
c) May be associated with anemia
d) May be a cause of sudden death during anti TB therapy
e) May present with prominent U waves in ECG
FTTTF
66. ECG changes in Addison's disease are
primarily due to hyperkalemia
caused by aldosterone hormone
deficiency.
• Peak T waves
• Widened QRS complex
67.
68. 5. Obese female with hirsutism, hypertension (150/100), amenorrhea
presents to the clinic. Which of the following investigations are needed to
come to a definitive diagnosis?
a) Serum T3/T4 levels
b) Urinary VMA
c) Serum cortisol
d) Dexamethasone suppression test
e) CT scan of the abdomen
TFFTT
69. 6. 28y old male with a BMI of 17 presented with tiredness & lethargy
for 8 months’ duration. Examination revealed a vitiligo, and BP
140/60mmHg, PR- 120/sec. Ix; WBC-5500, Hb- 10.5g/dl, 1MCV - 95,
serum Na-140, serum K+- 4.2, blood urea- 20, blood glucose -
150mg/dL. Most probable diagnosis is
a) Hypopituitarism
b) Thyrotoxicosis.
c) Type 1 DM
d) Pernicious anaemia.
e) Addison disease.
70. • Types
• Autoimmune polyendocrine syndrome type 1, an autosomal recessive
syndrome due to mutation of the AIRE gene resulting in
hypoparathyroidism, adrenal insufficiency, hypogonadism, vitiligo,
candidiasis and others.
• Autoimmune polyendocrine syndrome type 2, an autosomal dominant
syndrome due to multifactorial gene involvement resulting in adrenal
insufficiency plus hypothyroidism and/or type 1 diabetes.
• Immunodysregulation polyendocrinopathy enteropathy X-linked syndrome
(IPEX syndrome) is X-linked recessive due to mutation of the FOXP3 gene
on the X chromosome. Most develop diabetes and diarrhea and many die
due to autoimmune activity against many organs. Boys are affected, while
girls are carriers and might suffer mild disease
71. 7. 32 years old young female presented with dizziness & abdominal
pain. Her BP is 90/70mmHg with significant postural drop. Her Ix
results are as follows. S. Na+ -110 mmol/l (135-145 mmol/l), S. K+ -
5.1mmol/l (3.5-5mmol/l), RBS - 68mg/dl. What is the most important Ix
to arrive at a diagnosis?
a) 24hr urine collection for cortisol
b) 24hr urine collection for VMA
c) Dexamethasone suppression test
d) Short Synacthen test
e) USS abdomen