Post on 20-Dec-2015
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