Alexander ch23 lecture

Copyright © 2017, 2012 Pearson Education, Inc. All Rights Reserved.
Advanced EMT
A Clinical-Reasoning Approach, 2nd Edition
Chapter 23
Endocrine Disorders

• Applies fundamental knowledge to provide basic
and selected advanced emergency care and
transportation based on assessment findings for
an acutely ill patient.
Advanced EMT
Education Standard

1. Define key terms introduced in this chapter.
2. Describe the pathophysiology of type 1 and type 2
diabetes mellitus.
3. Given a patient’s blood glucose level, determine whether
it is within normal limits.
4. Recognize the brain’s particular sensitivity to decreased
blood glucose levels.
5. Predict the consequences of insufficient glycogen stores.
6. Compare and contrast the speed of onset and signs and
symptoms of hypoglycemia and hyperglycemia.
Objectives (1 of 3)

7. Compare and contrast diabetic ketoacidosis (DKA)
and hyperosmolar hyperglycemic state (HHS).
8. Describe how to conduct direct history taking and
assessment to obtain information relevant to the
patient with a diabetic emergency.
9. List common complications of diabetes.
10.Given a scenario with a patient suffering a diabetic
emergency, provide emergency medical care for
the patient.
11.Identify indications and contraindications to the
administration of oral glucose, intravenous dextrose,
and intramuscular glucagon.
Objectives (2 of 3)

12.Describe the reassessment of a patient with a
diabetic emergency.
13.Document the assessment and management of a patient
with a diabetic emergency.
14.Give a brief overview of the pathophysiology and the
signs and symptoms of hyperthyroidism and
hypothyroidism.
15.Give a brief overview of the pathophysiology and the
signs and symptoms of disorders of the adrenal glands,
including Cushing’s syndrome and Addison’s disease.
Objectives (3 of 3)

• Endocrine system
– Consists of glands that secrete chemical messengers
called hormones
– Hormones affect individual body cells to regulate
body functions.
 Energy metabolism
 Response to stressors
 Thirst
 Reproduction
 Many others
Introduction (1 of 3)

• Complex system leads patient to present with
various signs and symptoms.
– Abdominal pain
– Nausea and vomiting
– Cardiac dysrhythmias
– Altered mental status
– Dehydration
– Fatigue
– Weakness

• Endocrine system plays crucial role in maintaining
homeostasis.
– Cannot respond well to stressors, such as injury,
illness, and surgery
– Can exacerbate the underlying endocrine problem,
resulting in an endocrine emergency
• Most urgent endocrine problems are dysfunction
of pancreas, thyroid, and adrenal glands.

Think About It
• What are the next steps Will and Mia should take?
• How can they determine whether the patient’s
coworker is right about her condition?
• If the patient’s blood sugar is low, what are the
steps in treating the condition?

Figure 23-1
Structures of the endocrine system.

Anatomy and Physiology Review
• Releasing hormones
– Act on other endocrine glands, causing them
to release hormones
• Inhibiting hormones
– Decrease action
• Only cells with receptor for specific hormone
molecules affected by presence of hormone

Figure 23-3
The vast majority of hormones are regulated by negative feedback.
(Bledsoe, Bryan E.; Martini, Frederic H.; Bartholomew, Edwin F.; Ober, William C.;
Garrison, Claire W.; Anatomy & Physiology for Emergency Care, 2nd Edition, © 2008.
Reprinted with permission of Pearson Education, Inc., Upper Saddle River, NJ)

Anatomy and Physiology Review (1 of 6)
• Hormonal secretion is regulated by negative
feedback.
• Endocrine gland receives messages.
– Stimulated or inhibited by composition of extracellular
fluid or by hormones from other endocrine glands
– Controlled by release of neurotransmitters from
neurons

Table 23-1
Overview of Selected Endocrine Functions
Gland Stimulated By Hormones Released Hormone Targets and Effects
Hypothalamus Autonomic
nervous
system
Releasing and inhibiting hormones,
including growth hormone-releasing
hormone (GHRH), somatostatin
(growth hormone-inhibiting hormone
[GHIH]), corticotropin-releasing
hormone (CRH), thyrotropin-releasing
hormone (TRH), gonadatropic-
releasing hormone (GnRH), and
prolactin-releasing and inhibiting
hormones (PRH, PIH)
Anterior pituitary gland;
stimulation and inhibition of
anterior pituitary hormone
secretion.
Anterior pituitary
gland
Hypothalamic
hormones, levels
of various
hormones
Growth hormone (GH),
adrenocorticotropic hormone (ACTH),
thyroid-stimulating hormone (TSH),
follicle-stimulating hormone (FSH),
luteinizing hormone (LH), prolactin
(PRL)
GH affects all cells, ACTH affects
adrenal cortices, TSH acts on the
thyroid gland, FSH and LH act on
the ovaries and testes, and PRL
acts on the mammary glands.
Posterior pituitary
gland
Hypothalamus Antidiuretic hormone (ADH,
vasopressin), oxytocin
ADH acts on the kidneys to
prevent water loss, and oxytocin
acts on uterine and mammary
gland smooth muscle tissue.
Thyroid gland TSH, calcium level T3 and T4; calcitonin T3 and T4 affect all cells,
increasing cellular metabolism.
Calcitonin stimulates bone to
increase calcium uptake.

Table 23-1 (continued)
Overview of Selected Endocrine Functions
Gland Stimulated By Hormones Released Hormone Targets and Effects
Pancreas Levels of glucose
and amino acids
Glucagon (alpha cells), insulin (beta
cells), somatostatin (delta cells)
Glucagon promotes an increase in
glucose level through glycogenolysis
in the liver; insulin affects all cells,
promoting glucose uptake and
protein, glycogen, and fat synthesis;
and somatostatin acts locally to
inhibit alpha and beta cells
Adrenal cortex ACTH Glucocorticoids, mineralocorticoids,
small amounts of sex hormones
estrogen, testosterone,
progesterone)
Glucocorticoids, such as cortisol,
increase blood glucose and
suppress inflammation and immune
reaction. Mineralocorticoids, such as
aldosterone, regulate electrolyte and
fluid balance. Sex hormones have
effects on most cells in males and
females.
Adrenal medulla Sympathetic
nervous system,
via the
hypothalamus
Epinephrine, norepinephrine Epinephrine acts on the muscle,
liver, and cardiovascular system to
stimulate the fight-or-flight response.
Norepinephrine causes
vasoconstriction.

• Three main endocrine functions of hypothalamus
– Controlling pituitary gland through secretion of
releasing and inhibiting hormones
– Making two hormones that are released by posterior
pituitary gland
– Nervous stimulation of medullae of adrenal glands

• Pancreas and blood glucose level
– Glucose is the preferred source of energy for cells.
 Required for normal cell metabolism
 Glycogenesis
 Glycogenolysis
 Gluconeogenesis

• Pancreas and blood glucose level (continued)
– Brain cells
 Need constant glucose
 Cannot quickly convert to using fats
 Hypoglycemia: life-threatening emergency
 Unless glucose is restored, brain cells suffer damage and die.
– Other cells
 Can use fat as source of energy, but inefficiently
 Toxic byproducts accumulate in the blood.

Figure 23-4
The blood glucose level is regulated by the hormones glucagon and insulin. Glucagon
raises glucose levels, whereas insulin lowers glucose levels.

• Pancreas and blood glucose level (continued)
– Glucagon
 Secreted when BGL is low
 Accelerates glycogenolysis
 Stimulates gluconeogenesis
 Enhances glucose release into blood
– Insulin
 Secreted when BGL rises
 Allows glucose to enter cell

• Thyroid gland hormones
– Control rate of energy metabolism by cells (T3 and T4)
• Adrenal medullary hormones are epinephrine and
norepinephrine.
– Secreted in response to sympathetic nervous system
stimulation
– Mineralocorticoids control electrolyte balance.
– Glucocorticoids affect glucose metabolism.
– Androgens secreted from adrenal cortex

Assessment of Endocrine-Related
Complaints (1 of 4)
• Common presentations
– Altered mental status
– Weakness
– Fatigue
– Palpitations
– Fever
– Abdominal pain
– Other complaints

Table 23-3
Causes of Altered Mental Status
The mnemonic AEIOU TIPS helps you remember to investigate possible causes of altered
mental status, including those related to diabetes.
A – Acidosis (including diabetic ketoacidosis), alcohol
E – Epilepsy (hypoglycemia may result in seizures)
I – Infection (diabetics and patients with adrenal disease are prone to infection)
O – Overdose (may include overdose of insulin or antihyperglycemic agents)
U – Uremia, kidney failure (diabetics are prone to kidney failure)
T – Trauma, tumor, toxin
I – Insulin (too much or too little)
P – Psychosis, poison
S – Stroke, shock, seizures (diabetics are at higher risk for stroke)

Table 23-4
Medications That May Indicate an Endocrine Emergency
Medication Condition
levothyroxine (Synthroid), thyroid hormone Treats hypothyroidism; overdose may cause signs and
symptoms of hyperthyroidism.
methimazole (Tapazole) Treats hyperthyroidism by blocking thyroid hormone
synthesis. May indicate Graves’ disease.
propylthiouracil (PTU) Treats hyperthyroidism, including Graves’ disease, by
decreasing production of thyroid hormone.
steroids (prednisone, prednisolone, dexamethasone,
cortisone, hydrocortisone, methylprednisolone, others)
Corticosteroids are used to treat inflammatory conditions
and replace adrenal cortical hormones. Many have
mineralocorticoid effects in addition to the desired
glucocorticoid effects. May result in signs and symptoms
of Cushing’s syndrome. Sudden withdrawal can result in
adrenal insufficiency.
insulin (Humulin, Lispro, others) (various forms with
different durations of action, including regular, NPH,
Lente, Semi-lente, and Ultralente)
Increases cellular uptake of glucose; overdose may result
in hypoglycemia.
drugs for type 2 diabetes: Oral antihyperglycemics include
tolbutamide (Orinase), chlorpropramide (Diabinese),
metformin (Glucophage), glyburide (Micronase), glipizide
(Glucotrol), rosiglitazone (Avandia), sitagliptin (Januvia).
Injectable drugs include exenatide (Byetta).
Various mechanisms of action to increase insulin
production or enhance insulin use.

Complaints (2 of 4)
• Scene size-up
– Standard operational and patient care aspects
– Clue may be evident
– General appearance
– Chief complaint

Complaints (3 of 4)
• Primary assessment
– Level of responsiveness (AVPU)
– ABCs
– Need for oxygen
– Unresponsive or compromised airway, breathing, or
circulation is critical, high-priority patient

Complaints (4 of 4)
• Secondary assessment
– Obtain medical history.
– Tailor your questions for follow-up on chief complaint.
– Obtain vital signs, pulse oximetry, and blood glucose
level.
– Perform rapid physical exam on critical patients.
– Perform focused physical exam on noncritical patients.
– Reassess.

Diabetes and Diabetic Emergencies
(1 of 2)
• Type 1 diabetes
– Destruction of the beta cells in pancreas causing little
to no insulin production
– Onset is childhood, adolescence, or young adult
– Must take insulin to control blood sugar

Diabetes and Diabetic Emergencies
(2 of 2)
• Type 2 diabetes
– Occurs in middle-age, in obese patients
– Usually controlled by oral medications
– Decrease in amount of insulin produced or decrease
in cellular response to insulin

Table 23-5
Comparing and Contrasting Type 1 and Type 2
Diabetes Mellitus
Feature Type 1 Diabetes Type 2 Diabetes
Cause Autoimmune destruction of pancreatic
beta cells leading to insulin deficiency,
resulting in starvation metabolism and
hyperglycemia.
Reduced amount of insulin produced by pancreas and
increased resistance of cells to insulin, resulting in
hyperglycemia.
Risk factors Genetic factors. Genetic factors, obesity.
Hypoglycemia May occur when the amount of insulin
administered is too great for the
amount of calories ingested.
May occur when the dose of antihyperglycemic
medications is too great for the amount of calories
ingested.
Hyperglycemic
emergencies
Diabetic ketoacidosis (DKA) occurs in
undiagnosed or poorly controlled
diabetes or in response to increased
glucose levels produced by the stress
response as a complication of surgery,
infection, major illness, or trauma.
Hyperosmolar hyperglycemic state (HHS) may occur in
poorly controlled diabetes or in response to increased
glucose levels produced by the stress response as a
complication of surgery, infection, major illness, or
trauma.
Complications Blindness, cardiovascular disease,
stroke, kidney failure, amputation,
peripheral neuropathy, peripheral
vascular disease, nonhealing wounds,
gangrene.
Blindness, cardiovascular disease, stroke, kidney failure,
amputation, peripheral neuropathy, peripheral vascular
disease, nonhealing wounds, gangrene.
Management Diabetic diet, careful monitoring of
blood glucose level (BGL), insulin.
Weight loss through diet and exercise, diabetic diet,
careful monitoring of BGL, medications for type 2
diabetes, insulin in severe cases.

Diabetic Emergencies
• Normal blood glucose levels between 70 and
110 mg/dL
• Hypoglycemia
– Dangerously low (less than 60 mg/dL)
• Hyperglycemia
– Dangerously high (greater than 140 mg/dL)

Table 23-6
Comparing and Contrasting DKA and HHS
Feature DKA HHS
Type of diabetes Type 1 Type 2
Cause Inadequate insulin to allow glucose to enter cells
for metabolism, resulting in hyperglycemia and
use of fats for energy.
Decreased amount of insulin allows
some glucose into cells for metabolism
but cannot lower BGL to normal.
Consequences Hyperglycemia leads to dehydration through
osmotic diuresis. Electrolytes are lost through the
large amounts of urine. Use of fats for energy
results in ketone production,
lowering the blood pH. Dehydration, acidosis, and
electrolyte abnormalities lead to altered mental
status and increase the risk of cardiac
dysrhythmias. Kussmaul respirations are an
attempt to compensate for metabolic acidosis.
Hyperglycemia leads to dehydration
through osmotic diuresis. Electrolytes
are lost through the large amounts of
urine. Dehydration and electrolyte
abnormalities lead to altered mental
status and increase the risk of cardiac
dysrhythmias.
Onset Hours to days. May be preceded by surgery,
trauma, infection, or illness.
Several days. May be preceded by
surgery, trauma, infection, or illness.
Signs and symptoms Gradual onset of altered mental status; warm, dry
skin; poor skin turgor, orthostatic hypotension;
tachycardia; history of polyuria, polydipsia, and
polyphagia; Kussmaul respirations; acetone odor
on breath; abdominal pain; nausea, vomiting. BGL
may be 300–500 mg/dL.
Gradual onset of altered mental status;
warm, dry skin; poor skin turgor,
orthostatic hypotension; tachycardia;
history of polyuria, polydipsia, and
polyphagia. BGL may reach 1,000
mg/dL.
Prehospital
management
Management of airway, breathing, and
oxygenation; IV rehydration.
Management of airway, breathing, and
oxygenation; IV rehydration.

Diabetic Emergencies (1 of 8)
• Hyperglycemia
– Root problem in undiagnosed diabetes
– Insufficient amount of insulin for amount of glucose
present
– Causes
 Medication dose needs adjusting
 Noncompliance
 Excess calorie consumption
 Stressors such as surgery, infection, or myocardial infarction

• Diabetic ketoacidosis
– Abundant glucose but no insulin to allow entry into the
cell
– Cell begins using fatty acids for creating ATP
 Produces ketones and decreases pH
– Polyphagia
– Polyuria
– Polydipsia

• Diabetic ketoacidosis (continued)
– Body attempts to compensate by increasing CO2
elimination; Kussmaul respirations
 Causes fruity odor of acetone on breath
– Altered mental status, cardia dysrhythmias, weakness,
lethargic, dehydration, hypotension, vomiting with
relatively slow onset (hours to days)

• Diabetic ketoacidosis—treatment
– Supportive
– Ensure open airway and adequate ventilation and
oxygenation.
– Administer large volumes of isotonic crystalloid IV
fluids.
 Generally 1 to 2 L bolus followed by an infusion
 Check lung sounds for overload.

• Hyperosmolar hyperglycemic state
– Type 2 diabetes, still have some available insulin
– Osmotic diuresis, polyuria, polydipsia
– Signs and symptoms similar to DKA but no ketones or
Kussmaul respirations
– Support vital functions and begin rehydration.

• Hypoglycemia
– Low blood glucose level; sudden onset.
– Altered mental status most important; seizures may
occur.
– Check BGL of any patient with altered mental status;
goal is to increase blood glucose level.
– Triggers release of epinephrine, stimulates sympathetic
nervous system, and leads to early signs and
symptoms

Table 23-7
Signs and Symptoms of Hypoglycemia
• Sudden onset of altered mental status or bizarre behavior
• Irritability
• Weakness, loss of coordination
• Headache
• Weak, rapid pulse
• Pale, cool, diaphoretic skin

• Hypoglycemia—treatment
– Follow protocol.
– Awake and able to control airway
 Offer sugar to eat or drink.
– Decreases level of responsiveness
 25 grams dextrose 50% in strong vein
 1 mg glucagon IM if no IV

• Diabetics who refuse transport
– Once patient’s mental status normal, you cannot
transport him without his consent.
– Provide information to make informed decision.
– Unless backup source of energy, BGL will drop again.
– Document

Figure 23-7
Goiter results from an enlarged thyroid gland and can be associated with both
hypothyroidism and hyperthyroidism. (© Edward T. Dickinson, MD)

Thyroid Disorders
• Hyperthyroidism
– Increased metabolism, weight loss, heat intolerance,
other problems
• Hypothyroidism
– wWeight gain; cold intolerance; and, in severe cases,
coma
• Goiter
– Thyroid gland enlarged

Thyroid Disorders (1 of 2)
• Graves’ disease
– Form of hyperthyroidism
– Autoimmune disorder
– Increased production of thyroid hormones
– Characteristic feature of protruding eyes, or
exophthalmos

Thyroid Disorders (2 of 2)
• Hypothyroidism
– Iodine deficiency, surgical removal of the thyroid
gland, or damage to the gland from radiation therapy
– Mild cases due to autoimmune disease
– Myxedema coma
 Bradycardia, respiratory depression, and severe hypothermia

Table 23-8
Contrasting Hyperthyroidism and Hypothyroidism
Feature Hyperthyroidism Hypothyroidism
Cause Increased thyroid hormone levels Decreased thyroid hormone levels
Associated conditions Graves’ disease, goiter Goiter, surgical removal or radiation
damage of thyroid gland
Signs and symptoms Weight loss despite increased appetite,
anxiety, intolerance to heat, diarrhea,
palpitations, tachycardia, hypertension,
nonpitting pretibial edema
Weight gain despite decreased
appetite, fatigue and lack of energy,
lack of emotion, slowed mental
function, intolerance to cold,
myxedema in prolonged cases
Emergencies Thyrotoxicosis (thyroid storm), which may
present with heart failure, high fever,
vomiting, diarrhea, and psychosis
Myxedema coma, which may be
accompanied by bradycardia,
hypotension, respiratory depression,
elevated capnometry readings, and
severe hypothermia

Adrenal Disorders
• Addison disease
– Insufficient adrenal cortical hormones
– Damage to adrenal cortex
– Result of autoimmune disease, infection,
hypoperfusion

Adrenal Disorders
• Cushing’s syndrome
– Long-term overexposure to glucocorticoids
– Complications: osteoporosis, hypertension,
diabetes, muscle wasting, susceptibility to infection
– “Moon face” appearance, obese around trunk but
thin extremities, accumulation of excess fat in the
upper back

Table 23-9
Comparing and Contrasting Cushing’s Syndrome
and Addison’s Disease
Feature Cushing’s Syndrome Addison’s Disease
Cause Excess adrenal cortical hormones due to
glucocorticoid therapy (steroid medications) or
pituitary tumor, resulting in increased ACTH.
Insufficient secretion of adrenal
cortical hormones due to destruction
of adrenal cortex. Adrenal
insufficiency may occur as a result of
sudden withdrawal of corticosteroid
therapy.
Associated conditions COPD, asthma, cancer, or inflammatory conditions
requiring steroid therapy. Diabetes, infection.
Increased risk of cardiovascular disease and stroke.
Inability to respond to stressors such
as infection, surgery, trauma, or
illness.
Signs and symptoms Weight gain in the trunk, often with thin extremities.
“Moon face” appearance, accumulation of fat in the
upper back (“buffalo hump”). Thin, easily bruised
skin. Delayed wound healing. Development of facial
hair in women.
Hyperpigmentation of the skin and
gums, fatigue, weakness, weight loss.
Emergencies Increased risk of MI, stroke, and infection. Adrenal crisis (Addisonian crisis).
May present with hypoglycemia,
hypotension, and cardiac rhythm
disturbances due to electrolyte
abnormalities.

Chapter Summary (1 of 2)
• Signs and symptoms can be general (altered
mental status, weakness, or fatigue).
• In many cases, patient has known history of
endocrine disorder.
• You should have knowledge of the endocrine
system’s role in homeostasis and the
pathophysiology of endocrine disorders.

Chapter Summary (2 of 2)
• Ensure open airway, adequate ventilation,
oxygenation.
• Administer fluids to maintain adequate perfusion.
• Patients with hypoglycemia require oral or IV of
glucose, or IM of glucagon.
• Patients with thyroid problems may have difficulty
with temperature regulation.
• Be prepared to treat hyperthermia or hypothermia.

Alexander ch23 lecture

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