This document summarizes several key endocrine glands and hormones. It discusses the pituitary gland, thyroid gland, pancreas, and adrenal glands. For each gland, it outlines their location, cell types, hormones produced, functions, and disorders related to hormone imbalances like hyperthyroidism, hypothyroidism, diabetes mellitus, Cushing's syndrome, and Addison's disease. The roles of hormones like growth hormone, insulin, glucagon, cortisol, and thyroid hormones in regulating metabolism, growth, and development are also summarized.
In mammals, the adrenal glands (also known as suprarenal glands) are endocrine glands that sit at the top of the kidneys. They are chiefly responsible for releasing hormones in response to stress through the synthesis of corticosteroids such as cortisol and catecholamines such as adrenaline (epinephrine) and noradrenaline. They also produce androgens in their innermost cortical layer. The adrenal glands affect kidney function through the secretion of aldosterone, and recent data (1998) suggest that adrenocortical cells under pathological as well as under physiological conditions show neuroendocrine properties; within normal adrenal glands, this neuroendocrine differentiation seems to be restricted to cells of the zona glomerulosa and might be important for an autocrine regulation of adrenocortical function.
In mammals, the adrenal glands (also known as suprarenal glands) are endocrine glands that sit at the top of the kidneys. They are chiefly responsible for releasing hormones in response to stress through the synthesis of corticosteroids such as cortisol and catecholamines such as adrenaline (epinephrine) and noradrenaline. They also produce androgens in their innermost cortical layer. The adrenal glands affect kidney function through the secretion of aldosterone, and recent data (1998) suggest that adrenocortical cells under pathological as well as under physiological conditions show neuroendocrine properties; within normal adrenal glands, this neuroendocrine differentiation seems to be restricted to cells of the zona glomerulosa and might be important for an autocrine regulation of adrenocortical function.
At the end of this session,
Student are able to
1. Explain etiology and pathophysiology of adrenal cortex disorder
2. Identify the clinical manifestation related
3. Explain the diagnostic investigation related
4. Discuss the treatment, intervention and possible complication
5 Apply nursing art / caring value towards patient ~ nursing care
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Easy to understand the Physiology of these vital glands
1. What comprises the Endocrine system
2. Mechanisms of Hormonal alterations
3. Pituitary Gland- Anterior pituitary gland, posterior pituitary gland and their disorders
4. Thyroid gland and its disorders
5. Diabetes
6. Parathyroid Gland disorders
7. Adrenal Gland and its disorders
8. Thank you
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At the end of this session,
Student are able to
1. Explain etiology and pathophysiology of adrenal cortex disorder
2. Identify the clinical manifestation related
3. Explain the diagnostic investigation related
4. Discuss the treatment, intervention and possible complication
5 Apply nursing art / caring value towards patient ~ nursing care
Inborn errors of amino acid metabolismRamesh Gupta
Inherited disorders of amino acid metabolism e.g. phenylketonuria, maple syrup urine disease, alkaptonuria, homocystinuria, Hartnup disease etc for medical, biochemistry and biology undergraduates
Physiology of thyroid gland and pancreas
fail safe mechanism of pancreas
physiology in short with more pictures
Easy to understand the Physiology of these vital glands
1. What comprises the Endocrine system
2. Mechanisms of Hormonal alterations
3. Pituitary Gland- Anterior pituitary gland, posterior pituitary gland and their disorders
4. Thyroid gland and its disorders
5. Diabetes
6. Parathyroid Gland disorders
7. Adrenal Gland and its disorders
8. Thank you
pathology and Complications of type 2 diabetes mellitusAiswarya Thomas
explains in detail abou various complications of diabetes mellitus and its pathophysiology. Described about the peripheral, microvascular, macrovascular comlpication
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The endocrine system
1.
2.
3.
4. “Highly integrated and widely distributed
group of organs that provides homeostasis
among various tissues”
Signaling by Extracellular secreted
molecules:
Autocrine
Paracrine
Endocrine-Hormones
5. “Secretory molecules that act on target cells
distant from their site of synthesis”
Two types:
Interact with cell surface receptors
a) Peptide hormones i.e. Growth hormone and
insulin
b) Small molecules i.e. epinephrine
Interact with intracellular receptors
a) Lipd soluble hormones i.e. thyroxine
6.
7. Bean-shaped structure at base of brain.
Connected to Hypothalamus through a stalk
called Infundibulum.
Two lobes:
Adenohypophysis
Neurohypophysis
Release of trophic hormones is under
control of hypothalamic factors i.e either
stimulatory or inhibitory.
8.
9. Hyperpituitarism
Excessive secretion of trophic hormone
Causes:
Anterior lobe pituitary adenoma
Hypopituitarism
Deficiency of trophic hormone
Causes:
Ischemic injury
Surgery or radiation
Inflammatory reactions
10. Two bulky lateral lobes connected by isthmus
Located below or anterior to larynx
Lobules composed of dispersed follicles
Follicles- cuboidal to low columnar
epithelium
Thyroglobulin- presursor protein of thyroid
hormone
11.
12. Upregulation of carbohydrates and lipid
catabolism
Stimulation of protein synthesis in wide
variety of cells
Increase in basal metabolic rate
13. Hyperthyroidism:
Thyrotoxicosis due to elevated circulating
levels of free T3 and T4
GRAVES Disease – autoimmune disease
Autoantibodies to TSH receptor
Activate TSH receptors on thyroid epithelial
cells leads to hyperthyroidism
Hypertrophy and hyperplasia of follicles.
Ophthalmopathy
15. Inadequate levels of thyroid hormone.
Cretinism – infants
Iodine deficiency
Impaired development of skeletal system and
CNS
Goiter-impaired synthesis of thyroid
hormone
Compensatory rise in TSH
Enlargement of thyroid gland
17. Group of disorders with a common feature of
hyperlglycemia
Caused by deficient production or action of
insulin
Cause secondary damage to vital organs
Kidneys – end stage renal disease
Eyes – adult onset blindness
Nerves – non traumatic lower extremity
amputation
Blood vessels
18. Type I – IDDM (20%)
Type II – NIDDM (80-90%)
Monogenic forms i.e MODY– rare
19. Low level of glucose in body
High levels of glucose in body
Glucagon secretion
Insulin secretion
20.
21. Type-1 diabetes mellitus
Production of autoantibodies against b cells
of pancreas
No insulin production
Hyperglycaemia
Type-2 diabetes mellitus
Insulin production is sufficient
Cells involved in glucose metabolism become
desensitized
Do not respond to insulin
Hyperglycaemia
23. Obesity - Increased body fat
OUTCOMES:
Insulin resistance
Diabetes
Cardiovascular diseases like hypertention and
hyperlipidemia
24. Excess free fatty acids
FFA in B cells – release of IL-1B and other pro
inflammatory cytokines – recruit
macrophages and T cells – B cell dysfunction
and insulin resistance
Adipokines release from adipocyte cause B
cell dysfunction as described above.
25. FFA and glucose in B cells – release of IL-1B
and other pro inflammatory cytokines –
recruit macrophages and T cells – further
cytokine production
Amylin or IAPP release IL-IB
Cause B cell dysfunction and hyperglycemia
26. Multifactorial but main cause is
hyperglycemia and glucose toxicity
3 pathways:
Formation of advanced glycation end
products (AGEs)
Activation of protein kinase C
Disturbances in polyol pathways
45. Elevated glucocorticoid levels
Causes:
Exogenous glucocorticoids
Endogenous causes
-Primary hypothalamic-pituitary diseases
associated with hypersecretion of ACTH
-Secretion of ectopic ACTH by non-pituitary
neoplasm(tumor of thymus gland,
Small cell tumor of Lungs)
-Primary adrenocortical neoplasm (adenoma or
carcinoma)
-Primary cortical hyperplasia
46. Small cell carcinoma of lungs
Hypertention
Weight gain
Truncal obesity-moon faces (Fat redistribution)
Buffalo hump(Fat mass at lower cervical and
upper lumbar vertebra)
Atrophy
Weakness
Hyperglycemia
Glucosuria
Polydipsia (Excessive thirst)
Diabetes
47. When you do not succeed in taking giant
steps on the road to your goal,
be satisfied with little steps,
and wait patiently till the time that you are
able to run, or better still, to fly.
Be satisfied to be a little bee in the hive who
will soon become a big bee capable of making
honey…
Thank you …
47