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In this section, you will learn about the following topics:

•  DKA

• Hypothyroidism

• Hyperthyroidism

• Adrenal Insufficiency

DKA

Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes mellitus. It is characterized by hyperglycemia, ketosis, and metabolic acidosis. DKA primarily affects individuals with type 1 diabetes, but it can also occur in individuals with type 2 diabetes, especially during periods of stress or illness. It occurs when there is a relative or absolute deficiency of insulin in the body. Insulin is responsible for regulating blood glucose levels by facilitating the uptake of glucose into cells. In the absence of insulin, glucose cannot enter cells and accumulates in the bloodstream, leading to hyperglycemia.

The lack of insulin also triggers the breakdown of fat stores in the body as an alternative source of energy. This process, known as lipolysis, results in the release of fatty acids into the bloodstream. The liver converts these fatty acids into ketones, which are acidic byproducts of fat metabolism. In normal circumstances, ketones are efficiently metabolized and do not accumulate in significant amounts. However, in DKA, the excessive production of ketones overwhelms the body's ability to metabolize them, leading to ketosis.

The accumulation of ketones (specifically beta hydroxybuterate, or BHB) in the bloodstream causes the blood to become acidic, resulting in metabolic acidosis. Acidosis occurs when the pH of the blood falls below the normal range, impairing normal cellular function. If left untreated, severe acidosis can lead to organ dysfunction and even death.

The symptoms of DKA typically develop over a relatively short period, usually within 24 hours. Common symptoms include excessive thirst, frequent urination, abdominal pain, nausea, vomiting, fatigue, and altered mental status. As DKA progresses, individuals may experience deep and rapid breathing, known as Kussmaul breathing, as the body attempts to compensate for the acidosis.

The treatment of DKA involves a comprehensive approach aimed at correcting the underlying metabolic abnormalities and preventing complications. The main goals of treatment include:

1. Fluid replacement: DKA is associated with dehydration due to excessive urination and fluid loss. Intravenous fluids, typically isotonic saline, are administered to restore fluid balance and correct dehydration. It is important to give bolus of fluid first then start a continuous IV drip based off the glucose level (blood glucose>250, give d5 based fluid; blood glucose<250, given NS based fluid).

2. Insulin therapy: Insulin is the cornerstone of DKA treatment as it helps to lower blood glucose levels and suppress ketone production. Regular insulin is usually administered intravenously as a continuous infusion. Once the blood glucose level falls below 250 mg/dL, subcutaneous insulin may be initiated.

3. Electrolyte replacement: DKA is associated with electrolyte imbalances, including low levels of potassium, sodium, and phosphate. These imbalances need to be corrected to prevent cardiac arrhythmias and other complications. Specifically it is very important to monitor potassium levels since insulin causes potassium to shift into the cell - potassium will ALWAYS lower while on insulin. If the potassium is <3.5, you should not start an insulin drip. Electrolyte levels are closely monitored, and appropriate replacements are administered as needed.

Once the patient's condition stabilizes, and blood glucose and ketone levels are within the target range, a transition to subcutaneous insulin therapy can be initiated. The timing and dosage of subcutaneous insulin should be individualized based on the patient's needs and response to treatment.

Resources to complete:

FCCS Ch. 12 (part of it)

Marino 3rd ed: Pg 554-557; 4th ed: part of Ch 32

MedCram: DKA part 1 and 2

EM Basic Podcast Episode 12: DKA

Pulmcast - Endocrine Emergencies Part 1, DKA

Hypothyroidism

Hypothyroidism is a common thyroid disorder characterized by an underactive thyroid gland, which fails to produce enough thyroid hormones to meet the body's needs. There are several potential causes of hypothyroidism. The most common cause is an autoimmune condition called Hashimoto's thyroiditis, in which the body's immune system mistakenly attacks the thyroid gland. Other causes include surgical removal of the thyroid gland, radiation therapy to the neck area, certain medications, and congenital hypothyroidism (present at birth).

The symptoms of hypothyroidism can vary from person to person and may develop slowly over time. Some common symptoms include fatigue, weight gain, cold intolerance, dry skin, constipation, muscle weakness, depression, and memory problems. Additionally, individuals with hypothyroidism may experience menstrual irregularities, hair loss, and a hoarse voice. It is important to note that these symptoms can also be attributed to other health conditions, so a proper diagnosis is crucial.

To diagnose hypothyroidism, healthcare providers typically perform a thorough physical examination and order blood tests to measure the levels of thyroid-stimulating hormone (TSH) and thyroid hormones (T3 and T4) in the blood. Elevated TSH levels and low T3 and T4 levels are indicative of hypothyroidism.

The primary treatment for hypothyroidism is hormone replacement therapy, which involves taking synthetic thyroid hormones orally. The most commonly prescribed medication is levothyroxine, which is a synthetic form of the hormone thyroxine (T4). The dosage of medication is adjusted based on individual needs and regular monitoring of thyroid hormone levels. It is important for individuals with hypothyroidism to take their medication consistently and as prescribed to maintain optimal thyroid function.

Myxedema Coma

Myxedema coma is a rare but life-threatening condition that occurs in individuals with severe, untreated hypothyroidism. It is characterized by a significant decrease in thyroid hormone levels, leading to a slowing down of various bodily functions. It is is characterized by a profound slowing down of bodily functions. The signs and symptoms may include:

1. Hypothermia: Individuals with myxedema coma have significantly low body temperatures.

2. Bradycardia: The heart rate slows down, leading to bradycardia.

3. Respiratory depression: Breathing becomes shallow and slow, leading to respiratory depression.

4. Altered mental status: Individuals may exhibit confusion, lethargy, or even coma.

5. Swelling and puffiness: Myxedema coma can cause generalized swelling, particularly around the face, hands, and feet.

6. Dry and pale skin: The skin may appear dry, pale, and cool to the touch.

7. Constipation: Sluggish bowel movements and constipation are common symptoms of myxedema coma.

The treatment approach focuses on stabilizing the patient's vital functions and restoring thyroid hormone levels. The primary goals of treatment include hormone replacement therapy (IV levothyroxine), respiratory support if the patients breathing is severely slow, and supportive care.

Hyperthyroidism

Hyperthyroidism is a condition characterized by an overactive thyroid gland, which leads to an excessive production of thyroid hormones. This hormonal imbalance can have a significant impact on various bodily functions. The thyroid gland, located in the front of the neck, plays a crucial role in regulating metabolism and energy production in the body. When the thyroid gland becomes overactive, it produces an excess amount of thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3).

Hyperthyroidism can be caused by several factors, including Graves' disease, toxic multinodular goiter, and thyroiditis. Graves' disease is the most common cause of hyperthyroidism and is an autoimmune disorder in which the body's immune system mistakenly attacks the thyroid gland, leading to its overstimulation. Toxic multinodular goiter occurs when multiple nodules in the thyroid gland become overactive and produce excessive thyroid hormones. Thyroiditis, which can be caused by viral infections or autoimmune conditions, involves inflammation of the thyroid gland, leading to the release of stored hormones.

The symptoms of hyperthyroidism can vary from person to person, but some common signs and symptoms include:

• Weight loss: Individuals with hyperthyroidism often experience unexplained weight loss, despite having an increased appetite.

• Rapid heartbeat: An overactive thyroid can cause an increased heart rate, palpitations, and irregular heart rhythms.

• Nervousness and irritability: Hyperthyroidism can lead to feelings of restlessness, anxiety, and irritability.

• Heat intolerance: People with hyperthyroidism may have difficulty tolerating heat and may sweat excessively.

• Fatigue and muscle weakness: Despite having an increased metabolic rate, individuals with hyperthyroidism may experience fatigue and muscle weakness.

• Tremors: Fine tremors in the hands and fingers are common in hyperthyroidism.

• Changes in menstrual patterns: Women with hyperthyroidism may experience irregular menstrual periods or lighter flow.

• Changes in bowel movements: Hyperthyroidism can cause an increase in bowel movements, leading to diarrhea.

• Enlarged thyroid gland: In some cases, the thyroid gland may become enlarged, resulting in a visible swelling in the neck known as a goiter.

Thyroid Storm

Thyroid storm, also known as thyrotoxic crisis, is a rare but potentially fatal condition that occurs in individuals with untreated or poorly managed hyperthyroidism. It is characterized by a sudden and severe exacerbation of the symptoms of hyperthyroidism, leading to a cascade of physiological and metabolic disturbances. This often involves high fever, tachycardia, profuse sweating (even in cool environments), extreme anxiety/restlessness, fine tremors in the hand, nausea/vomiting, and confusion.

Medications such as propylthiouracil (PTU) or methimazole are administered to block the production of thyroid hormones. Beta-blockers like propranolol are used to control symptoms such as rapid heart rate and tremors. Intravenous fluids, electrolyte replacement, and temperature regulation are essential to maintain the patient's stability. Additional interventions may be required to address specific complications, such as antibiotics for infections or anticoagulants for thromboembolism.

Adrenal Insufficiency

Adrenal insufficiency, also known as Addison's disease, is a rare and chronic condition that occurs when the adrenal glands do not produce enough of certain hormones, particularly cortisol and sometimes aldosterone. The adrenal glands are small, triangular-shaped glands located on top of the kidneys. Despite their small size, these glands play a crucial role in maintaining overall health and well-being.

The adrenal glands are responsible for producing several hormones that are essential for various bodily functions. Cortisol, often referred to as the "stress hormone," helps regulate metabolism, blood pressure, and the body's response to stress. Aldosterone helps regulate the balance of salt and water in the body, which is important for maintaining blood pressure and electrolyte levels. When the adrenal glands fail to produce adequate amounts of these hormones, it can lead to a range of symptoms and complications. Adrenal insufficiency can be classified into two main types: primary adrenal insufficiency and secondary adrenal insufficiency.

• Primary adrenal insufficiency, also known as Addison's disease, occurs when the adrenal glands themselves are damaged or destroyed. This can be due to an autoimmune response, where the body's immune system mistakenly attacks and damages the adrenal glands. Other causes of primary adrenal insufficiency include infections, such as tuberculosis or fungal infections, and genetic disorders that affect the adrenal glands' function.

• Secondary adrenal insufficiency, on the other hand, occurs when the pituitary gland, located at the base of the brain, fails to produce enough adrenocorticotropic hormone (ACTH). ACTH is responsible for stimulating the adrenal glands to produce cortisol. Without sufficient ACTH, the adrenal glands do not receive the signal to produce cortisol, leading to adrenal insufficiency. Common causes of secondary adrenal insufficiency include pituitary tumors, pituitary surgery, or long-term use of corticosteroid medications, which can suppress the production of ACTH.

The symptoms of adrenal insufficiency can vary depending on the severity of hormone deficiency and the underlying cause. Common symptoms include fatigue, weakness, weight loss, loss of appetite, low blood pressure, dizziness, salt cravings, nausea, vomiting, abdominal pain, muscle or joint pain, and darkening of the skin. These symptoms can be vague and nonspecific, often leading to a delayed or missed diagnosis.

Blood tests are used to measure the levels of various hormones, including cortisol and adrenocorticotropic hormone (ACTH). Low cortisol levels and high ACTH levels are indicative of primary adrenal insufficiency, while low levels of both cortisol and ACTH suggest secondary adrenal insufficiency.

The diagnosis of adrenal insufficiency can be challenging, as symptoms can be nonspecific and overlap with other conditions such as sepsis. Once diagnosed, the treatment for adrenal insufficiency involves hormone replacement therapy to replace the deficient hormones. The primary hormone replacement is cortisol, which is usually taken orally in the form of hydrocortisone. In some cases, aldosterone replacement may also be necessary, particularly in primary adrenal insufficiency. This is typically achieved through the use of fludrocortisone tablets.

Adrenal Crisis

Adrenal crisis is a life-threatening condition that can occur in individuals with adrenal insufficiency. It is a medical emergency that requires immediate attention and treatment. In this section, we will explore the causes, symptoms, and management of adrenal crisis.

Adrenal crisis can be triggered by various factors, including:

• Stress: Physical or emotional stress can put a significant strain on the adrenal glands, leading to an adrenal crisis. This can include illness, surgery, trauma, or emotional distress.

• Infection: Infections, particularly severe ones such as pneumonia or sepsis, can overwhelm the body and cause the adrenal glands to fail in producing enough cortisol to meet the increased demand.

• Sudden withdrawal of corticosteroid medications: If an individual with adrenal insufficiency abruptly stops taking their prescribed corticosteroid medications, it can result in an adrenal crisis. These medications are essential for replacing the hormones that the adrenal glands are unable to produce.

• Trauma or injury: Physical trauma or injury, such as a car accident or severe fall, can lead to an adrenal crisis due to the stress it places on the body.

Symptoms of adrenal crisis include severe fatigue, abdominal pain, low blood pressure, rapid heart rate, confusion/altered mental state, and electrolyte imbalances. Treatment in the hospital involves IV fluids, glucocorticoid replacement (such as hydrocortisone), electrolyte correction and monitoring on telemetry.