Transcript Endocrine System - faculty at Chemeketa

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:
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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
Thyroid Stimulating Hormone
Specific Hormones
Growth Hormone
Anterior
Pituitary
Adrenocorticotropic
Hormone
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:
Medulla
-Epinephrine
Norepinephrin
e
Cortex
-Aldosterone
-Cortisol
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
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Infection
Inflammation
Myocardial ischemia or infarction
Trauma
Surgery
Emotional stress
Pregnancy
Drug treatment
S/S of Hyperglycemia/Insulin
Insufficiency or Resistance
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Polyuria
Polydipsia
Nocturia
Weight Loss
Fatigue
Blurred vision
Control
• Oral
• Transplant
– Islet cells
– Pancreas
Oral Hypoglycemic Drugs
Generic name
Initial dosage
Glyburide
1.25-5.0 mg PO qd
Duration
of activity
(hr)
24-60
Glipizide
2.5-5.0 mg PO qd
12-24
Chlorpropamide
100-250 mg PO qd
48-90
Tolazamide
100-250 mg PO qd
10-24
Acetohexamide
250-500 mg PO qd
12-24
Tolbutamide
250-500 mg PO bid
6-12
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