Endocrine System

I’m hot, I’m cold, I’m fast, I’m slow.

EMT-Paramedic Program

The System Itself

• The other regulating system of the body– Closely linked to nervous

system

• Uses glands and tissues• Via hormones, the

system regulates:– growth– the use of foods for energy– pH of body fluids– fluid balance– reproduction– provides resistance to stress

Hormones

• Chemical messengers to either:– Body organs– Tissues– Or Both

• Binding depends on:– Quantity – Quality of receptor

sites

• They may be divided into three groups:– Amines

• Tyrosine, epi, norepi

– Proteins• amino acids; insulin, GH,

calcitonin, ADH, oxytocin

– Steroids• cholesterol; cortisol,

aldosterone, estrogen, progesterone, and testosterone

Hormone Secretion

• Negative feedback mechanism

• Endocrine glands respond to blood level changes or other hormones present

• Secretion of hormone until stimulus is negated or changed

Pituitary “Master Gland”

• Posterior holds hypothalamus hormones ADH and oxytocin

• Anterior produces GH, TSH, ACTH, prolactin, FSH, LH

Specific Hormones

• ADH – maintains BP by

reabsorption of water by kidney tubules and vasoconstriction

• Oxytocin– stimulates

contraction of uterus and release of milk

Specific HormonesThyroid Stimulating Hormone

Growth Hormone

Adrenocorticotropic Hormone

Anterior Pituitary

Thyroid Gland

• Produces:– T4 - Thyroxine– T3 – Triiodothyronine

• Contain Iodine• Regulate energy

production & growth– Calcitonin –

• Regulates calcium• Maintains strong

bones…– Also feeds back

through pituitary

Parathyroid Glands

• “Pair-a-thyroids?” • Produces parathyroid

hormone– Also involved in

calcium & blood phosphate levels

Disorders Associated with Thyroid Gland• Issues directly associated with gland

– Tumor• Pituitary malfunction indirectly affecting• Hypothyroidism (Myxedema)• Hyperthyroidism

(Grave’s Disease)– Thyrotoxicosis– Thyrotoxic Crisis

(Thyroid Storm)

Disorders of the Thyroid Gland

• Thyroid Storm– Severe Tachycardia, Dysrhythmias– Heart Failure– Shock– Hyperthermia– Restlessness, Agitation & Paranoia– Abdominal pain– Delirium, Coma

• What else does this look like?• What could help you distinguish?• Danger in becoming a cynic?

Adrenal Glands

Each adrenal has:

Cortex -Aldosterone-Cortisol

Medulla -Epinephrine-Norepinephrine

Trouble Associated with Adrenal Gland

Cushing’s Syndrome– ACTH Levels too

high• Enlarges adrenal

gland– May be associated

with pituitary tumor

Disorders Associated with Adrenal Glands

Addison’s Disease– Deficiency of cortisol & aldosterone– Slow, gradual onset– Progressive

• Fluid volume deficit• Hyperpigmentation (bronze)

Adrenal Gland Disorders

Addisonian Crisis– Acute episode preceded by:

• Physical or emotional stress– Surgery– Alcohol intoxication– Trauma– Infection– Hypoglycemia

– Adrenal cortex cannot comply with body’s increased demand

Ovaries

Secrete

– Estrogen

– Progesterone

progesterone

Testes

Secrete

– Testosterone

– Inhibin

Pancreas

• U R&L Q• Islets of

Langerhans– Produce Glucagon

& Insulin

Pancreatic Hormones

• Glucagon – Alpha Cells– stimulates liver to change

glycogen to glucose– raises blood glucose

levels• Insulin – Beta Cells

– lowers blood glucose levels by increasing transport of glucose into the cells

Glucose/Dextrose (D-glucose)

• An intermediate in metabolism of carbohydrates

• The most important carbohydrate, and is formed during digestion; absorbed from intestines into blood of portal vein; in passage through liver, is converted into glycogen

Glucose

• May be:– Used immediately – Stored in muscles– Stored in fat

• Brain cannot store it’s food– Requires continuous circulating volume– Reason neuro s/s develop quickly

Disorders Associated with Pancreatic Dysfunction

Diabetes Mellitus

– Hyperglycemia

– Hypoglycemia

– DKA

– HHNK

Diabetes Mellitus

• 16 million in U.S. & rising• 3 diagnostic types:

– IDDM Type I– NIDDM Type II– Other (Secondary) DM

Diabetes Mellitus

• IDDM type 1• Most commonly occurs in children and

young adults– Genetic predisposition; Immune mediated

destruction of insulin-producing cells

Diabetes Mellitus

• NIDDM type II– Usually occurs after age 30. – A strong genetic

predisposition is evident but pathogenesis is different.

– Most individuals obese– Resistance to insulin action is

present. – Exogenous insulin not

required.

Promotion of Hyperglycemia

• Increased dietary intake (esp. carbohydrates)

• Limitation of physical activity

• Reduction of hypoglycemic therapy

• Limitation of endogenous insulin production– Pancreatic diseases– Drug treatment– Electrolyte disorders

Diabetes Mellitus

• Other (secondary) DM– Associates hyperglycemia to another

cause including:• Pancreatic disease/Pancreatectomy• Drugs or chemical agents• Others too

• Gestational diabetes– Develops during pregnancy and resolves

with birth but increased risk of DM later.

Development of Insulin Resistance

• Infection• Inflammation• Myocardial ischemia or infarction• Trauma• Surgery• Emotional stress• Pregnancy• Drug treatment

S/S of Hyperglycemia/Insulin Insufficiency or Resistance

• Polyuria

• Polydipsia

• Nocturia

• Weight Loss

• Fatigue

• Blurred vision

Control

• Oral

• Transplant– Islet cells– Pancreas

Oral Hypoglycemic Drugs

Metformin 500-1000 mg PO tid

Avandia 4 mg PO qd

Insulin

Insulin Route Onset Peak Duration

Novolog

Aspart

SQ 15 min 1-3 hr 3-5 hr

Humalog

Lispro

SQ 15 min 30-90 min 3-5 hr

Regular IV 10-30 min 15-30 min 30-60 min

Humulin Regular

SQ 30-60 min 2-4 hr 5-7 hr

NPH SQ 3-4 hr 6-12 hr 18-24 hr

Lantus Glargine

SQ 1.1 hr None 24 hr

70/30 NPH/regular

SQ 30 min 4-8 hr 24 hr

Diabetic Ketoacidosis

• A result of severe insulin insufficiency

and an excess of glucagon. Type I

• Common causes:

– Interruption of insulin therapy

– Stress, infection

– Non-compliance frequently a factor

• Onset slow, from 12-24 hours.

Diabetic Ketoacidosis

• Transition from glucose to lipid metabolism– Forms ketones & increase to toxic levels

(diuresed)– Metabolic Acidosis

• Symptoms • Causes severe osmotic diuresis and

severe dehydration• Tx: Requires close monitoring

– Draw red-top– Give IV fluids (Typically 3-5 L Low)– Consider thiamine

• All vitamins & Electrolytes grossly deranged

Non-Ketotic Hyperglycemic Hyperosmolar Coma (HHNK)

• Complication of Type II – Typically preceded by infection &/or

diuretics– Hyperglycemic state causes

hyperosmolar diuresis– Pronounced volume loss (Towards 10L)

• CBG (PG) levels 1000 & higher• Only mild metabolic acidosis

– Non-Ketotic– Many electrolytes within normal levels

Hypoglycemia

• Common causes– Excessive insulin– Stress– Overexertion– Infection– Under eating

• Symptoms• Treatment

– O2, IV, CBG (Red Top), 50% dextrose IV

Endocrine Summary

• A VERY complicated system

• A specialty of it’s own

• Much of EMS treatment is symptom oriented

• Much of care is cause oriented– Important distinction