The document summarizes adrenal hormones and their functions. It discusses that the adrenal glands are composed of the adrenal cortex and medulla. The cortex produces steroid hormones like cortisol, aldosterone and androgens. The medulla produces catecholamines including epinephrine and norepinephrine. It describes the synthesis, regulation and effects of these hormones. It also discusses adrenal disorders like Cushing's syndrome, Conn's syndrome and adrenal insufficiency.
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
Posterior Pituitary or Neurohypophysis composed mainly of glial-like cells called pituicytes.
The pituicytes do not secrete hormones.
They act simply as a supporting structure for large numbers
of terminal nerve fibers and terminal nerve endings from nerve tracts.
That originate in the supraoptic and paraventricular
nuclei of the hypothalamus.
Thyroid hormone (The Guyton and Hall physiology)Maryam Fida
THYROID HORMONE
Location:
The thyroid gland located below the larynx on each side of and anterior to the trachea.
Largest Endocrine Hormone
Secretion:
secretes:
1. thyroxine (T4)
2. triiodothyronine (T3)
3. Also secretes calcitonin (an important hormone for calcium metabolism)
Cell: Thyrotopes
secretion is controlled by thyroid-stimulating hormone (TSH) from the anterior pituitary gland.
93% T4 & 7% T3
T4→T3 in tissues
Qualitatively same
Differ in Rapidity & Intensity of action.
T3 is 4 times more potent than T4, but decrease conc. In blood & decrease half life.
T3 and T4 combine mainly with thyroxine-binding globulin.
More than 90% of Thyroid hormone that binds with cellular receptors is T3.
T4
No effect for 2-3 days after injection
Long Latent Period.
Activity peaks in 10-12 days & ↓↓ with a half life of 15 days.
In some cases it takes 6 weeks-2 months.
T3
4 times rapid
Latent Period 6-12 hours
Peak in 2-3 days
Composed of large numbers of closed follicles filled with colloid and lined with cuboidal epithelial cells that secrete into the interior of the follicles
The major component of colloid is the large glycoprotein Thyroglobulin contains the thyroid hormones within its molecule.
50mg/year, 1mg/week
Ingested iodine in the form of iodides
Iodides ingested orally are absorbed from GIT
⅕ removed from the blood by thyroid cells for synthesis of hormones; rest excreted through kidneys.
Basal membrane of thyroid cells has an active pump to push iodides to interior (Iodine Pump).
Normally 30% more conc. Inside
Max. active 250% more conc. Inside
The rate of Iodine trapping is influenced by conc. of TSH
TSH stimulates and hypophysectomy greatly diminishes the activity of the iodide pump in thyroid cells.
Biochemistry Of Hormones
Contains All Important topics with best key points....
Made By Sanjay kumar (Student Of PharmD Faculty of Pharmacy Hamdard University)
Posterior Pituitary or Neurohypophysis composed mainly of glial-like cells called pituicytes.
The pituicytes do not secrete hormones.
They act simply as a supporting structure for large numbers
of terminal nerve fibers and terminal nerve endings from nerve tracts.
That originate in the supraoptic and paraventricular
nuclei of the hypothalamus.
Thyroid hormone (The Guyton and Hall physiology)Maryam Fida
THYROID HORMONE
Location:
The thyroid gland located below the larynx on each side of and anterior to the trachea.
Largest Endocrine Hormone
Secretion:
secretes:
1. thyroxine (T4)
2. triiodothyronine (T3)
3. Also secretes calcitonin (an important hormone for calcium metabolism)
Cell: Thyrotopes
secretion is controlled by thyroid-stimulating hormone (TSH) from the anterior pituitary gland.
93% T4 & 7% T3
T4→T3 in tissues
Qualitatively same
Differ in Rapidity & Intensity of action.
T3 is 4 times more potent than T4, but decrease conc. In blood & decrease half life.
T3 and T4 combine mainly with thyroxine-binding globulin.
More than 90% of Thyroid hormone that binds with cellular receptors is T3.
T4
No effect for 2-3 days after injection
Long Latent Period.
Activity peaks in 10-12 days & ↓↓ with a half life of 15 days.
In some cases it takes 6 weeks-2 months.
T3
4 times rapid
Latent Period 6-12 hours
Peak in 2-3 days
Composed of large numbers of closed follicles filled with colloid and lined with cuboidal epithelial cells that secrete into the interior of the follicles
The major component of colloid is the large glycoprotein Thyroglobulin contains the thyroid hormones within its molecule.
50mg/year, 1mg/week
Ingested iodine in the form of iodides
Iodides ingested orally are absorbed from GIT
⅕ removed from the blood by thyroid cells for synthesis of hormones; rest excreted through kidneys.
Basal membrane of thyroid cells has an active pump to push iodides to interior (Iodine Pump).
Normally 30% more conc. Inside
Max. active 250% more conc. Inside
The rate of Iodine trapping is influenced by conc. of TSH
TSH stimulates and hypophysectomy greatly diminishes the activity of the iodide pump in thyroid cells.
Biochemistry Of Hormones
Contains All Important topics with best key points....
Made By Sanjay kumar (Student Of PharmD Faculty of Pharmacy Hamdard University)
Describe the structures, relations, and functions of the adrenal gland.
describe the histological structures and clinical importance of the adrenal gland
Coagulation cascade PowerPoint templates designed by skilled, experienced and professional graphic designers that are intended to solve the big issue of time consumption. These are fully editable slides and organized in a way to simplify the most complex topics and present it in an attractive manner. You can easily incorporate charts, diagrams and animations along with the content to these layouts in order to explore new technologies and trends of businesses in a unique way. All editable slides are digitally created to pinpoint and clarify the message, and summarize information regarding topic.
A small gland that makes steroid hormones, adrenaline, and noradrenalineRuvarasheMutadza1
A small gland that makes steroid hormones, adrenaline, and noradrenaline. These hormones help control heart rate, blood pressure, and other important body functions. There are two adrenal glands, one on top of each kidney. Also called suprarenal gland.
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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.
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
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
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.
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
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. Adrenal glands
• Small, triangular glands loosely
attached to the kidneys
• Divided into two morphologically distinct
regions
- adrenal cortex (outer)
- adrenal medulla (inner)
3.
4. Steroid Hormones
• Steroid hormones are produced by the gonads
and adrenal cortex.
• Steroid hormones are made from cholesterol
in the smooth endoplasmic reticulum and
mitochondria of endocrine cells.
5. • Steroid hormones cannot be stored in vesicles
in the endocrine cells that produce them. As
soon as steroid hormones are produced, they
diffuse out of the endocrine cell and enter the
bloodstream.
• Steroid hormones are lipid soluble and their
receptors are located in the cytoplasm target
cell.
6. Steroid hormone transport
• Lipid soluble hormones require transport
proteins
• albumin and transthyretin (prealbumin)
• specific transport molecules (steroid-
binding globulin)
• only unbound form can enter the cell
•Steroid and thyroid hormones are 99%
7. Adrenal Medulla
• an extension of the sympathetic
nervous system
• acts as a peripheral amplifier
• activated by same stimuli as the
sympathetic nervous system
(examples – exercise, cold, stress,
hemorrhage, etc.)
8.
9. Hormones of the Adrenal Medulla
•Hormones synthesized in adrenal
medulla are catacolamines. They are:
•dopamine
•adrenaline/ noradrenaline
epinephrine/norepinephrine
•80% of released catecholamine is
epinephrine
•Hormones are secreted and stored in
the adrenal medulla and released in
response to appropriate stimuli
10. Tyrosine
(+)O2 (1) Tyrosine hydroxylase
Dopa
PLP (2) Dopa decarboxylase
CO2
Dopamine
Cu++
(3) Dopamine hydroxylase
Vit C
Norepinephrine
SAM (4) N-METHYL TRANSFERASE
SAH
Epinephrine
SAM (5) Catechol-O-methyl transferase
SAH
Metanephrine
(6) Mono amino oxidase
VMA (Vanillyl mandalic acid)
Synthesis of
Catecholamines
11. Mechanism of Action
• receptor mediated – adrenergic receptors
• peripheral effects are dependent upon the
type and ratio of receptors in target tissues
Receptor α β
Norepinephrin
e
+++++ ++
Epinephrine ++++ ++++
12.
13. Differences between Epinephrine and
Norepinephrine
Epinephrine >> norepinephrine – in terms of cardiac
stimulation leading to greater cardiac output (β
stimulation).
• Epinephrine < norepinephrine – in terms of
constriction of blood vessels – leading to increased
peripheral resistance – increased arterial pressure.
• Epinephrine >> norepinephrine –in terms of
increasing metabolism Epi = 5-10 x Norepinephrine
14. Effects of Epinephrine
Metabolism:
- glycogenolysis in liver and skeletal muscle
- mobilization of free fatty acids
- increased metabolic rate
• can lead to hyperglycemia
• O2 consumption increases
15.
16.
17. Pheochromocytoma
• a catecholamine-secreting tumour of
chromaffin cells of the adrenal medulla
• paraganglioma – a catecholamine
secreting tumour of the sympathetic
paraganglia
adrenal pheochromocytoma (90%)
extra-adrenal pheochromocytoma
19. Diagnosis and Treatment
• diagnosed by high plasma catecholamines
and increased metabolites in urine
• no test for adrenal or extra-adrenal
• treatment is surgical resection
20. Adrenal Cortex
•Hormones produced by the adrenal cortex
are referred to as corticosteroids.
•These comprise mineralocorticoids,
glucocorticoids and androgens.
•The cortex is divided into three regions:
•zona glomerulosa
• zona fasciculata
• zona reticularis
21. Zona Glomerulosa
• Outermost zone – just below the adrenal
capsule
• Secretes mineralocorticoids.
• Mineralocorticoids are it is termed as they
are involved in regulation of electrolytes in
ECF.
• The naturally synthesized
mineralocorticoid of most importance is
aldosterone.
22. Zona Fasciculata
• Middle zone – between the glomerulosa
and reticularis
• Primary secretion is glucocorticoids.
• Glucocorticoids, as the term implies, are
involved the increasing of blood glucose
levels. However they have additional
effects in protein and fat metabolism.
• The naturally synthesized glucocorticoid of
most importance is cortisol.
23. Zona Reticularis
• Innermost zone – between the fasciculata
and medulla
• Primary secretion is androgens.
• Androgenic hormones exhibit
approximately the same effects as the
male sex hormone – testosterone.
24.
25.
26. Hormones of the Adrenal Cortex
• all adrenal cortex hormones are steroids
• not stored, synthesized as needed
O
HO
O
C = O
HO
OH
CH2OH
testosterone cortisol
27. Aldosterone
• a steroid hormone
•essential for life (acute)
• responsible for regulating Na+
reabsorption in the distal tubule and the
cortical collecting duct
• target cells are called “principal (P) cell”
- stimulates synthesis of more
Na/K-ATPase pumps
28.
29. Effects of Aldosterone
• Renal and circulatory effects … covered
(ECF volume regulation, sodium and
potassium ECF concentrations)
• Promotes reabsorption of sodium from
the ducts of sweat and salivary glands
during excessive sweat/saliva loss.
• Enhances absorption of sodium from the
intestine especial. colon. – absence leads
to diarrhea.
30. Regulation of Aldosterone Release
• direct stimulators of release
• indirect stimulators of release
- increased extracellular K+
- decreased osmolarity
- ACTH
- decreased blood pressure
- decreased macula densa blood flow
31. Glucocorticoids - Cortisol
• a steroid hormone
• essential for life (long term)2hr
• the net effects of cortisol are catabolic
- prevents against hypoglycemia
- plasma bound to corticosteroid
binding globulin (CBG or transcortin)
32.
33.
34. Physiological Actions of Cortisol
• promotes gluconeogenesis
• promotes breakdown of skeletal muscle
protein
• enhances fat breakdown (lipolysis)
• suppresses immune system
• breakdown of bone matrix (high doses)
35. Anti-inflammatory Effects of Cortisol
• reduces phagocytic action of white blood
cells
• reduces fever
• suppresses allergic reactions
• wide spread therapeutic use
36. Effect on Blood Cells and Immunity
• Decrease production of eoisinophils and
lymphocytes
• Suppresses lymphoid tissue systemically therefore
decrease in T cell and antibody production there
by decreasing immunity
• Decrease immunity could be fatal in diseases such
as tuberculosis
• Decrease immunity effect of cortisol is useful
during transplant operations in reducing organ
rejection.
37. Regulation of Cortisol Release
• cortisol release is regulated by ACTH
• release follows a daily pattern - circadian
• negative feedback by cortisol inhibits the
secretion of ACTH and CRH
38.
39. Regulation of Cortisol Release
Enhanced release can be caused by:
• physical trauma
• infection
• extreme heat and cold
• exercise to the point of exhaustion
• extreme mental anxiety
40. Adrenal Cortex Dysfunctions
Hypoadrenalism – Addison’s Disease
• adrenal cortex produces inadequate
amounts of hormones
• caused by autoimmunity against
cortices 80%
• also caused by tuberculosis, drugs,
cancer
• plasma sodium decreases and may
lead to circulatory collapse
41. Mineralocorticoid Deficiency
• Lack of aldosterone:
– Increased sodium, chloride, water loss
– Decrease ECF volume
– Hyperkalemia
– Mild acidosis
– Increase RBC concentration
– Decrease cardiac output – shock - death within 4
days to a 2 weeks if not treated
42. Glucocorticoid Deficiency
• Loss of cortisol
–Disruption in glucose concentration
–Reduction in metabolism of fats and
proteins
–Patient is susceptible to different types of
stress
–Sluggishness of energy mobilization result in
weak muscle even when glucose and other
nutrients are available – cortisol is needed
for metabolic function
43. Melanin Pigmentation
• Characteristic of Addison’s disease is uneven
distribution of melanin deposition in thin skin
eg. Mucous membranes, lips, thin skin of the
nipples.
• Feedback and effect on MSH
44. Treatment
• Total destruction, if untreated, could lead to
death with a few days.
• Treatment – small quantities of
mineralocorticoids and glucocorticoids daily.
45. Hyperadrenalism – Cushing’s Syndrome
• caused by exogenous glucocorticoids
and by tumours (adrenal or pituitary)
• zg tumour increases aldosterone
• zr tumour increases cortisol
-increased sodium, blood pressure
-80% suffer from hypertension
- excess protein catabolism,
redistribution of fat
46. Characteristics
• Buffalo torso
–Redistribution of fat from lower parts
of the body to the thoracic and upper
abdominal areas
• Moon Face
–Edematous appearance of face
–Acne & hirsutism( excess growth of
facial hair)
47. What Would the Feedback Loop Look
Like for Cushing’s Syndrome?
48. Effects on Carbohydrate Metabolism
• “Adrenal diabetes”
–Hypersecretion of cortisol results in
increase blood glucose levels, up to 2 x
normal (200mg/dl)
–Prolonged oversecretion of insulin
“burns out” the beta cells of the
pancreas resulting in life long diabetes
mellitus
49. Effects on Protein Metabolism
• Decrease protein content in most parts
of the body resulting in muscle weakness
• In lymphoid tissue – decrease protein
synthesis results in suppression of the
immune system
• Lack of protein deposition in bones can
result in osteoporosis
• Collagen fibers in subcutaneous tissue
tear forming striae
51. Treatment
• Removal of adrenal tumor if this is the cause
• Microsurgical removal of hypertrophied
pituitary elements to reduce ACTH secretion
• Partial or total adrenalectomy followed by
administration of adrenal steroids to
compensate insufficiencies that develop
52. Adrenogenital syndrome (AG syndrome)
• There is conegenital deficiency of steroid
hydroxylases leading to deficient secretion of
cortisol.
• Since cortisol, the major feedback effector is not
present, ACTH secretion continues leading to
congenital adrenal hyperplasia (CAH).
53. 21 –Hydroxylase Deficiency:
• 21 –Hydroxylase Deficiency is the most
common type, where the production of
cortisol is totally absent.
• The lack of feedback leads to increased
androgen synthesis.
• This would result in Virilization of female
children who develop ambiguous genitalia.
precocious puberty is seen in male children.
• Early diagnosis and supplementation of
cortisol is effective in children.
54. 11-Hydroxylase Deficiency:
• In this condition, the symptoms are more
serious.
• The hypertensive variety of the AG syndrome
manifests and the child may not survive.
55. Estimation of Glucocorticoids secrtion:
1) Basal level of cortisol: The plasma cortisol
level is determined by
• RIA
• ELISA
• CLIA (chemiluminiscent immuno assay )
• The normal range is 5-25 microgram/dl of
at 9AM and 2-5 microgram/dl at 10 pm.
56. 2) Estimation of urinary free cortisol:
• The free cortisol in plasma is the biologically
active fraction.
• High levels are seen in hyperfunction and low
levels in hypoactivity
3) Plasma ACTH:
Suppressed ACTH levels are seen in
hyperadrenalism and high ACTH levels in
hypoadrenalism as well as in Cushing’s disease.
57. 4) Dexamethasone suppression test
• Dexamathasone produce a fall in cortisol
secretion due to feedback suppression ofACTH.
5) Urinary steriods
Estimation of 17-ketogenic steriods is indecated
only in AG syndrome.
6) Stimulation test
Infusion of synthetic ACTH ( synacthen or tetra
cosactrin ) is given
In the absense of reserve, stimulation tests fail to
the any response
58. 7) Metyrapone test :
• metyrapone inhibits the hydrolase enzyme.
• when it is given, cortisol is not formed.
• Then there is no feedback inhibitory effect.
• Hence, alternate pathways of sex steriods are
more operative and the urinary excretion of 17-
ketosteriods tends to elevate.
8) CRH test:
The test is of importance in establishing the cause
of adrenal hyperfunction ( primary, secondary or
tertiary)
60. NORMAL VALUE OF
CORTISOL : plasma
9 AM -------------------------130 – 600 nmol / L
MIDNIGHT---------------30 –- 130 nmol / L
Immunoassay for 17- alpha-hydroxy
progesterone
Normal value : urine
female : 5.5 – 22 μmol / d
MALE : 8 – 22 μmol / d
61. 1) VMA (Vanilimandilic acid) :
normal level 2-6mg/day
Estimated by antibody method
2) HVA (Homovanilic acid) in urine: metabolite
of dopa and dopamine
VMA /HVA ratio >1 has better prognosis in
neuroblastoma