Endocrine Endocrine EmergenciesEmergencies

Endocrine System Physiology/Patho Function

Disorders of the Pancreas Disorders of the Thyroid Gland Disorders of the Adrenal Glands

Endocrine System Physiology/Patho Function

Disorders of the Pancreas Disorders of the Thyroid Gland Disorders of the Adrenal Glands

Endocrine Disorders Endocrine Disorders and Emergenciesand Emergencies

Endocrine SystemEndocrine System

Consists of glands that secrete hormones

Maintains homeostasis with the use of hormonal chemical messengers…tend to be widespread in effect

Consists of glands that secrete hormones

Maintains homeostasis with the use of hormonal chemical messengers…tend to be widespread in effect

HormonesHormones

Are released as changes in the internal environment occur

Transported by the blood throughout the body

One may control the secretion of another

Hormonal action controlled by negative feedback

Are released as changes in the internal environment occur

Transported by the blood throughout the body

One may control the secretion of another

Hormonal action controlled by negative feedback

They are located throughout the body.

Hypothalamus Pituitary Thyroid Parathyroid Thymus

Hypothalamus Pituitary Thyroid Parathyroid Thymus

There are eight major glands in the endocrine system:

Pancreas Adrenals Gonads Pineal

The Endocrine The Endocrine SystemSystem

The Major Glands of the The Major Glands of the Endocrine SystemEndocrine System

Disorders of the Disorders of the PancreasPancreas

Beta Cells secrete insulin to decrease blood sugar

Alpha Cells secrete glucagon to increase blood sugar

Delta cells secrete somatostatin suppresses secretion of glucagon and insulin

Beta Cells secrete insulin to decrease blood sugar

Alpha Cells secrete glucagon to increase blood sugar

Delta cells secrete somatostatin suppresses secretion of glucagon and insulin

Disorders of the Disorders of the PancreasPancreas Glucose Metabolism

anabolism & catabolism

Glucose Metabolism anabolism & catabolism

Disorders of the Disorders of the PancreasPancreasInsulin is required for glucose

metabolism Presence of enough insulin to meet

cellular needs. Ability to bind in a manner to stimulate

the cells adequately. When unable to obtain energy from

glucose, the body begins to use fatty stores.

•Ketones and ketosis.

Regulation of Blood Glucose Hypoglycemia and hyperglycemia Role of pancreas, liver, and kidneys Osmotic diuresis and glycosuria

Insulin is required for glucose metabolism

Presence of enough insulin to meet cellular needs.

Ability to bind in a manner to stimulate the cells adequately.

When unable to obtain energy from glucose, the body begins to use fatty stores.

•Ketones and ketosis.

Regulation of Blood Glucose Hypoglycemia and hyperglycemia Role of pancreas, liver, and kidneys Osmotic diuresis and glycosuria

InsulinInsulinRegulated by glucose in the

body After a meal

>>>hyperglycemia pancreas stimulates

insulin via the islet cells [beta cells]

Secretion is halted when the blood glucose is low >>>hypoglycemia

[Negative Feedback]

Regulated by glucose in the body

After a meal >>>hyperglycemia

pancreas stimulates insulin via the islet cells [beta cells]

Secretion is halted when the blood glucose is low >>>hypoglycemia

[Negative Feedback]

GlucagonGlucagon Insulin antagonist

– actions are opposite

Secreted during low levels of glucose >>>hypoglycemia

Causes glucose to move from cells, specifically the liver

Insulin antagonist – actions are opposite

Secreted during low levels of glucose >>>hypoglycemia

Causes glucose to move from cells, specifically the liver

Regulation of Insulin Regulation of Insulin SecretionSecretion

glucagon

somatostatin insulin

GLUCOSEGlut-2

Increased secretionof Insulin

Decreasesblood glucose

Liver

Releasesglucoseandketones Endocrine Pancreas

Pathogenesis Pathogenesis of Diabetesof Diabetes

Impaired Transport of Glucoseinto Cells

HYPERGLYCEMIA CELL ENERGY

breakdown offat and protein

ketogenesis

blood osmolality

cells shrink glycosuria

dehydration

thirst HR warm,dryFruity Kussmaul Comabreath resp

Diabetes MellitusDiabetes Mellitus Type I Diabetes Mellitus

Also called juvenile or insulin-dependent diabetes mellitus (IDDM).

Characterized by low production of insulin. Closely related to heredity.

Results in pronounced hyperglycemia. Symptoms of untreated Type I DM

include polydipsia, polyuria, polyphagia, weight loss, and weakness.

Untreated or noncompliant patients may progress to ketosis and diabetic ketoacidosis.

Type I Diabetes Mellitus Also called juvenile or insulin-

dependent diabetes mellitus (IDDM). Characterized by low production of

insulin. Closely related to heredity.

Results in pronounced hyperglycemia. Symptoms of untreated Type I DM

include polydipsia, polyuria, polyphagia, weight loss, and weakness.

Untreated or noncompliant patients may progress to ketosis and diabetic ketoacidosis.

Diabetes MellitusDiabetes Mellitus Type II Diabetes Mellitus

Also called adult-onset or non-insulin-dependent diabetes mellitus (NIDDM).

Results from decreased binding of insulin to cells. Related to heredity and obesity. Accounts for 90% of all diagnosed

diabetes patients. Less risk of fat-based metabolism.

Results in less-pronounced hyperglycemia. Hyperglycemic hyperosmolar nonketotic

acidosis. Managed with dietary changes and oral

drugs to stimulate insulin production and increase receptor effectiveness.

Type II Diabetes Mellitus Also called adult-onset or non-insulin-

dependent diabetes mellitus (NIDDM). Results from decreased binding of insulin

to cells. Related to heredity and obesity. Accounts for 90% of all diagnosed

diabetes patients. Less risk of fat-based metabolism.

Results in less-pronounced hyperglycemia. Hyperglycemic hyperosmolar nonketotic

acidosis. Managed with dietary changes and oral

drugs to stimulate insulin production and increase receptor effectiveness.

Diabetic Diabetic EmergenciesEmergencies

Diabetic Diabetic EmergenciesEmergencies

Diabetic Diabetic EmergenciesEmergencies Diabetic Ketoacidosis - Hyperglycemia

Pathophysiology Results from the body’s change to fat

metabolism. Continuous buildup of ketones produces

significant acidosis. Signs and Symptoms

Extended period of onset (12–24 hours). Sweet, fruity breath odor. Potassium-related cardiac dysrhythmias. Kussmaul’s respiration. Decline in mental status and coma.

Diabetic Ketoacidosis - Hyperglycemia Pathophysiology

Results from the body’s change to fat metabolism.

Continuous buildup of ketones produces significant acidosis.

Signs and Symptoms Extended period of onset (12–24 hours). Sweet, fruity breath odor. Potassium-related cardiac dysrhythmias. Kussmaul’s respiration. Decline in mental status and coma.

Diabetic EmergenciesDiabetic EmergenciesAssessment and ManagementAssessment and Management

Focused History & Physical Exam• Obtain SAMPLE and OPQRST histories.• Look for medical identification.

Management• Maintain airway and support breathing as

indicated.• Determine blood glucose level and obtain

blood sample.• If blood glucose unknown, administer 25g 50%

dextrose.• Establish IV and administer normal saline per

local protocol.• Monitor cardiac rhythm and vital signs.• Expedite transport.

Focused History & Physical Exam• Obtain SAMPLE and OPQRST histories.• Look for medical identification.

Management• Maintain airway and support breathing as

indicated.• Determine blood glucose level and obtain

blood sample.• If blood glucose unknown, administer 25g 50%

dextrose.• Establish IV and administer normal saline per

local protocol.• Monitor cardiac rhythm and vital signs.• Expedite transport.

The futureThe future

1 - Continuous glucose sensor monitors blood sugar level

2 - Data transmitted for the computer program to work out insulin dose

3 - Insulin pump delivers the dose

1 - Continuous glucose sensor monitors blood sugar level

2 - Data transmitted for the computer program to work out insulin dose

3 - Insulin pump delivers the dose

Diabetic Diabetic EmergenciesEmergencies Hyperglycemic Hyperosmolar

Nonketotic (HHNK) Coma Pathophysiology

Found in Type II diabetics. Results in blood glucose levels far

above the norm Insulin activity prevents buildup of

ketones. Sustained hyperglycemia results in

marked dehydration.• Often related to dialysis, infection, and

medications. Very high mortality rate.

Hyperglycemic Hyperosmolar Nonketotic (HHNK) Coma Pathophysiology

Found in Type II diabetics. Results in blood glucose levels far

above the norm Insulin activity prevents buildup of

ketones. Sustained hyperglycemia results in

marked dehydration.• Often related to dialysis, infection, and

medications. Very high mortality rate.

Hyperglycemic Hyperosmolar Hyperglycemic Hyperosmolar Nonketotic (HHNK) ComaNonketotic (HHNK) Coma

Signs & Symptoms Gradual onset over days. Increased urination and thirst,

orthostatic hypotension, and altered mental status.

Assessment & Management Difficult to distinguish from diabetic

ketoacidosis in the prehospital setting.

Treatment is identical to diabetic ketoacidosis.

Signs & Symptoms Gradual onset over days. Increased urination and thirst,

orthostatic hypotension, and altered mental status.

Assessment & Management Difficult to distinguish from diabetic

ketoacidosis in the prehospital setting.

Treatment is identical to diabetic ketoacidosis.

Diabetic Diabetic EmergenciesEmergencies Hypoglycemia

Pathophysiology True medical emergency resulting

from low blood glucose levels; rarely seen outside diabetics.

By the time signs and symptoms develop, most of the body’s stores have been used.

Diabetics with kidney failure are predisposed to hypoglycemia.

Hypoglycemia

Pathophysiology True medical emergency resulting

from low blood glucose levels; rarely seen outside diabetics.

By the time signs and symptoms develop, most of the body’s stores have been used.

Diabetics with kidney failure are predisposed to hypoglycemia.

HypoglycemiaHypoglycemia Signs & Symptoms

Altered mental status with rapid onset Frequently involves combativeness.

Diaphoresis and tachycardia Hypoglycemic seizure and coma

Assessment and Management Focused History & Physical Exam

Obtain SAMPLE and OPQRST histories.

Look for medical identification.

Signs & Symptoms Altered mental status with rapid

onset Frequently involves combativeness.

Diaphoresis and tachycardia Hypoglycemic seizure and coma

Assessment and Management Focused History & Physical Exam

Obtain SAMPLE and OPQRST histories.

Look for medical identification.

ManagementManagementDiabetic EmergenciesDiabetic Emergencies

• Maintain airway and support breathing as indicated.

• Determine blood glucose level and obtain blood sample.

• Establish IV access.• If blood glucose <4.0 mmol/L or is

unknown, administer 50 ml of 50% Dextrose IV.

• If IV cannot be established, administer 0.5–1.0mg glucagon intramuscularly.

• Monitor cardiac rhythm and vital signs.• Expedite transport.

• Maintain airway and support breathing as indicated.

• Determine blood glucose level and obtain blood sample.

• Establish IV access.• If blood glucose <4.0 mmol/L or is

unknown, administer 50 ml of 50% Dextrose IV.

• If IV cannot be established, administer 0.5–1.0mg glucagon intramuscularly.

• Monitor cardiac rhythm and vital signs.• Expedite transport.

The Canadian Diabetes Association 2003 Clinical Practice Guidelines recently lowered the blood glucose (sugar) target levels. Canadians with type 2 diabetes need to understand what those new levels are, and how meeting these new targets can help them stay healthy and live well with diabetes.

The Canadian Diabetes Association 2003 Clinical Practice Guidelines recently lowered the blood glucose (sugar) target levels. Canadians with type 2 diabetes need to understand what those new levels are, and how meeting these new targets can help them stay healthy and live well with diabetes.Recommended Targets for People With Diabetes*Recommended Targets for People With Diabetes*

   AICAIC A1C Fasting blood glucose / blood glucose before meals (mmol/L)

A1C Fasting blood glucose / blood glucose before meals (mmol/L)

Blood glucose two hours after eating(mmol/L)

Blood glucose two hours after eating(mmol/L)

Blood Pressure

Blood Pressure

CholesterolCholesterol

Target for most patients with diabetes Target for most patients with diabetes

=7.0%

=7.0%

4.0 to 7.04.0 to 7.0 5.0 to 10.05.0 to 10.0 130 / 80 130 / 80 LDL: below 2.5 Total Cholesterol to HDL ratio:

below 4

LDL: below 2.5 Total Cholesterol to HDL ratio:

below 4

Normal range Normal range =6.0%=6.0% 4.0 to 6.04.0 to 6.0 5.0 to 8.05.0 to 8.0   

Onset any age adultsWeight underweight obeseImmune-mediated YES NOKetoacidosis YES NOInsulin secretion NO YESBeta cell function NO YESGenetic predisposition Moderate Very

Strong

Onset any age adultsWeight underweight obeseImmune-mediated YES NOKetoacidosis YES NOInsulin secretion NO YESBeta cell function NO YESGenetic predisposition Moderate Very

Strong

Type 1

Compare Type 1 and Compare Type 1 and Type 2Type 2 Type 2

HIGHBlood Sugar

HIGHBlood Sugar

LOW Blood Sugar

LOW Blood Sugar

Increased thirst and urination

hunger

ketones in urine

aching, weak

heavy breathing

nausea,vomiting

Fatigue

seizure

Increased thirst and urination

hunger

ketones in urine

aching, weak

heavy breathing

nausea,vomiting

Fatigue

seizure

cold sweats

headache

trembling

pounding heart

sleepiness

personality change

hunger

cold sweats

headache

trembling

pounding heart

sleepiness

personality change

hunger

KNOW THE DIFFERENCEKNOW THE DIFFERENCE

DiabetesDiabetes

Now that you mastered

Diabetes Mellitus

There is More!!!!!

What is Diabetes Insipidus?

Now that you mastered

Diabetes Mellitus

There is More!!!!!

What is Diabetes Insipidus?

Grave’s Disease Pathophysiology

Probably hereditary in nature. Autoantibodies are generated that

stimulate thyroid tissue to produce excessive hormone.

Signs & Symptoms Agitation, emotional changeability,

insomnia, poor heat tolerance, weight loss, weakness, dyspnea.

Tachycardia and new-onset atrial fibrillation.

Protrusion of the eyeballs or goiters.

Grave’s Disease Pathophysiology

Probably hereditary in nature. Autoantibodies are generated that

stimulate thyroid tissue to produce excessive hormone.

Signs & Symptoms Agitation, emotional changeability,

insomnia, poor heat tolerance, weight loss, weakness, dyspnea.

Tachycardia and new-onset atrial fibrillation.

Protrusion of the eyeballs or goiters.

Disorders of the Disorders of the Thyroid GlandThyroid Gland

Assessment & Management Usually arise from cardiovascular

signs/symptoms.• Manage signs and symptoms.

Thyrotoxic Crisis (Thyroid Storm) Pathophysiology

Life-threatening emergency, usually associated with severe physiologic stress or overdose of thyroid hormone.

Results when thyroid hormone moves from bound state to free state within the blood.

Assessment & Management Usually arise from cardiovascular

signs/symptoms.• Manage signs and symptoms.

Thyrotoxic Crisis (Thyroid Storm) Pathophysiology

Life-threatening emergency, usually associated with severe physiologic stress or overdose of thyroid hormone.

Results when thyroid hormone moves from bound state to free state within the blood.

Disorders of the Disorders of the Thyroid GlandThyroid Gland

Signs & Symptoms High fever (106º F or higher) Reflected in increased activity of

sympathetic nervous system.• Irritability, delirium or coma• Tachycardia and hypotension• Vomiting and diarrhea

Assessment and Management Support airway, breathing, and

circulation. Monitor closely and expedite

transport.

Signs & Symptoms High fever (106º F or higher) Reflected in increased activity of

sympathetic nervous system.• Irritability, delirium or coma• Tachycardia and hypotension• Vomiting and diarrhea

Assessment and Management Support airway, breathing, and

circulation. Monitor closely and expedite

transport.

Disorders of the Disorders of the Thyroid GlandThyroid Gland

Hypothyroidism and Myxedema Pathophysiology

Can be inherited or acquired. Chronic untreated hypothyroidism

creates myxedema.• Thickening of connective tissue in skin

and other tissues.• Infection, trauma, CNS depressents, or

a cold environment can trigger progression to a myxedemic coma.

Hypothyroidism and Myxedema Pathophysiology

Can be inherited or acquired. Chronic untreated hypothyroidism

creates myxedema.• Thickening of connective tissue in skin

and other tissues.• Infection, trauma, CNS depressents, or

a cold environment can trigger progression to a myxedemic coma.

Disorders of the Disorders of the Thyroid GlandThyroid Gland

Signs & Symptoms Fatigue, slowed

mental function Cold

intolerance, constipation, lethargy

Absence of emotion, thinning hair, enlarged tongue

Cool, pale doughlike skin

Coma, hypothermia, and bradycardia

Signs & Symptoms Fatigue, slowed

mental function Cold

intolerance, constipation, lethargy

Absence of emotion, thinning hair, enlarged tongue

Cool, pale doughlike skin

Coma, hypothermia, and bradycardia

Disorders of the Thyroid Disorders of the Thyroid GlandGland

Assessment and Management Focus on maintaining ABCs. Closely monitor cardiac and

pulmonary status. Establish IV access, but limit fluids. Expedite transport.

Assessment and Management Focus on maintaining ABCs. Closely monitor cardiac and

pulmonary status. Establish IV access, but limit fluids. Expedite transport.

Disorders of the Disorders of the Thyroid GlandThyroid Gland

Signs & Symptoms Weight gain “Moon-faced”

appearance Fat

accumulation on the upper back

Skin changes and delayed healing of wounds

Mood swings Impaired

memory or concentration

Signs & Symptoms Weight gain “Moon-faced”

appearance Fat

accumulation on the upper back

Skin changes and delayed healing of wounds

Mood swings Impaired

memory or concentration

Disorders of the Thyroid Disorders of the Thyroid GlandGland

Hyperadrenalism (Cushing’s Syndrome) Pathophysiology

Often due to abnormalities in the anterior pituitary or adrenal cortex.

May also be due to steroid therapy for nonendocrine conditions such as COPD or asthma.

Long-term cortisol elevation causes many changes.• Atherosclerosis, diabetes, hypertension• Increased response to catecholamines• Hypokalemia and susceptibility to infection

Hyperadrenalism (Cushing’s Syndrome) Pathophysiology

Often due to abnormalities in the anterior pituitary or adrenal cortex.

May also be due to steroid therapy for nonendocrine conditions such as COPD or asthma.

Long-term cortisol elevation causes many changes.• Atherosclerosis, diabetes, hypertension• Increased response to catecholamines• Hypokalemia and susceptibility to infection

Disorders of the Disorders of the Adrenal GlandAdrenal Gland

Assessment & Management Support ABCs. Use caution when establishing IV access. Report any observations indicative of

Cushing’s Syndrome to the receiving facility.

Adrenal Insufficiency (Addison’s Disease) Pathophysiology

Due to destruction of the adrenal cortex. Often related to heredity. Stress may trigger Addisonian crisis.

Assessment & Management Support ABCs. Use caution when establishing IV access. Report any observations indicative of

Cushing’s Syndrome to the receiving facility.

Adrenal Insufficiency (Addison’s Disease) Pathophysiology

Due to destruction of the adrenal cortex. Often related to heredity. Stress may trigger Addisonian crisis.

Disorders of the Disorders of the Adrenal GlandAdrenal Gland

May be related to steroid therapy.• Sudden withdrawal can trigger

Addisonian crisis.

Signs & Symptoms Progressive weakness, fatigue,

decreased appetite, and weight loss Hyperpigmentation of skin and

mucous membranes Vomiting or diarrhea Hypokalemia and other electrolyte

disturbances Unexplained cardiovascular collapse

May be related to steroid therapy.• Sudden withdrawal can trigger

Addisonian crisis.

Signs & Symptoms Progressive weakness, fatigue,

decreased appetite, and weight loss Hyperpigmentation of skin and

mucous membranes Vomiting or diarrhea Hypokalemia and other electrolyte

disturbances Unexplained cardiovascular collapse

Disorders of the Disorders of the Adrenal GlandAdrenal Gland

Assessment and Management Maintain ABCs. Closely monitor cardiac and

pulmonary status. Obtain blood glucose level and treat

for hypoglycemia if present. Establish IV and provide aggressive

fluid resuscitation. Expedite transport.

Assessment and Management Maintain ABCs. Closely monitor cardiac and

pulmonary status. Obtain blood glucose level and treat

for hypoglycemia if present. Establish IV and provide aggressive

fluid resuscitation. Expedite transport.

Disorders of the Disorders of the Adrenal GlandAdrenal Gland

SummarySummary

Endocrine Disorders and Emergencies

Endocrine Disorders and Emergencies