The Endocrine System

Endocrine System

Endocrine vs. Exocrine

Organs are not physically connected

Alters activities of target organs/cells

Purpose: Growth/Development

Reproduction

Regulation

Stress Reactions

Hormones are Activated By

Hormonal

Humoral

Neural

Gland/Hormone Functions

Some glands produce >1 hormone

Some hormones produced by >1 gland

Some organs have >1 function

Some hormones have >1 function

Functions of Endocrine Glands

Endocrine Functions only

Production

Secretion

Contained within other organs which have other functions

Categories of Glands

Central: PituitaryHypothalamus

Peripheral: Thyroid PinealAdrenals GonadsParathyroids PancreasThymus Others

Hypothalamus

Found on floor of diencephalon

Neural and endocrine functions

Biofeedback mechanism for:

Osmotic pressures

Temperature regulations

Metabolic functions

Pituitary

Extends from Hypothalamus-behind sphenoid bone

“Master Gland” of body

Anterior- Portal network

Posterior- Neural-contains axons of

Hypothalamus neurons

Anterior Pituitary

GH- Growth Hormone

Prolactin

TSH- Thyroid Stimulating Hormone

ACTH- Adrenocorticotropic

FSH- Follicle Stimulating Hormone

LH- Luteinizing Hormone

Posterior Pituitary

ADH- Anti-Diuretic Hormone

Oxytocin

Pituitary Disorders

Acromegaly- Hypersecretion of GH

Dwarfism- Hyposecretion of GH

Thyroid

Inferior to larynx

2 Lobes

T3- Triiodothyronine

T4- Thyroxine

Calcitonin

Thyroid Disorders

Hypothyroidism- Hyposecretion

Hyperthyroidism- HypersecretionGraves Disease

Goiters- iron deficiencies

Parathyroids

4 small glands posterior surface of thyroid

Parathyroid hormone

Responsible for osteoclast of bone

Decreases blood phosphate levels

(By way of kidneys)

Enhances activation of Vitamin D

Parathyroid Disorders

Hyperparathyroidism

“Moan and groan, stones and bones”

Pineal Gland

Forms part of diencephalon

Melatonin

Inhibits hypothalamus release of gonadotropins

Melatonin-decreases in light/increase in dark (circadian rhythm)

Thymus Gland

Posterior to sternum, around great vessels

Thymosin

Both lymphatic and endocrine

Lymphatic- produces T-lymphocytes

Endocrine- ‘programs’ T-cells

The Adrenals

Located on superior end of each kidney

Medulla- inner gland

Cortex- outer gland

Adrenal Medulla

Sympathetic preganglionic fibers synapse on cells in medulla

Release of epinephrine/norepinephrine into general circulation

Adrenal Cortex

Produce over 30 steroid hormones

Three main cortical hormones

Mineralocorticoids

Glucocorticoids

Sex hormones

Mineralocorticoids

Regulate levels of electrolytes and water in extracellular fluid

95% are aldosteroneSodium reabsorption Potassium excretion

Glucocorticoids

Influence carbohydrate metabolism

Important in body’s response to stress

95% cortisol (hydrocortisone)

stimulates gluconeogenesis

secretion is regulated by ACTH

Sex Hormones

Androgens (testosterone)

Estrogens

Both are secreted in greater numbers by gonads

Adrenal Disorders

Cushing’s disease-

cortisol over-production secondary to

increased ACTH

Addison’s Disease-

cortisol/aldosterone deficiencies

Gonads

Testes- males

Testosterone

Ovaries- females

Estrogens

Progesterone

Both produce hormones/gametes

Pancreas

Retroperitoneal-posterior to stomach

Exocrine & Endocrine

Endocrine- islets of Langerhans

Alpha

Beta

Delta

Alpha cells

20% of islets

Hormone glucagon

Stimulates breakdown of glycogen in liver- raises glucose levels in blood

(glycogenolysis & glyconeogenesis)

Beta Cells

75% of islets

Hormone- insulin

Decreases glucose levels

Glucose Metabolism

Organic components of food:

Carbohydrates (instant-energy)

Glucose

Fats

Fatty acids/glycerols

Proteins

Amino acids

Carbohydrate Metabolism

Insulin is released by humoral, hormonal, neural means

Increased glucose

Parasympathetic stimulation

Gastrointestinal hormones

Carbohydrate Metabolism

60% of carbohydrates are stored as

glycogen in liver

If muscles are not exercised after eating-stored as muscle glycogen

Glycolysis

Glucose is broken down into pyruvate

and lactate- releasing 2ATPs

(Anaerobic metabolism)

Krebs Cycle

Fat Metabolism

A third of any glucose passing through liver is converted to fatty acids

Fatty acids are converted to triglycerides and stored in adipose tissue

Fat Metabolism

Without insulin, fat is broken back down into triglycerides/cholesterol CAD

Fatty acids are also broken down into ketone bodies

Protein Metabolism

In absence of insulin- protein storage stops and breakdown begins (muscle)

Amino acid breakdown for energy leads to increased urea in urine organ dysfunction

Pancreas Disorders

Diabetes-

Type 1- Juvenile onsetType 2- Mature onset Gestational diabetes

Type 1 Diabetes

Insulin dependant

S/S:polyuria

polydipsia

polyphagia

blurred vision

weight loss

Type 2 Diabetes

Generally non-insulin dependant

Has ability to make small amounts of

insulin

Can develop into insulin dependant

Gestational Diabetes

Develops during pregnancy

Deficiencies in insulin leads to inability to metabolize carbohydrates

Generally disappears after delivery

Insulin Agents

Early- porcine, bovine

Recent- genetic engineered human insulin

Protein

Rapid, intermediate and long-term

Combination of long-term, rapid each day

Insulin Types

Regular- Fast acting

0.5-1 hour onset

6-8 hour duration

NPH- Intermediate

1-1.5 hour onset

24 hour duration

Insulin Types

Ultralente- Long acting4-6 hour onset36 hour duration

Oral agents:Diabinese (chlorpropamide)Orinase (tolbutamide)Micronase (glyburide)Glucotrol

Diabetic Emergencies

Hypoglycemia

Hyperglycemia

Diabetic Ketoacidosis (DKA)

Hyperosmolar Hyperglycemic Nonketotic Coma (HHNK)

Hypoglycemia

Rapid on-set

< 60 mg/dl

Causes: too much insulin

decreased intake salicylates

excessive activity beta blockers

emotional stress hypothermia

chronic alcoholism sepsis

S/S of Hypoglycemia

Altered LOCs- irritability, nervousness,

confusion, combative

Cool, clammy

Weak, rapid pulse

Snoring, salivation

Normal BP

Diabetic Ketoacidosis

Fat metabolism leads to ketoacids

Acidosis leads to K+ in circulation &

hyperkaluria K+ deficiency

Osmotic diuresis dehydration,

electrolyte imbalances

S/S of DKA

Warm, dry skin

Dry mucous membranes

Tachycardia, thready pulse

Postural hypotension

Weight loss

‘Polys’

S/S of DKA

Abdominal pain

Anorexia, nausea/vomiting

Acetone breath

Kussmauls

Decreased LOC

Hyperosmolar Hyperglycemic Nonketotic

ComaGenerally Type II diabetic

Osmotic diuresis secondary to sugars

Not acidotic as in DKA

Factors: Geriatric

Preexisting diseases

Increased insulin requirements

Medication use- thiazide, diuretics

Parenteral/enteral feedings

S/S of HHNK

Weakness

Thirst

Polyuria

Weight Loss

Extreme dehydration

Treatment of Diabetic Emergencies

Hypoglycemia- ABCs

IV- NS

Monitor ECG

Oral, IV Dextrose

Poss. Glucagon IM

Poss. Thiamine

Monitor glucose!

Treatment of Diabetic Emergencies

Hyperglycemia (DKA, HHNK)-

ABCs

O2

IV- NS

Monitor ECG for abnormalities