Unit 5: Pharmacotherapy of

Endocrinologic Disorders

ZANDRA MAE P. LISTON, RPh

Endocrine review
QUIZ
 Unit 5: Pharmacotherapy of Endocrinologic
Disorders

Unit 5 delves into the pharmacological treatments used to

manage a range of endocrinologic disorders. The endocrine
system is responsible for regulating vital processes in the
body through the secretion of hormones. When these
hormones are imbalanced, various health conditions can
arise, affecting growth, metabolism, reproduction, and
overall physiological function. The pharmacotherapy in this
unit focuses on correcting these imbalances through drug
interventions, offering relief, and improving quality of life for
patients.
TOPICS:

Hyperthyroi
dism
Growth Reproductiv Diabetes
and
Diseases e Diseases Mellitus
Hypothyroid
ism
 HYPERTHYROIDISM

Hyperthyroidism occurs
when the thyroid gland
produces an excess of
thyroid hormones (T3 and
T4), leading to an
accelerated metabolism.
 HYPERTHYROIDISM

Pathophysiology
 Triiodothyronine (T3) and thyroxine (T4) are thyroid hormones produced by the thyroid gland.

1.Regulation of Metabolism:
Both T4 and T3 are crucial in regulating the body's metabolism. They help control how the body uses energy by
influencing the rate at which cells and organs function.

2.Growth and Development:

T4 and T3 are essential for normal growth and development, particularly during childhood. They play a critical role
in the development of the brain and other organs.

3.Temperature Regulation:
These hormones help regulate body temperature by increasing the metabolic rate, which in turn generates heat.

4.Cardiovascular Function:
T4 and T3 have an impact on the heart, helping to increase heart rate and the strength of heart contractions.

5.Protein Synthesis and Breakdown:

They influence the synthesis of proteins and also affect the breakdown of proteins, carbohydrates, and fats in the
body.
 HYPERTHYROIDISM

 The pathophysiology of hyperthyroidism primarily revolves around an overactive thyroid

gland, and the main mechanisms leading to this state include:
• Graves' Disease: This is the most common cause of hyperthyroidism, an autoimmune
disorder where the body produces antibodies called thyroid-stimulating
immunoglobulins (TSIs) that bind to the thyroid-stimulating hormone (TSH) receptor on
thyroid cells. This leads to an overproduction of T3 and T4, despite low levels of TSH due to
negative feedback.
• Toxic Multinodular Goiter (Plummer’s Disease): This condition is caused by the
formation of multiple autonomously functioning thyroid nodules, which secrete excessive
thyroid hormones independently of TSH regulation.
• Thyroiditis: Inflammation of the thyroid gland can cause the release of stored thyroid
hormones into the bloodstream, leading to transient hyperthyroidism.
• Excessive Iodine Intake: Too much iodine, often from medications like amiodarone or
from iodine contrast agents used in imaging studies, can induce hyperthyroidism by
HYPERTHYROIDISM

Toxic Multinodular Goiter (Plummer’s

Graves' Disease Disease) Hashimoto’s Thyroiditis
 HYPERTHYROIDISM

Factors That May Induce or Potentiate Hyperthyroidism

• Autoimmune Disorders: In particular, Graves' disease, which is associated with genetic
predisposition (HLA-DR3, HLA-B8) and environmental triggers such as infections, stress, or
trauma.
• Excessive Iodine Intake: High intake of iodine-rich substances (e.g., iodized salt, certain
medications like amiodarone) can stimulate the thyroid gland, especially in individuals with pre-
existing thyroid conditions.
• Pregnancy: During pregnancy, the body’s demand for thyroid hormones increases, and pre-
existing thyroid disease may become exacerbated. The hormone hCG (human chorionic
gonadotropin) can also mimic TSH, potentially leading to increased thyroid hormone production.
• Medications: Drugs such as amiodarone (a class III antiarrhythmic), interferons, and certain
chemotherapy drugs can increase thyroid hormone levels by either inducing thyroiditis or
stimulating the thyroid.
• Infections or Stress: Physical or emotional stress can potentially trigger an exacerbation of
 HYPERTHYROIDISM

Clinical Presentation

1. Unexplained Weight Loss 8. Sleep Disturbances

2. 9. Menstrual Changes
Increased Heart Rate (Tachycardia)
3. 10. Enlarged Thyroid (Goiter)
Nervousness, Anxiety, or Irritability
4. Heat Intolerance and Sweating 11. Digestive Changes
5. Fatigue or Muscle Weakness 12. Eye Issues (in Graves' Disease)
6. Tremors 13. Thinning Hair and Brittle Hair
7. Increased Appetite 14. Elevated Blood Pressure
 HYPERTHYROIDISM

Therapeutic Outcomes and Pharmacotherapy

• Antithyroid Medications: Thionamides
MOA: Thionamides work by blocking the thyroid gland's ability to produce thyroid
hormones.
• Methimazole (Tapazole): The first-line drug for hyperthyroidism in most cases,
it inhibits thyroid hormone synthesis by blocking the enzyme thyroid peroxidase.
The typical dose starts at 10-30 mg daily and can be adjusted based on the
patient’s thyroid levels. Treatment generally lasts 12-18 months.
• Propylthiouracil (PTU): Another antithyroid drug, often used in Graves'
disease during pregnancy (due to its lower transfer across the placenta) or in
severe cases. It blocks both thyroid hormone synthesis and the peripheral
conversion of T4 to T3. Initial dosing typically starts at 300-600 mg daily,
divided into 3 doses, and tapered over time.
 HYPERTHYROIDISM

• Radioactive Iodine (RAI) Therapy:

• RAI therapy (I-131) involves the ingestion of radioactive iodine, which is selectively
absorbed by the thyroid gland, causing the gland to shrink and reduce hormone
production. This treatment is commonly used for Graves' disease and toxic
multinodular goiter. The usual dose is between 10-20 mCi, and the effects can
take several weeks to months to manifest.
• Thyroidectomy:
• Surgical removal of part or all of the thyroid gland may be indicated for patients with
large goiters, intolerant to antithyroid medications, or those with cancer. This is a
more invasive
 HYPOTHYROIDISM

Hypothyroidism is a
condition where the
thyroid gland is
underactive, leading
to a deficiency in
thyroid hormone
production.
 HYPOTHYROIDISM

Pathophysiology
• Primary Hypothyroidism: This occurs due to a problem within the thyroid
gland itself, such as:
• Autoimmune thyroiditis (Hashimoto’s thyroiditis): The most common cause,
where the immune system attacks the thyroid gland, impairing its ability to produce
hormones.
• Iodine deficiency: Insufficient iodine in the diet leads to reduced thyroid hormone
synthesis. This is rare in areas where iodine is added to salt.
• Thyroid surgery or radiation therapy: Removal of the thyroid or destruction of
thyroid tissue via radiation can lead to a decreased ability to produce thyroid
hormones.
• Medications: Certain drugs, such as lithium, amiodarone, and interferons, can
interfere with thyroid hormone production.
 HYPOTHYROIDISM

• Secondary Hypothyroidism: This occurs when there is insufficient secretion

of thyroid-stimulating hormone (TSH) from the pituitary gland, leading to
low thyroid hormone production. This is less common and is often caused by
pituitary tumors or hypothalamic disorders.
• Tertiary Hypothyroidism: This rare form occurs due to problems in
the hypothalamus, which leads to insufficient secretion of thyrotropin-
releasing hormone (TRH), resulting in low TSH and subsequently low thyroid
hormone levels.
 HYPOTHYROIDISM

 Factors That May Induce or Potentiate

• Autoimmune Disorders: The most common cause of hypothyroidism in developed countries

is Hashimoto’s thyroiditis, an autoimmune disorder where the immune system produces antibodies that
attack the thyroid gland, leading to its destruction over time.
• Iodine Deficiency: In regions where iodine is not supplemented in the diet, insufficient iodine can lead to
thyroid hormone deficiency. Iodine is required for the synthesis of T4 and T3.
• Medications: Drugs such as lithium (used for bipolar disorder), amiodarone (a medication for
arrhythmias), and interferon-alpha (used in cancer and viral treatments) can interfere with thyroid
hormone production.
• Pregnancy: Pregnancy-related changes can affect thyroid function. Women may
develop hypothyroidism due to Hashimoto’s thyroiditis or due to transient changes in thyroid function
during pregnancy.
• Radiation Therapy: Radiation treatment for head and neck cancers can damage the thyroid gland, leading
to hypothyroidism. Additionally, radioactive iodine treatment for hyperthyroidism may result in permanent
hypothyroidism.
• Pituitary and Hypothalamic Disorders: Tumors or other conditions affecting the pituitary or
 HYPOTHYROIDISM

Clinical Presentation
 1. Fatigue and Weakness: 8. Muscle and Joint Pain:
 2. 9. Puffy Face:
Unexplained Weight Gain:
10. Slow Heart Rate (Bradycardia):
 3. Cold Sensitivity: 11. Hoarseness or Throat Tightness:
 4. Dry Skin and Hair: 12. Elevated Blood Cholesterol:
 5. Constipation: 13. Heavy or Irregular Menstrual
 6. Depression or Low Mood: Periods:
 7. 14. Thinning Eyebrows:
Memory Problems and Brain Fog:
15. Goiter (Enlarged Thyroid):
 HYPOTHYROIDISM

 Diagnostic and Laboratory Tests

• Serum TSH (Thyroid Stimulating Hormone): The most sensitive test for diagnosing
hypothyroidism. In primary hypothyroidism, TSH levels are elevated due to the pituitary gland's
attempt to stimulate the thyroid when hormone levels are low. In secondary hypothyroidism, TSH
levels are low or normal, reflecting a problem with the pituitary or hypothalamus.
• Free T4 (Thyroxine): Low levels of free T4 confirm the diagnosis of hypothyroidism. This is the key
thyroid hormone that directly affects metabolism.
• Free T3 (Triiodothyronine): This test is usually lower in hypothyroid patients, though T3 is less
commonly tested in routine evaluation.
• Thyroid Antibodies: In cases of autoimmune hypothyroidism, such as Hashimoto’s thyroiditis,
elevated levels of thyroid peroxidase antibodies (TPO-Ab) and thyroglobulin antibodies (Tg-
Ab) are often present.
• Ultrasound: In some cases, an ultrasound of the thyroid gland may be performed if a goiter is present
to evaluate the gland's size and structure.
• Fine Needle Aspiration (FNA): If a nodule or mass is detected in the thyroid, an FNA may be used
 HYPOTHYROIDISM

Therapeutic Outcomes and Pharmacotherapy

 The mainstay of treatment is thyroid hormone replacement therapy.
• Levothyroxine (L-thyroxine):
• Levothyroxine is the most commonly prescribed medication for hypothyroidism. It is a synthetic
form of T4, which is converted into the active T3 in the body.
• Starting dose: The initial dose of levothyroxine typically ranges from 1.6 to 1.8 mcg/kg/day,
which is based on body weight. For example, for a patient weighing 70 kg, the starting dose would
be approximately 112-126 mcg/day.
• Maintenance dose: The dose is adjusted based on the patient’s TSH levels, typically aiming for a
TSH level between 0.4–4.0 mU/L. Most patients require 75-150 mcg/day.
• Adjustment: Dosages are adjusted at 6-week intervals based on laboratory tests until TSH levels
stabilize. Elderly patients or those with heart disease may need lower starting doses (e.g., 25-50
mcg/day).
• Liothyronine (T3):
• Liothyronine is a synthetic form of T3, but it is not commonly used as the primary therapy due to
its shorter half-life and potential for causing more fluctuations in hormone levels. It is sometimes
 HYPOTHYROIDISM

• Desiccated Thyroid Extract:

• Desiccated thyroid extract (e.g., Armour Thyroid) is a natural thyroid product
derived from porcine thyroid glands that contains both T3 and T4. While it may be
used by some patients, it is not recommended as first-line therapy due to potential
variability in hormone content and lack of standardized dosing.
• Therapeutic Monitoring: Patients should have regular follow-up visits to
assess their response to therapy. TSH levels should be measured every 6-8
weeks until the target range is achieved, and then annually once stable.
 GROWTH DISORDERS

Growth disorders are conditions that affect the normal growth and development of
children and adolescents. These disorders may result from hormonal imbalances,
genetic mutations, nutritional deficiencies, or other systemic conditions that
interfere with growth. The disorders can broadly be classified into conditions
associated with growth hormone deficiency (GHD), abnormalities in growth
hormone receptors, and excess growth hormone production, as well as
other conditions that affect growth indirectly.
 GROWTH DISORDERS

 Classes of Growth Disorders

• Growth Hormone Deficiency (GHD): The most common cause of growth
disorders, GHD occurs when the pituitary gland does not produce enough
growth hormone (GH), which is essential for stimulating growth in bones and
tissues.
• Acromegaly and Gigantism: These conditions are caused by excess
production of growth hormone. Gigantism occurs in children and adolescents
when excess GH causes abnormal growth of long bones, leading to abnormally
tall stature. Acromegaly occurs in adults after the growth plates have
fused, resulting in abnormal enlargement of tissues and organs, particularly
hands, feet, and facial features.
GROWTH DISORDERS
GROWTH DISORDERS
 GROWTH DISORDERS

• Dwarfism: Dwarfism is a condition in which individuals have short stature

resulting from genetic factors or hormonal deficiencies. Achondroplasia is the
most common form of genetic dwarfism, where abnormal cartilage
development leads to short limbs.
• Constitutional Growth Delay (CGD): A variation of normal growth, CGD
involves slower growth during childhood but typically catches up with peers by
the time the child reaches puberty. Children with CGD have delayed bone age
but normal final adult height.
• Nutritional Deficiency Growth Disorder: Insufficient nutrition, especially
protein and calorie intake, can stunt growth. Malnutrition can lead to failure to
thrive in infants and children.
 GROWTH DISORDERS

 Pathophysiology

• Growth Hormone Deficiency (GHD): Growth hormone is produced by the anterior

pituitary and stimulates the liver to release insulin-like growth factor 1 (IGF-1),
which promotes growth. When GHD occurs, it results in insufficient GH secretion,
leading to a reduction in IGF-1 levels and poor growth of bones and tissues.
• Acromegaly/Gigantism: These conditions are typically caused by pituitary tumors
that secrete excessive GH, which leads to elevated levels of IGF-1. In gigantism,
the excess GH affects growing bones, causing extreme height, while in acromegaly,
the excess GH leads to the thickening of bones and tissues, especially in the hands,
feet, and face, as growth plates have already fused in adults.
• Achondroplasia (Dwarfism): This is caused by mutations in the FGFR3 (Fibroblast
Growth Factor Receptor 3) gene that lead to abnormal cartilage development in the long
bones, particularly the limbs. This leads to disproportionate short stature with a
normal-sized trunk.
 GROWTH DISORDERS

• Constitutional Growth Delay (CGD): This is thought to be a variation of

normal growth, where there is a delay in skeletal maturation. These children
often have a delayed onset of puberty and tend to catch up in growth later in
life.
• Nutritional Deficiency: Inadequate nutrition, especially deficiencies in protein,
vitamins (like vitamin D), and minerals (such as zinc), can directly affect growth
processes and lead to stunted growth. In some cases, poor nutrition causes
failure to thrive, especially in infancy.
 GROWTH DISORDERS

 Factors That May Induce or Potentiate

• Genetic Factors: Mutations in the genes responsible for growth hormone
production, receptor function, or bone development are significant contributors
to growth disorders. For example, achondroplasia is caused by a dominant
mutation in the FGFR3 gene, leading to dwarfism.
• Pituitary Tumors: Tumors in the pituitary gland that overproduce growth
hormone can lead to gigantism or acromegaly, depending on the age of the
individual at the time of onset.
• Nutritional Deficiency: Lack of essential nutrients such as proteins, calories,
and vitamins can significantly affect growth, particularly in children.
• Chronic Diseases: Conditions like chronic kidney disease, celiac disease,
or hypothyroidism can lead to growth retardation due to the body’s inability to
 GROWTH DISORDERS

 Clinical Presentation
• Growth Hormone Deficiency
(GHD):
• Short stature (height significantly
below age-based growth percentiles)
• Delayed growth and development
• Proportional body size (small body
stature, normal body proportions)
• Delayed or absent puberty (lack of
pubertal changes)
• Hypoglycemia in infancy
 GROWTH DISORDERS

• Acromegaly/Gigantism:
• In gigantism: Extreme height (tall stature,
typically above 8 feet in some cases) with
proportionally long limbs
• In acromegaly: Enlarged hands and feet, facial
changes (e.g., protruding jaw, enlarged nose),
joint pain, excessive sweating, and increased risk
of cardiovascular issues.
 GROWTH DISORDERS

• Endocrine Disorders: Other hormonal imbalances, such

as hypothyroidism or sex hormone deficiencies, can interfere with growth.
For example, congenital hypothyroidism often leads to stunted growth unless
treated early with thyroid hormone replacement.
• Infections and Medications: Certain infections, such as human growth
hormone deficiency, or medications like glucocorticoids, can impair growth.
 GROWTH DISORDERS

• Achondroplasia (Dwarfism):
• Short stature with disproportionately short
limbs (arms and legs shorter than the
trunk)
• Normal intelligence and life expectancy
• Large head, broad forehead, and flattened
bridge of the nose
 GROWTH DISORDERS

• Constitutional Growth Delay (CGD):

• Slower-than-average growth during childhood, with normal height gain during
puberty
• Bone age delayed compared to chronological age
• Normal final adult height

• Nutritional Deficiency Growth Disorder:

• Delayed growth, failure to thrive in infants, underweight, and short stature in
children
• Muscle wasting, thin skin, and irritability due to malnutrition
 GROWTH DISORDERS

 Diagnostic and Laboratory Tests

• Growth Hormone Deficiency (GHD):
• IGF-1 levels: Low IGF-1 is indicative of growth hormone deficiency.
• Growth hormone stimulation tests: If GH deficiency is suspected, tests
like arginine or clonidine stimulation tests are used to stimulate GH production
and measure its response.
• MRI of the pituitary gland: To check for pituitary tumors.

• Acromegaly/Gigantism:
• IGF-1 levels: Elevated IGF-1 levels suggest excess growth hormone production.
• Oral glucose suppression test: GH levels do not decrease normally after glucose
intake in acromegaly.
• MRI of the pituitary: To identify pituitary tumors causing excess GH production.
 GROWTH DISORDERS

• Achondroplasia (Dwarfism):
• Genetic testing: Diagnosis is confirmed by identifying mutations in
the FGFR3 gene.
• X-rays: Radiographs can show characteristic features such as short, thickened
bones, particularly in the limbs.
• Constitutional Growth Delay (CGD):
• Bone age assessment: X-rays of the left hand and wrist to assess bone maturity
(delayed bone age).
• Growth charts: Slower growth velocity in early childhood but normal growth by
adolescence.
• Nutritional Deficiency Growth Disorder:
• Serum albumin and protein levels: To check for signs of malnutrition.
• Vitamin D, calcium, and zinc levels: To assess nutritional status.
 GROWTH DISORDERS

 Therapeutic Outcomes and Treatment

• Growth Hormone Deficiency (GHD):

• Recombinant human growth hormone (rhGH):
• Treatment: Somatropin (e.g., Humatrope, Norditropin, Genotropin) is the most common
therapy.
• Dosing: For children, the typical starting dose is 0.16–0.30 mg/kg/week given as
subcutaneous injections, divided into daily doses.
• Therapeutic Outcomes: Improvement in growth velocity, normalization of growth patterns,
and the onset of puberty in children with delayed development.

• Acromegaly/Gigantism:
• Surgical removal of pituitary adenomas (if present).
• Somatostatin analogs (e.g., octreotide): These inhibit GH release.
• Dosing: Octreotide is usually given at 50–200 mcg subcutaneously 2 to 3 times a day.
• GH receptor antagonists (e.g., pegvisomant) block GH effects at the tissue level.
•
 GROWTH DISORDERS

• Achondroplasia (Dwarfism):
• There is no cure, but growth hormone therapy may help in some cases to
increase height during childhood.
• Orthopedic surgeries may be needed to address joint issues.

• Nutritional Deficiency:
• Nutritional support with a focus on protein, calories, and specific vitamin or
mineral supplements as needed.
• Therapeutic Outcomes: Improved growth velocity, resolution of failure to thrive,
and normal development once proper nutrition is restored.
 REPRODUCTIVE DISORDERS

 Reproductive disorders encompass a broad range of conditions affecting both male and female
reproductive systems. These disorders can involve hormonal imbalances, structural
abnormalities, infections, and genetic factors, which may affect fertility, sexual function, or
hormonal regulation.
 The major types of reproductive disorders include:

• Female Reproductive Disorders:

• Polycystic Ovary Syndrome (PCOS)
• Endometriosis
• Premature Ovarian Insufficiency (POI)
• Uterine Fibroids
• Infertility (Male and Female Causes)
• Male Reproductive Disorders:
• Male Infertility
• Hypogonadism
• Erectile Dysfunction
 REPRODUCTIVE DISORDERS

Activity:
• Explain the pathophysiology of the disorders ; Identify the factors that may induce or
potentiate the disorders ; Describe the clinical presentation of the disorders, including
diagnostic and laboratory tests; Evaluate the therapeutic outcomes INCLUDE SPECIFIC
MEDICINES AND DOSING-HANDWRITTEN YELLOW PAPER
• Female Reproductive Disorders:
• Polycystic Ovary Syndrome (PCOS)
• Endometriosis
• Premature Ovarian Insufficiency (POI)
• Uterine Fibroids
• Infertility (Male and Female Causes)
• Male Reproductive Disorders:
• Male Infertility
• Hypogonadism
• Erectile Dysfunction
 DIABETES MELLITIS

Diabetes mellitus is a chronic metabolic disorder characterized by high blood

glucose (hyperglycemia) resulting from defects in insulin secretion, insulin action,
or both. Diabetes leads to disturbances in carbohydrate, fat, and protein
metabolism, and over time, it can lead to complications such as cardiovascular
disease, neuropathy, nephropathy, and retinopathy.
 There are two primary types of diabetes:
• Type 1 Diabetes Mellitus (T1DM): An autoimmune disorder leading to the
destruction of insulin-producing beta cells in the pancreas.
• Type 2 Diabetes Mellitus (T2DM): Characterized by insulin resistance and a
gradual decline in insulin secretion.
 DIABETES MELLITIS

 Pathophysiology

• Type 1 Diabetes Mellitus (T1DM):

• Autoimmune Destruction of Beta Cells: T1DM occurs when the body's immune system
attacks and destroys the insulin-producing beta cells in the pancreas. This leads
to absolute insulin deficiency, meaning the body cannot produce insulin to regulate
blood sugar levels.
• Hyperglycemia: Without insulin, glucose cannot enter cells for energy and accumulates in
the bloodstream, leading to high blood sugar levels.
• Type 2 Diabetes Mellitus (T2DM):
• Insulin Resistance: In T2DM, the body’s cells become resistant to the effects of insulin.
The pancreas initially compensates by producing more insulin, but over time, beta-cell
function declines.
• Relative Insulin Deficiency: Eventually, insulin production is insufficient to overcome
insulin resistance, leading to hyperglycemia.
• Impaired Insulin Action: Insulin resistance primarily affects muscle, fat, and liver cells,
 DIABETES MELLITIS

 Factors That May Induce or Potentiate

• Genetic Factors: Both T1DM and T2DM have genetic components. A family history of
diabetes significantly increases the risk, particularly for T2DM.
• Obesity: In T2DM, obesity is a major contributor to insulin resistance. Excess fat,
particularly visceral fat, leads to increased inflammation and hormonal changes that impair
insulin action.
• Age: The risk of developing T2DM increases with age, especially after 45 years.
• Sedentary Lifestyle: Lack of physical activity contributes to insulin resistance and weight
gain, both of which potentiate T2DM.
• Diet: A diet high in refined carbohydrates, processed foods, and fats can increase the risk
of T2DM by contributing to weight gain and insulin resistance.
• Autoimmune Disorders: In T1DM, genetic predisposition is combined with environmental
triggers (such as viral infections) that initiate autoimmune destruction of the pancreas.
 DIABETES MELLITIS

• Gestational Diabetes: Women who have had gestational diabetes are at an

increased risk of developing T2DM later in life.
• Other Conditions: Diseases such as hypertension, polycystic ovary
syndrome (PCOS), and dyslipidemia can increase the risk of
developing T2DM.
 DIABETES MELLITIS

 Clinical Presentation
 The clinical presentation of diabetes varies depending on the type of diabetes and the degree of
control over blood glucose levels. Common symptoms of both T1DM and T2DM include:
• Polyuria: Frequent urination due to excess glucose in the urine.
• Polydipsia: Excessive thirst due to dehydration from frequent urination.
• Polyphagia: Increased hunger due to cells being deprived of glucose.
• Fatigue: Due to inadequate glucose utilization by cells.
• Unexplained Weight Loss: In T1DM, weight loss is common because the body begins to break
down fat and muscle for energy due to a lack of insulin.
• Blurred Vision: Caused by fluctuations in blood glucose levels affecting the lens of the eye.
• Slow Healing of Wounds: A common complication of both types, particularly in poorly controlled
diabetes.
•
 DIABETES MELLITIS

 Specific Signs in Type 1 Diabetes:

• Rapid onset of symptoms: T1DM symptoms may appear suddenly, with more
severe hyperglycemia.
• Ketoacidosis: In some cases, the body produces ketones when cells cannot
access glucose, leading to diabetic ketoacidosis (DKA), a life-threatening
condition characterized by nausea, vomiting, abdominal pain, fruity-smelling
breath, and confusion.
 Specific Signs in Type 2 Diabetes:
• Gradual onset: Symptoms tend to develop more slowly in T2DM and may be
less noticeable in the early stages.
• Skin Changes: Acanthosis nigricans (dark, thick patches of skin) may appear in
 DIABETES MELLITIS

 Diagnostic Tests
• Fasting Plasma Glucose (FPG): A fasting blood test that measures blood glucose after an
overnight fast.
• Diagnosis: ≥126 mg/dL (7.0 mmol/L) indicates diabetes.

• Oral Glucose Tolerance Test (OGTT): Measures blood glucose before and after consuming a
glucose solution.
• Diagnosis: A 2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) indicates diabetes.

• Glycated Hemoglobin (HbA1c): Reflects average blood glucose levels over the past 2–3
months. It is used for monitoring long-term glucose control.
• Diagnosis: An HbA1c ≥6.5% is diagnostic of diabetes.

• Random Plasma Glucose Test: A blood test taken at any time of the day.
• Diagnosis: A random glucose level ≥200 mg/dL (11.1 mmol/L), along with symptoms of
hyperglycemia, suggests diabetes.
• Urine Tests: To check for the presence of glucose or ketones in the urine (in T1DM for signs of
 DIABETES MELLITIS

 Therapeutic Outcomes and Treatment

 Type 1 Diabetes Mellitus (T1DM)
 Treatment: Insulin therapy is the cornerstone of treatment for T1DM.

• Insulin: Insulin is required for all patients with T1DM, as they lack insulin
production.
• Rapid-acting insulins: (e.g., lispro, aspart, glulisine)
• Dosing: Typically given before meals to control postprandial glucose spikes. Dosing depends
on carbohydrate intake and blood glucose levels, usually around 1-2 units per 10–15
grams of carbohydrate.
• Long-acting insulins: (e.g., glargine, detemir, degludec)
• Dosing: Typically administered once or twice a day for basal insulin control, with dosages
based on body weight (starting dose around 0.3–0.5 units/kg/day).

• Continuous Glucose Monitoring (CGM): CGMs may be used to closely monitor

 DIABETES MELLITIS

 Treatment: In T2DM, the focus is on lifestyle changes (diet and exercise) and oral medications, with insulin
added when necessary.
• Metformin: The first-line therapy for T2DM, which works by reducing hepatic glucose production and
improving insulin sensitivity.
• Dosing: Starting dose of 500 mg once or twice daily, increasing up to 2000-2500 mg daily in divided doses.

• Sulfonylureas (e.g., glipizide, glimepiride): These stimulate insulin secretion from the pancreas.
• Dosing: Starting dose for glipizide is 5 mg once daily, adjusted based on response.

• DPP-4 Inhibitors (e.g., sitagliptin, linagliptin): These increase insulin secretion and decrease glucagon
production.
• Dosing: Sitagliptin is typically dosed at 100 mg once daily.

• SGLT-2 Inhibitors (e.g., empagliflozin, canagliflozin): These block glucose reabsorption in the kidneys,
promoting glucose excretion.
• Dosing: Empagliflozin is typically dosed at 10 mg once daily.

• Insulin Therapy: If oral medications fail to control blood glucose levels, insulin may be added, usually
starting with long-acting insulin (e.g., glargine) to provide basal insulin.
 Therapeutic Outcome: The goal for T2DM is also to maintain an HbA1c of <7%, with regular monitoring of
END
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