The endocrine system

“Highly integrated and widely distributed

group of organs that provides homeostasis

among various tissues”

Signaling by Extracellular secreted

molecules:

Autocrine

Paracrine

Endocrine-Hormones

“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

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.

Hyperpituitarism

Excessive secretion of trophic hormone

Causes:

Anterior lobe pituitary adenoma

Hypopituitarism

Deficiency of trophic hormone

Causes:

Ischemic injury

Surgery or radiation

Inflammatory reactions

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

Upregulation of carbohydrates and lipid

catabolism

Stimulation of protein synthesis in wide

variety of cells

Increase in basal metabolic rate

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

Sympathetic

overstimulation.

Accumulation of

loose connective

tissue behind

orbits

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

Pancreatic cells – islets of langerans

Contain 4 cells

Alpha cell releasing glucagon

Beta cell releasing insulin

Delta cell releasing somatostatin

PP cells releasing VIP

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

Type I – IDDM (20%)

Type II – NIDDM (80-90%)

Monogenic forms i.e MODY– rare

Low level of glucose in body

High levels of glucose in body

Glucagon secretion

Insulin secretion

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

Target tissue fails to response insulin

Decreased glucose uptake

Gluconeogenesis

Decreased glycolosis

Decreased fatty acid oxidation

Obesity - Increased body fat

OUTCOMES:

Insulin resistance

Diabetes

Cardiovascular diseases like hypertention and

hyperlipidemia

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.

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

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

Diabetic nephropathy

Retinopathy

Hypertension

Peripheral neuropathy

Microangiopathy

Macrovascular disease

Myocardial infarction

Ketoacidosis

Diabetic coma

Hyperosmolar non-ketotic coma

Weakness

Polyuria

Polydipsia

Polyphagia

Ketoacidosis

Metabolic derangements

Glucose, fat and protein metabolism

Glycosuria

Osmotic diuresis

Proteolysis

Weightloss

Muscle weakness

Ketogenesis

Ketonemia

Ketonuria

Polyuria

Polydipsia

Obesity

Weakness

Weight loss

Hyperosmolar non-ketotic coma

Dehydration

Osmotic diuresis

Urinary fliud loss

Normal glucose level= 70-120mg/dl

Random glucose level >200 or =200mg/dl

Fasting glucose level >126 or =126mg/dl

OGTT – oral glucose tolerance test

>200mg/dl or =200mg/dl

Euglycemic fasting glucose level

<110mg/dl, OGTT<140mg/dl

Prediabetes fasting glucose level >110

but<126 mg/dl , OGTT>140 &<200 mg/dl

Glycaemic control- %age of glycosylated

hemoglobin (HbA1C)

HbA1C<7 = tight glycaemic control

Medical nutrition therapy

Oral hypoglycaemic therapy

Insulin therapy

First line of defense for type-2 diabetics

Adequate diet – low cholesterol intake

Excursive

1. Weight reduction

2. Improves insulin sensitivity

3. Lower blood glucose level

Metformin

Type-2 diabetes

Reduce hepatic glucose production

Sulphonylureas

Tolbutamide

Tolazamide

Increase insulin release

Pramlintide

Type-1 diabetes

Type-1 diabetes main treatment

Portable pen injectors

Subcutaneous injection

Insulin glargine……..

Blood glucose monitoring

Body weight monitoring

Personal hygeine

Healthy lifestyle

Reducing excessive salt intake

Paired organs having cortex and medulla

Synthesize

1. Glucocorticoids

2. Mineralocorticoids

3. Sex steroids

It can be :

Primary hypoadrenalism

1. Acute adrenocortical insufficiency

2. Chronic adrenocortical insufficiency

Secondary hypoadrenalism

ADDISON DISEASE:

Adrenal cortex destruction

Causes

1. Autoimmune adrenalitis

2. Tuberculosis

3. AIDS

4. Fungal

5. Metastatic cancer

It includes:

Cushing syndrome

Hyperaldosteronism

Adrenogenital syndrome

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

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

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 …

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