DISORDERS OF THE ENDOCRINE SYSTEM

ANAPHY

A. Ductless glands

• Growth and development

• Metabolism of energy // Cellular metabolism

• Muscle and adipose tissue

• Distribution // Blood sugar levels

• Sexual development // Reproductive function

• Fluid & electrolyte balance

• Inflammation and immune responses

B. Stimulus of hormone release

• Hormones: released into blood

• Control of hormone release:

◦Hormonal stimulus

◦Humoral stimulus

◦Neural stimulus

HOMEOSTASIS

A. Feedback mechanism

• Negative: results when a change in condition triggers action that reverses the change

• Positive: results in having the body react to a change by amplifying it

DISORDERS OF THE PITUITARY GLAND

ANAPHY

• Anterior and posterior lobe

• Hypophysis

• Master gland

• Controlled by hypothalamic hormones

Anterior Pituitary Gland

• Adenohypophysis — glandular component

• Hormones:

◦Somatotropin / Growth Hormone (GH)

◦Prolactin (PRL)

◦Thyroid Stimulating Hormone (TSH)

◦Adrenocorticotropic Hormone (ACTH)

◦Gonadotropic Hormones — LH & FSH

 ◦Melanocyte Stimulating Hormone

• Hyperpituitarism: hypersecretion or oversecretion of ACTH & GH

• Hypopituitarism: undersecretion or undersecretion of all hormones of adenohypophysis

HYPERPITUITARISM

• Oversecretion of anterior pituitary gland, most commonly involves ACTH & GH

• May result in Cushing’s Syndrome or Acromegaly

• Etiology:

◦Anterior pituitary gland adenoma

◦Anterior pituitary gland hyperplasia

◦Carcinoma

• Clinical manifestations:

◦Amenorrhea

◦Galactorrhea

◦Infertility

◦Impotence and loss of libido

◦Blurred/Double vision

◦Parasthesia

◦Headache

◦Nausea & vomiting

◦Seizures

• GIGANTISM
 ◦Growth hormone excess in children

◦Happens before puberty or before closure of the epiphyses

◦Etiology: pituitary adenomas or damage secondary to trauma

• ACROMEGALY

◦Growth hormone excess in adults

◦Happens after puberty or closure of the

epiphyses of the long bones

◦Etiology: pituitary adenomas and damage

secondary to trauma

◦Clinical manifestations:

‣ Enlarged bones of hands and feet

‣ Enlarged membranous bones of the face and skull

‣ Enlarged cartilaginous structure of larynx and respiratory tract

‣ Kyphosis 2 to vertebral changes

‣ Arthralgia, degenerative arthritis of the spine, hips and knees

‣ Cardiomegaly and accelerated atherosclerosis

HYPOPITUITARISM

• Undersecretion, usually involves all of interior pituitary hormones

• Etiology:

◦Destruction of pituitary lobe

◦Diseases of pituitary or hypothalamus

 ◦Radiation therapy

◦Space occupying lesions

• Clinical manifestations

◦Decreased growth in children

◦Impairment of GH secretion

◦Amenorrhea

◦Decreased libido

◦Erectile dysfunction

◦Hypogonadism

◦Cold intolerance

◦Dry skin

◦Mental dullness

◦Weakness

◦Nausea

◦Anorexia

• GROWTH HORMONE DEFICIENCY

◦Etiology

‣ Pituitary adenomas (tumors)

‣ Damage secondary to trauma

◦Congenital Growth Hormone Deficiency

‣ Decreased birth length

‣ Decrease in growth rate

 ‣ In Children:

• Normal intelligence

• Short stature (dwarfism)

• Obesity with immature facial features

• Some delay in skeletal maturation

• Delayed puberty

‣ In adults:

• Decrease in lean body mass

• Increase in fat mass

• Hyperlipidemia

• Decreased bone mineral density

• Reduced exercise capacity

• Etiology:

◦Pituitary adenomas

◦Damage secondary to trauma

• DIAGNOSTICS: ANTERIOR PITUITARY GLAND DISORDERS

◦Assessment of visual acuity and visual fields

◦CT scans and MRI are used to diagnose presence and extend of pituitary tumors

◦Serum levels of pituitary hormones

• MANAGEMENT:

◦Hypophysectomy

‣ Surgical removal of pituitary tumor through a transphenoidal approach

 ‣ Usual treatment

Posterior Pituitary Gland

• Neurophypophysis — Neural C component

• Hormones:

◦Vasopressin or antidiuretic hormone (ADH)

◦Oxytocin

Posterior Pituitary Gland Disorders

• Diabetes insipidus

• Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

DIABETES INSIPIDUS

• NEPHROGENIC DI

◦Genetic or acquired failure of renal tubules to

respond to ADH

◦Related to disorder and drugs that damage renal

tubules

• NEUROGENIC/CENTRAL DI

◦Head trauma

◦Brain tumor

◦Surgical abrasion
 ◦Surgical ablation

◦Irridation of pituitary gland

◦CNS infection

• Clinical Manifestations: cannot be controlled by

limiting fluid intake

◦Polydipsia

◦Polyuria

◦Nocturia

• Diagnostics

◦Fluid deprivation test

◦Measurement of:

‣ Plasma levels of ADH

‣ Plasma and urine osmolality

• Management

◦Replacement of ADH with synthetic vasopressin (DESMOPRESSIN)

‣ Considerations: used in caution in patients with CAD

◦Ensure adequate fluid replacement

◦Identify correct underlying intracranial pathology

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

• Excessive secretion of ADH from pituitary gland

• Etiology:
 ◦Head injury

◦Brain surgery

◦Tumor

◦Infection

• Clinical manifestations

◦Inability to excrete dilute urine

◦Weight gain due to fluid retention

◦Dilution hyponatremia

• Diagnostics

◦Serum sodium

◦Serum & urine osmolality

• Management

◦Elimination of underlying cause

◦Restricting fluid intake

◦Diuretics (Furosemide)

◦Close monitoring of I&O, daily weight, urine, blood chem,

neuro status

◦Hypertonic Saline for emergency correction of hyponatremia in severe SIADH

DRUGS FOR PITUITARY DISORDERS

GROWTH HORMONES

• Treats deficiency of GH
• Examples:

◦mecasermin

◦somatropin

• Side effects:

◦Headache

◦Vomiting

◦Fatigue

◦Muscle pain

GROWTH HORMONE RECEPTOR ANTAGONIST

• Treats acromegaly

• Examples:

◦Pegvisomant

◦Octerotide

• Side effects:

◦Diarrhea

◦Nausea

◦Blurred vision

ANTIDIURETIC HORMONES

• Treats Diabetes Insipidus

• Examples!

◦Vasopressin

◦Desmopressin acetate
• Side effects:

◦Water intoxication

◦Hypertension

• Intervention:

◦Monitor weight

◦Monitor I&O

DISORDERS OF THE THYROID GLAND

ANAPHY

• Butterfly shaped organ

• Lower neck, anterior of trachea

• Two lateral lobes connected by an isthmus

Thyroid Hormones:

• Thyroxine (T4): contains 4 iodine atoms in each molecule

• Triiodothyronine (T3): contains 3 iodine atoms in each

molecule
hyperkalemia
ponies to
depth bones
• Calcitonin/Thyrocalcitonin: secreted in response to high

plasma levels of Ca+ and reduces plasma Ca+ by

increasing deposition in bones

• Function:

◦Control cellular metabolic activity

 ◦Accelerate metabolic process

◦Enhance cell replication for growth

HYPOFUNCTION OF THE THYROID GLAND

CRETINISM/CONGENITAL HYPOTHYROIDISM

• Inadequate secretion of thyroid hormone during

fetal/neonatal development

GOITER

• Inadequate secretion of thyroid hormone during fetal or neonatal development

T ly compensatory TSH
• Iron deficiency causing low thyroid hormones causing

increased TSH

• INCREASED TSH — overproduction of thyroid hormone and

hypertrophy of thyroid gland

autoimmune thyroiditis
HYPOTHYROIDISM
Hashimoto's disease
• Suboptimal levels of thyroid hormone with

increased TSH and TRH

• Etiology:

◦Autoimmune thyroiditis (Hashimoto’s

disease)

◦Atrophy of thyroid gland

 ◦Therapy for hyperthyroidism
Abnormal 1 level
◦Iodine deficiency and excess

◦Pituitary tumors

◦Traumatic brain injury

• MYXEDEMA extremehypothyroidism

◦Advanced form of hypothyroidism

◦Presence of nonpitting mucous type

edema caused by accumulation of

hydrophilic mucopolysaccharide

substance in connective tissues throughout the body

• Clinical Manifestations:

◦Extreme fatigue

◦Hair loss

◦Brittle nails

◦Dry skin

◦Amenorrhea

◦Loss of libido

◦Lethargy

◦Weight gain

◦Generalized flowing of body functions

◦Cold intolerance — subnormal body temp

◦Puffy face and periorbital edema

 ◦Decreased GI motility

◦Impairment of muscle function

◦Pericardial and pleural effusion may develop

• Myxedema Coma

◦Decompensated state of severe hypothyroidism

◦Hypothermic and unconscious

◦May initially show signs of depression, somnolence, lethargy and diminished cognitive status

• Management

◦Synthetic Thyroid Hormone — Levothyroxine (Synthroid or Levothroid)

◦Prevention of cardiac dysfunction and monitoring of angina, ischemia and infarction

◦Prevention of medication interaction: thyroid hormones may increase blood glucose levels and

increase the pharmacological effects of other drugs

DRUGS FOR HYPOTHYROIDISM

LEVOHYROIXINE

• Side effects

◦Signs of hyperthyroidism

• Interventions

◦Monitor T3, T4 and TSH levels

◦Take drugs in the morning 30-60mins before meals

◦Monitor pulse rate in cases of hyperthyroidism

HYPERFUNCTION OF THE THYROID GLAND

HYPERTHYROIDISM
• Oversecretion of thyroid hormones

• Increased metabolic rate

• Etiology:

◦Hyperactivity of thyroid gland

◦Adenoma of thyroid and thyroiditis

◦Multibodular goiter excessive intake of thyroid hormone

◦Grave’s disease

• Clinical Manifestations

◦Nervousness and apprehensive

◦Palpitations with abnormally rapid pulse

◦Heat intolerance

◦SOB

◦Flushed, warm and moist skin — excessive sweating

◦Exopthalmos bulging of eyes

◦Pretibial myxedema

◦Increased appetite

◦Progressive weight loss

◦Fatigability and weakness

◦Tremors

◦Muscle cramps

◦Amenorrhea

◦Diarrhea
 ◦Elevated BP

◦Cardiac dysrhythmias

• Thyroid Storm

◦Acutely exaggerated manifestation of the thyrotoxic state

◦Clinical Manifestations:

‣ Very high fever

‣ Extreme cardiovascular effects

• Angina

• Congestive Failure

• Tachycardia

‣ Severe CNS effects

• Agitation

• Restlessness

• Delirium

◦Management

‣ Radioactive Iodine Therapy

• Destroys the overactive thyroid cells

• Observe for signs of thyroid storm

• CI:

◦Pregnancy and breastfeeding, to prevent fetal hypothyroidism

• Anti thyroid Medications

◦Functions
 ‣ Inhibit one or more stages in thyroid hormone synthesis or hormone release

‣ Block the utilization of iodine

‣ Reduces amount of thyroid tissue resulting to decreased thyroid hormone production

◦Propylthiouracil (PTU) / Methimazole (Tapazole)

‣ Blocks the conversion of T4 to T3

‣ Watch for signs of agranulocytosis and thrombocytopenia

• Thyroidectomy

◦Surgical removal of the thyroid gland

• Diagnostics

◦Serum TSH

◦Serum free T4

◦Serum T3 and T4

◦Fine needle aspiration biopsy

◦Thyroid scan

• Radioactive Iodine Uptake

◦Measures rate of iodine uptake by thyroid

◦Patient is administered a tracer dose of

iodine and a count over the thyroid gland,

detecting the gamma rays released from

the breakdown of iodine

PARATHYROID GLAND

• Anaphy

◦4 structures

◦Situated in the neck

◦Embedded in the posterior aspect of the thyroid gland

• Parathormone

◦Regulates calcium and phosphorus metabolism

◦Increases calcium absorption from the kidney, intestines and bones raising the blood Ca levels

◦Reduces the reabsorption of phosphate from the proximal tubule of the kidney lowering blood

phosphorus level through the urine

DRUGS FOR HYPERTHYROIDISM

• Drugs:

◦Propylthiouracil (PTU)

‣ Causes agranulocytosis
 ‣ Monitor for fever and sore throat

‣ Check CBC with differential for neutropenia

◦Methimazole

◦Potassium iodide

◦Iodine solution (Lugol’s solution)

◦Iodine 131

• Side effects:

◦Signs of hypothyroidism

• Interventions:

◦Monitor T3, T4, TSH levels

◦Monitor weight

◦Take with meals

• Foods that block thyroid gland function

◦Cruciferous veggies

◦Cauliflower

◦Cabbage

◦Turnips

◦Strawberries

◦Peaches

◦Spinach

◦Kale

◦Brussel sprouts
 ◦Radish

◦Peas

PARATHYROID DRUGS

calcitonin

HYPERPARATHYROIDISM

• Overproduction of parathormone

• Characterized by bone decalcification and the development of renal calculu containing calcium and

hypercalcemia

• Etiology:

◦Parathyroid adenomas

◦Parathyroid hyperplasia

◦Parathyroid carcinoma

◦Compensatory Response to Chronic Hypocalcemia

◦Vitamin D deficiency

◦Decreased renal activation of Vitamin D (Renal failure)

• Clinical Manifestations:

◦Hypercalcemia
 ◦Hypercalciuria due to increased renal filtration load of calcium

◦Hypophosphatemia

◦Hyperphosphaturia excreted through urine

◦Renal calculi/Kidney stones

◦Pathological fractures, deformities, kyphosis, compressional fractures of the vertebrae

◦Fatigue, muscle weakness

◦Hypertension and cardiac dysrythmias

◦Psychological effects (Psychosis) caused by the direct action of calcium on the brain and

nervous system

• Diagnostics:

◦Serum Parathromone radiommunoassay

◦Serum calcium levels

◦Bone scans and x-rays

◦Parathyroid utz, MRI

◦Fine needle aspiration biopsy

• Management:

◦Parathyroidectomy — treatment of choice

‣ Watch for hypocalcemia or tetanus

◦Hydration therapy w/ restricted Ca diet

◦Monitor manifestations of renal calculi

‣ Abdominal pain and hematuria

◦Mobility is encouraged
• Bisphosphonates

◦Treats hypercalcemia by inhibiting osteoclasts bone resorption

◦Alendronate (Fosamax)

• Calcitonin and corticosteroids

◦Combination administration given to hypercalcemia crisis

◦Reduce serum calcium levels by increasing deposition in bone

DRUGS FOR HYPERPARATHYROIDISM & HYPERCALCEMIA

• Drugs:

◦Gallium nitrate

◦Cinacalcet hydrochloride

◦Paricalcitol

◦Doxercalciferol

• Side effects:

◦Nausea

◦Vomiting

◦Diarrhea

• Interventions:

◦Foods rich in calcium

• Vitamin D function:

◦Enhances absorption of calcium in the GI tract

• Calcitonin function:

◦Decreases serum calcium and inhibits bone breakdown (resorption)

HYPOPARATHYROIDISM

• Inadequate parathormone secretion

• Deficiency of PTH results in increased blood phosphate

and decreased blood calcium levels.

• Etiology: damage to parathyroid glands during

parathyroidectomy, thyroidectomy or radical neck dissection

• Clinical Manifestations:

◦Hypocalcemia

◦Compensatory hypocalciuria due to low serum calcium

◦Hyperphosphatemia

◦Hypophosphaturia

◦Tetany secondary to hypocalcemia:

‣ Numbness

‣ Tingling and cramps in the extremities

‣ Bronchospasm

‣ Laryngeal and carpopedal spasm

◦Cardiac Dysrhythmias

◦Seizures and delirium

• Diagnostics

◦Positive Trousseau’s sign BP cuff

◦Positive Chvostek’s sign cheek contraction

◦Serum calcium levels

 ◦Serum phosphate levels

◦Increased bone density in x-rays and bone scans

• Management:

◦Monitoring for early signs of tetany and hypocalcemia in Post-Op patients of thyroidectomy,

parathyroidectomy or radical neck dissection

◦IV Calcium Gluconate: must be kept bedside for immediate treatment and tetany post

thyroidectomy to increase serum calcium levels

◦Parenteral Parathormone:

‣ Treatment of acute hypoparathyroidism with tetany

‣ Monitor closely for allergic reactions and changes in serum calcium levels

◦Provide environment free from noise, bright lights or sudden movement because of

neuromuscular irritability

◦Prepare for emergency tracheostomy, mechanical ventilation and bronchodilator agents for

respiratory distress

◦Low phosphorus and high calcium diet

◦High VitD diet to enhance calcium absorption from the GIT

ADRENAL GLAND

ANAPHY

• Pair of organs attached to the upper portion of each kidney

• Each gland is 2 glands with separate independent functions

• Adrenal Medulla
 ◦Inner portion

◦SNS (neural control)

◦Cathecolamines

• Adrenal Cortex

◦Outer portion

◦HPA Axis (hormonal control)

◦Glucocorticoids, mineralocorticoids,

androgens

Catecholamines

• Epinephrine & Norepinephrine

◦Stimulate the flight of fight response

◦Regulate metabolic pathways to promote

catabolism and stored fuels to meet caloric

needs from endogenous source

◦Decrease blood flow to tissues not needed in emergency situations

◦Increase blood flow to tissues that are important for effective fight or flight

◦Elevate blood glucose levels and the basal metabolic rate

• Glucocorticoids

◦Cortisol

‣ Influence metabolism on all organs especially on glucose metabolism — increasing blood

glucose levels
 ‣ Indirectly acts on bone by blocking calcium absorption high decreases bone cell growth

GLUCOCORTICOIDS

• Fights inflammation

• Treats allergy

• Helps cope with stress

• Examples:

◦Dexamethasone

◦Prednisone

◦Hydrocortisone

• Side effects:

◦Cushing’s Syndrome:

‣ Hypernatremia

‣ Hypokalemia

‣ Hyperglycemia

‣ Osteoporosis

‣ Weight gain

‣ Mood swings

‣ Cataracts

‣ Acne

• Interventions:

◦Monitor blood sugar

◦High K+ diet
 ◦Monitor for GI bleed

◦Take drug in the morning

• Mineralocorticoids

◦Aldosterone

◦Aldosterone functions for electrolyte metabolism — blood volume and salt balance

◦Increasing sodium ions reabsorption at the renal tubules and GI epithelium in exchange for

potassium of hydrogen ions excretion

◦Conserves water and increases blood pressure — important for fluid loss from severe

bleeding

MINERALOCORTICOIDS

Fludocortisone Acetate

• Replaces hormones in Addison’s Disease

• Side effects:

◦Signs of Cushing’s Syndrome

◦GI Bleed

• Interventions

◦ Take drugs with food or milk

◦High K+ diet

• Androgens

◦Steroid hormones that exert effects similar to those of the male sex hormones

◦Adrenal gland may also secrete small amounts of some estrogens or female sex hormones

ANDROGENS
Methyl testosterone

• Replaces androgen hormones

• Treats certain types of breast cancers

• Risk for prostate cancer

• Side effects

◦Masculinization

◦Priapism

◦Acne

• Interventions

◦Menstrual irregularities

◦Changes in libido

◦Take with food or snacks

STEROID DRUGS

• Should not be stopped abruptly

• Takes a while for adrenal gland to produce its own steroids after it is shut down from prolonged

steroid use.

• Dose must be tapered to prevent a fatal adrenal crisis

HYPERFUNCTION OF THE ADRENAL GLAND

• PHEOCHROMOCYTOMA

◦Tumor

◦Usually benign
◦Originates from chromaffim cells (neuroendocrine cells) of the adrenal medulla

◦Causes a sympathetic nervous system over activity due to increased catecholamine secretion

◦Etiology: mutated genetic inheritance

◦Clinical manifestations

‣ Hypertension

‣ Headache excessive sweating

‣ Diaphoresis

‣ Palpitations

‣ Tachycardia

‣ Flushing

‣ Tremor

‣ Hyperglycemia

◦Diagnostics:

‣ Urine and plasma levels of

catecholamines and metanephrine (MN),

a catecholamine metabolite, are the most direct and conclusive tests

‣ Clonidine (catapres) suppression test

• May be performed if plasma and urine catecholamine results are inconclusive

‣ Imaging studies:

• CT scan

• MRI

• UTZ
 ◦Management:

‣ Bed rest with of bed elevated promoting orthotic decrease in blood pressure

‣ Close monitoring with ECG changes and careful administration of anti-hypertensives

‣ Adrenalectomy

• Surgical removal of the tumor

• Definitive treatment

• Hypotension and hypoglycemia may occur in the post-op period because of sudden

withdrawal of excessive amount of catecholamine

• Manipulation of the tumor during surgical incision may cause release of stored

epinephrine and norepinephrine with marked increases in blood pressure and

changes in the heart rate

• CUSHING’S SYNDROME cortisol

◦Excessive adrenocortical activity

◦Symptoms are a result of over secretion of

glucocorticoids and androgens

◦Mineralocorticoid secretion may also be affected

◦Etiology:

‣ Excessive use of corticosteroids medication

‣ Hyperplasia of the adrenal cortex

‣ Tumor of the pituitary gland

‣ Ectopic and non-pituitary ACTH secreting tumor

◦Clinical manifestations:
 ‣ Glucose intolerance and insulin

resistance

‣ Hyperglycemia

‣ Immunosuppresion

‣ Weight gain

‣ Truncal obesity: heavy trunk with thin

extremities

‣ Buffalo hump and moon face

‣ Arrest of growth

‣ MSK changes: osteoporosis, kyphosis, compression fractures

‣ Muscle wasting due to increased catabolism of proteins

‣ Thin fragile skin with ecchymosis and striae

‣ Weakness

‣ Hypertension or heart failure

‣ Virilization:

• Appearance of mascular traits and recession of feminine traits: hirituism, atrophy of

breast, clitoris enlarges, voice depends and loss of libido

‣ Mood changes and psychosis may occur

‣ Gastric ulceration and bleeding

◦Diagnostics

‣ Dexamethasone suppression test

• Widely used and most sensitive

 ‣ Increased serum sodium levels

‣ Decreased potassium levels

‣ Serum glucose levels

‣ Serum and 24hr urine cortisol levels

‣ Serum radioimmunoassay of ACTH

‣ CT, MRI, IUTZ to localize tumors

◦Management

‣ Transsphenoidal hypophysectomy

• Surgical removal of the pituitary tumor

‣ Radiation of the pituitary gland

‣ Adrenalectomy — Treatment of choice with primary hypertrophy

‣ Temporary replacement therapy with hydrocortisone post operativel

HYPOFUNCTION OF ADRENAL GLAND

• ADDISON’S DISEASE Hortisol

◦Adrenocortical insufficiency occurs

◦Adrenal cortex function is inadequate to meet the patient’s need for cortical hormones

◦Etiology:

‣ Autoimmune or idiopathic atrophy

‣ Infection

‣ Surgical removal of adrenal glands

‣ Corticosteroid use
 ‣ Rapid withdrawal resulting to adrenal cortical

atrophy

‣ Pituitary gland hyposecretion

◦Clinical manifestations:

‣ Hypoglycemia

‣ GI Symptoms and anorexia

‣ Muscle weakness

‣ Fatigue

‣ Emaciation

‣ Hyponatremia

‣ Hyperkalemia

‣ Confusion and restlessness

‣ Dark pigmentation of mucous membranes and skin of knuckles, elbows and knees

‣ Decreased cardiac output and hypotension

◦Addisonian Crisis:

‣ With disease progression and acute hypotension

• Circulatory shock

• Cyanosis

• Pallor

• Apprehension

• Rapid and weak pulse

• Rapid respirations
 • Low blood pressure

◦Diagnostics:

‣ Serum cortisol

‣ Plasma ACTH

‣ Serum glucose levels

‣ Decreased serum sodium levels

‣ Increased serum potassium levels

◦Management:

‣ Administering fluids and restoring blood circulation

‣ Corticosteroid administration with hydrocortisone

‣ Antibiotics if condition is precipitated by an infection in the adrenals

‣ Possible lifelong replacement of corticosteroids and mineralocorticoids to prevent

recurrence of adrenal insufficiency

‣ IV administering of fluids, glucose and electrolytes

DISORDERS OF THE ENDOCRINE PANCREAS

ANAPHY

• Relies on humoral control

• Influenced also by neural factors for enzymatic and hormonal secretion

• Exocrine pancreas: secretion of pancreatic enzymes in to the GIT through the pancreatic duct

• Endocrine pancreas: secretion of insulin, glucagon and somatostatin directly into the bloodstream

ENDOCRINE PANCREAS
• Islet of Langerhans

◦Collection of cells embedded in the pancreatic

tissue

◦Alpha cells — glucagon

◦Beta cells — insulin

◦Delta cells — somatostatin

• Insulin

◦Lowers blood glucose levels

◦Stimulate glycogenesis

◦Transports and metabolizes glucose for energy

◦Inhibits glycogenolysis & gluconeogensis

◦Enhances storage of dietary fat in adipose tissue

◦Accelerates transport of amino acids (from dietary protein) into cells

• Glucagon

◦Raises blood glucose levels

◦Stimulates glycogenolysis

• Hypopituitarism

◦Growth hormone inhibiting hormone (GHIH)

◦Lower blood glucose levels by inhibiting GH and glucagon release

Nutrient Metabolism and Storage

• Carbohydrates
 ◦Glucose — quick source of energy and fuel needed for vital functions

◦Glycogen — stored from glucose in liver

◦Glycogenesis — conversion of extra glucose into glycogen in liver

◦Glycogenolysis — conversion of extra

glucose into glycogen in liver

◦Glycogenolysis — conversion of glycogen

back to glucose in liver during hypoglycemia

• Fats

◦Most efficient form of fuel storage

◦When there is high saturation of glycogen,

excess glucose is converted into fatty acids stored as triglycerides

• Proteins

◦Essential for formation of all body structure

‣ Genes, enzymes, muscles, bone matrix & blood

◦Amino acids are the building blocks of proteins

• Fats & Proteins

◦Gluconeogenesis

◦Generation of glucose from non-carbohydrate carbon substances such as fatty acids and

amino acids in the liver, especially during hypoglycemia

DIABETES MELLITUS

• Group of metabolic diseases

• Characterized by increased levels of glucose in blood (hyperglycemia) resulting from defects in

insulin action and secretion

• Risk Factors:

◦Family history of DM

◦45yo+

◦History of gestational diabetes

◦High HDL cholesterol levels and

triglyceride levels

◦Obesity

◦Hypertension

• INSULIN DEPENDENT DIABETES

MELLITUS (IDDM)

◦Type 1 DM Ming
◦Acute onset

◦Before 30 years of age

◦Etiology: destruction of pancreatic beta cells

due to genetic, immunologic and possibly

environmental factors (viral)

• NON INSULIN DEPENDENT DIABETES MELLITUS (NIDDM)

◦Type 2 DM

◦Occurs randomly in people older than 30yo and obese

◦Etiology:
 ‣ Insulin resistance

‣ Impaired insulin resistance due to genetic factors

• GESTATIONAL DIABETES MELLITUS (GDM)

◦Any degree of glucose intolerance during pregnancy

◦Occurs in 14% of pregnant women

◦Increases risk for HPN disorders during pregnancy

◦Etiology: secretion of placental hormones leading to insulin resistance

• Clinical manifestations:

◦Hyperglycemia

◦Glycosuria

◦Osmotic diuresis

◦Polyuria

◦Polydipsia

◦Polyphagia

◦Fatigue and weakness

◦Ketonuria

◦Vision changes

◦Tingling or numbness in hands and feet

◦Slow healing ounces and lesions

◦Recurrent infections

◦Weight loss

• Diagnostics:
 ◦Fasting blood sugar

◦Random blood sugar

◦Postprandial sugar

◦HGBA1C/Haemoglobin A1C (glycohemoglobin/glycated hemoglobin/glycosated hemoglobin)

◦Oral glucose tolerance test (OGTT)

◦Urine glucose and ketone levels — urine

dipstick

◦Urine test for albumin

◦Serum cholesterol and triglyceride levels

• Management:

◦Goal: normalize insulin activity and blood glucose levels to reduce the development of

vascular and neuropathic complication

◦Nutritional Theraphy:

‣ Nutrition and meal planning

‣ Weight control, weight loss for obese patients

◦Exercise:

‣ Increases the glucose uptake by body muscles

‣ Improves insulin utilization

◦Self monitoring of blood glucose

‣ Enables diabetic people to adjust their treatment regimen

‣ To obtain optimal blood glucose control

‣ Continuous Glucose Monitoring System (CGMS): Uses a sensor attached to an infusion

 set inserted subq @ abdomen and connected to the

device worn on a belt

• Pharmacological Therapy

◦Insulin

‣ Basal Insulin/Background Insulin: necessary to

maintain blood glucose levels irrespective of meals

‣ Types of insulin:

• Rapid acting

◦Rapid onset

◦Short duration

◦Instruct patient to eat no more

than 5 to 15 minutes after

injection

◦Used with intermediate acting

insulins

◦CLEAR

◦AKA:

‣ Insulin Aspart (NovoLog)

‣ Insulin Glulisine (Apidra)

‣ Insulin Lispro (Humalog)

◦ONSET: 15 MINUTES

◦PEAK: 30-90 MINUTES

 ◦DURATION: 3-5 HOURS

◦IMPLICATION!

‣ Given immediately before meals

‣ SQ or IV

‣ MAY MIX WITH NPH INSULIN

• Short acting

◦Regular insulin

◦Clear solution

◦Given 20 to 30 min before meals, either alone or in combination with

intermediate acting insulins

◦Approved for IV use

◦CLEAR

◦AKA:

‣ Insulin regular (Humulin R, Novolin R)

‣ ONSET: 30 - 60 MINUTES

‣ PEAK: 2 - 4 HOURS

‣ DURATION: 5 - 8 HOURS

‣ IMPLICATION:

• Given 30 minutes BEFORE meals

• SQ or IV

• MAY MIX WITH NPH INSULIN

• Intermediate acting
 ◦Appear white and cloudy

◦May function as basal insulins but split into 2 injections for 24hr coverage

◦Often combined with rapid or short acting insulins

◦CLOUDY

◦AKA:

‣ Insulin NPH human (Humulin N, Novolin N)

◦ONSET: 1 - 3 HOURS

◦PEAK: 8 HOURS

◦DURATION: 12 - 16 HOURS

◦IMPLICATION

‣ Lowers blood glucose elevations when RA insulins stop working

‣ SQ

‣ May mix with RA or SA insulin

• Long acting

◦Approved for use as basal insulin

◦Absorbed very slowly for 24hr and is given OD

◦Not mixed with other insulins for it may cause precipitation

◦Lowers blood glucose when rapid acting insulins stop working

◦CLEAR

◦AKA:

‣ Insulin Glargine (Lantus, Toujeo)

‣ Insulin Detemir (Levemir)

 ◦ONSET: 1 HOUR

◦PEAK:

‣ Lantus — NO PEAK

‣ Levemir — 6 TO 8 HOURS

◦DURATION: 20 TO 24 HOURS

◦IMPLICATIONS:

‣ Lowers blood glucose elevations when RA insulins stop working

‣ SQ

‣ Usually taken OD

‣ May mix with RA or SA insulin

• Mixed Insulin

◦CLOUDY

◦AKA:

‣ Humulin 70/30

‣ Novolin 70/30

‣ Region 70/30

◦ONSET: 30 MINS

◦PEAK: 2 TO 12 HOURS

◦DURATION: 24 HOURS

◦IMPLICATION:

‣ Usually taken OD

‣ SQ
 ‣ DO NOT MIX WITH OTHER INSULINS

‣ TIPS

• Always know the peak times of insulin medications

• Rationale:

◦It is the period where clients most likely develop hypoglycemic or insulin

reactions

‣ FAQs

• Why is insulin not given orally?

◦It is destroyed by gastric secretions.

• What are the sites for insulin injections?

◦Abdomen (preferred), posterior arm, anterior thigh, and hips.

• Why rotate injection sites?

◦To prevent lipodystrophy that will result into erratic insulin absorption.

• What is the needle gauge for insulin injection?

◦G27 - NEEDLE 29, 1/2”

• Why do we roll the insulin vial between the palms before preparation?

◦To properly dissolve the insulin solution and restores appearance

• Can an insulin vial be shaken?

◦NO, bubbles will expand insulin volume.

• How to draw insulin?

◦Draw insulin from clear vial first the cloudy to maintain the purity and clarity of

the clear solution.

 • What insulins are not compatible for mixing with other types of insulin (even though

they are clear)

◦Glargine (Lantus)

◦Insulin detemir (Levemir)

• How is insulin injected?

‣ Give SQ @ 45-90 degree angle, 45-60 degree in THIN clients

• Is aspiration needed when insulin injected?

◦NO

• What insulins can be given IV?

◦SHORT ACTING + RAPID ACTING

◦Complications of insulin therapy

‣ Local allergic reactions

‣ Systemic allergic reactions

‣ Insulin lipodystrophy

• Lipoatrophy: loss of subq fat with dimpling or pitting

• Lipohypertrophy: development of fibrofatty masses at the injection site

‣ Resistance to injected insulin

‣ Morning hyperglycemia

• Elevated blood glucose level on arising in the morning caused by insufficient level of

insulin

‣ Causes:
 • Dawn Phenomenon:

hypercalcemia at around 3am,

surges of GH secretion

increasing the need of insulin

◦Due to DECREASED effect

of bedtime insulin dose

◦HYPERGLYCEMIA occurs between 2:00 & 8:00 AM (early morning)

◦May need to INCREASE the insulin dose

• Somogyi effect: nocturnal hypoglycemia followed by rebound hyperglycemia

◦“TOO MUCH INSULIN”

◦A “rebound hyperglycemia” in response to LOW BLOOD GLUCOSE at night

◦May need to DECREASE the insulin dose or provide snacks at bedtime

• Insulin waning: progressive increase in blood glucose from bedtime to morning

‣ TIPS

• CHECK BS level between 2:00 - 3:00 AM

• Hypoglycemia consistently present (SOMOGYI PHENOMENON)

• If BS level usually high or normal — SUSPECT DAWN PHENOMENON

• Oral Antidiabetic agents

◦Oral hypoglycemic agents

‣ Used only in the treatment of DM2 (involving resistance to secreted insulin or synthetic

insulin)

‣ Sulfonylureas
 • Stimulate beta cells to secrete insulin

• May improve binding between insulin and insulin receptors or increase the number of

insulin receptors

• Glipizide, glyburide, glimepiride

‣ Biguanides

• Inhibit production of glucose by the liver and increase the body tissues sensitivity to

insulin

• Metformin

‣ Alpha-glucosidase Inhibitors

• Delay absorption of complex carbs in the intestine and slow entry of glucose into

systemic circulation

• Acarbose, miglitol

‣ Non-sulfonylurea insulin secretagogues

• Stimulate pancreas to secrete insulin

• Repaglinide, nateglinide

‣ Thiazolidinediones/Glitazones

• Sensitize body tissue to insulin

• Stimulate insulin receptor sites to lower blood glucose and improve insulin action

• Pioglitazone, rosiglitazone

‣ Dipeptidyl Peptidase-4 (DPP-4) Inhibitor

• Increase and prolog the action of incretin (hormone, increases insulin resistance &

decreasing glucagon level) with the result of improved glucose control

 • Sitagliptin, vildagliptin

• REDUCES GLUCAGON

• RISK FOR PANCREATITIS

• Ogliptin, Saxagliptin, Sitagliptin, Linagliptin

• SIDE EFFECTS:

◦Headache

◦Runny nose

◦Chills

• INTERVENTIONS

◦Report severe abdominal pain (PANCREATITIS)

• Education

◦Insulin treatment/replacement

◦Blood sugar monitoring

◦Monitoring for side effects of treatment

◦Monitoring for complications of DM

• Complications

◦HYPOGLYCEMIA

‣ Occurs when the blood glucose falls to less than 50-60mg/Dl

‣ Because of too much insulin/oral hypoglemic agents, too little food or excessive physical

activity

◦Diagnostics: serum glucose testing

◦Clinical manifestations
 ‣ Sweating

‣ Tremors

‣ Tachycardia and palpitations

‣ Nervousness

‣ Hunger

‣ Lightheadedness

‣ Confusion and memory lapses

‣ Impaired coordination

‣ Double vision

‣ Drowsiness

‣ Disoriented behavior

‣ Seizures

‣ Difficulty arousing from sleep

‣ Loss of consciousness

◦Management

‣ 15g of fast acting carbs

• 4-6oz of fruit juice, soda

• 6-10 hard candies

• 2-3tsp of sugar or honey

‣ Glucagon 1mg IM or subq

‣ 25-50ml of D50W

• DIABETIC ACIDOSIS (DKA)

◦Caused by increased fat breakdown in response to energy needs in the absence of proper

glucose utilization due to inadequate amount of insulin

◦Fat breakdown results in an increased production of ketone bodies as a byproduct causing

acidosis

◦Usually affects DM1

◦Diagnostics

‣ Serum glucose testing

‣ Low serum bicarbonate

‣ Low serum pH, 6.8 to 7.3 acidic

‣ Blood and urine ketone test

‣ ABG — low PaCO2

‣ Serum sodium and potassium

‣ Serum creatinine, BUN & HCT —

CBC

◦Clinical Manifestations

‣ Hyperglycemia

‣ Polydipsia

‣ Blurred vision

‣ Weakness

‣ Headache

‣ Orthostatic hypertension

‣ Dehydration and electrolyte loss due to polyuria

 ‣ Acidosis

‣ Abdominal pain

‣ Nausea and vomiting

‣ Hyperventilation — Kussmaul

respirations

‣ Fruity breath odor (acetone breath)

‣ Loss of consciousness

◦Management

‣ Insulin treatment Clear IV insulin mg humalorin R

‣ Fluid and electrolyte replacement

‣ Reversing acidosis through insulin treatment

• HYPERGLYCEMIC HYPEROSMOLAR NONKETONIC SYNDROME (HHNS)

◦Severe condition of hyperosmolarity and hyperglycemia with alterations of the sensorium

precipitated by an acute illness

◦Ketosis and acidosis do not occur in HHNS when compared to DKA due to the presence of

minimum insulin to prevent fat breakdown

◦Usually affects DM2

◦Diagnostics

‣ Serum glucose levels

‣ Electrolytes, serum sodium

‣ Blood urea nitrogen

‣ CBC
◦Clinical manifestations

‣ Hyperglycemia

‣ Glycosuria

‣ Polyuria

‣ Dehydration

‣ Hypernatremia and increased osmolarity

‣ Hypotension

‣ Alterations in sensorium

◦Management

‣ Fluid replacement

‣ Correction of electrolyte imbalances

‣ Insulin treatment

◦Long term complications

‣ Macrovascular Complications

• BV wall thickens and become occluded by plaque that adheres to the walls and

eventually blocks flow — atherosclerotic changes

• CAD — MI

• Cerebrovascular disease — CVA, Stroke

• Peripheral Vascular disease — DVT

‣ Microvascular complications

• Increase in blood glucose levels thickens the baseline membrane of the capillaries

into several times its normal thickeness, decreasing blood supply

 • Diabetic nephropathy

• Diabetic neuropathy

• Diabetic retinopathy

• Foot and leg problems

NOM INSULIN DRUGS FOR DM

• Amylinomimetic

◦Reduces glucagon secretion after meals

◦Examples: Primlintide

◦Side effects:

‣ Anorexia

‣ Weight loss

‣ Hypoglycemia

◦Interventions: AVOID ALCOHOL

• Glucagon-like Peptides (GLP 1 RECEPTOR ANTAGONISTS)

 ◦Increases insulin and decreases glucagon

◦All are injectable’s (SQ)

◦Incretins

‣ Hormones that stimulate insulin secretion after eating, before blood glucose become

elevated

◦Examples:

‣ Albiglutide

‣ Exenatide

‣ Liraglutide

‣ Dulaglutide

◦Side effects:

‣ Nausea and vomiting

‣ Diarrhea

‣ Dizziness

◦Interventions

‣ Report severe abdominal pain (PANCREATITIS)

• Sodium Glucose Transporter 2 (SGLT 2) inhibitors

◦Prevents the kidney from retaining glucose

◦Examples:

‣ Dapagliflozin (Farxiga)

‣ Empagliflozin

‣ Canagliflozin
 ◦Side effects:

‣ Hypotension

‣ Dehydration

‣ Glycosuria

‣ Weight loss

◦Interventions:

‣ Monitor for dehydration

• Inhaled Insulin

◦Ultra rapid insulin (faster than rapid acting)

◦Example:

‣ Afrezza

◦Side effects:

‣ Hypoglycemia

‣ Cough

‣ Sore throat

◦AVOID in asthmatic & COPD patients

What dietary alterations for Cushing's

A High protein high carbohydrate low kt
B Low carbohydrate high calorie lowsodium
c low protein high carbonate low calcium

D High carbohydrate low potassium fluid restriction

 Cushing's disease opposite of Addison's
hormones
L excess of salt sugar d sex
L moon face shape buffalo hump due to fat
distribution

L Thin fragile skin purple striae

L Low sodium TBP caution with Nat retention
L LOW sugar
L Low calorie as Px are usually overweight

what complication is the client with hypercortisolism at

greater risk
A Skin breakdown infection GI ulceration

B Anorexia constipation hypotension

C Kidney stones weight loss cataracts

D Diabetes insipidus bradycardia arthritis

Hypercortism Cushing's steroid production

steroid production
L
Heavy on 61 can cause ulcerations bleeding
L makes bones porous FRACTURES

yyyyyy.mg

Thin fragile skin

 INHALED
They are taken nonparentally

c They cannot shrink their bones

clear yellow tinged CSF hasglucose

Do not document unless all actions were taken

B There is no indication of pathogenic exposure

D 2ndpriority
 A Pituitary always give t manifestation

D We are suspecting Addisonians crisis which is a medical

emergency
A We are not done withthe situation justyet
B We don't need BP as our priority is to give medication to client
c it will not change theirmedical emergency status

prednisone steroid changes fat distribution

in months years
L moonface buffalohump

Cushing's

A Nevergivefakereassurance
B Fatdistribution will still happen withmedication
D Antagonistic response

Steroids irritateGI

never stop medications abruptly always wean off

steroids
Cause GI irritation bleeding
Hyperglycemia due to glucose
Makes bones porous fractures

Mask S S of infections

Steroids Aspirin
GI irritation
Self increasing dosage can be done at own discretion

ea

pp

It HCl production

Aldosterone Na K
normal Nat 135 145 hyponatremia
kt 3.5 5 hypokalemia

Salt substitutes have hidden Kt

L this can cause hyperkalemia

Spironolacting k sparring diuretic

L holds onto kt

This can equal to HYPERKALEMIA

Sodium is already high Causing hypernatremia

HYPERKALEMIA is a bigger priority
but

Nah
Why 101
Acetaminophen has no affect
Tumor found in abdomen kidneys
Palpating can cause cancercells to spread
Hypertensive crisis from catecholamine secretion due
to palpation

works directly against ADH

SIADH ADHT fluid retention fluid overload

Urinespecific gravity Osmolality

complications from fluid overload due to fluid retention

Pituitary Thyroid

for GHdisorders

pituitary isdoingok
viscera bone deformities acromegaly GH
Sandostatin GH release

NSAIDs are given to help w patients who have Nephrogenic

diabetes insipidus

Due to ADH they have IN

osmolarity

Giving lactate Ringer's to replace fluids

Monitor Ido

Urineoutput urine osmolality check specificgravity

Will cause further FV AKD

MIO QH
Even when DI A DM have no connection the medication
is given to strengthen the ADH action

Sulfonylurea wake up insulin during hyperglycemia

strengthen ADH action

can cause hypoglycemia

Never abmpley change medication

PX has no hx of DM so if hypoglycemia sugar
intake
Px is experiencing dry mouth

Usually for DM Px

SIADH
output serum osmolality Tunnegravity
L dil sodium due to excreted Na thru write

weare concerned w
Hinitimia areto ele Nat mosely being excreted in
urine
CNS seizures coma

2 doesn't mean effectiveness

 kidney'snot
responding

2 This is an NSAID
Pts w Dl it helps to concentrate the urine

For neurogenic DI
Contradictory

Desmopressin for neurogenic DI

PT is neurogenic DI Rx Vasopressin
Administer in evening to better hold on to PV prevent bathroom

at night promotesleep

Noaffecton this medication

The medication is IM injection
DDAVP is intranasally
Hypothyroidism
HR BP cognition a
Pt is being medicated so 5 5 should be alleviated

Synthroid speeds things up

Pt is an elderly physiological toxicity
kidney excretion suspect meds still in body

liver metabolism

hypothyroidism

Manipulation of thyroid gland after surgery

pregnant

Pt is radioactive for week

Adverse affect of PTO AGRUNOLOCYTOSIS
L Risk for infection

E
Pt w hypothyroidism
Being nervous is not a s s of hypothyroidism
l
s s for hyperthyroidism
withhold the med suspect pt to be at loxic level
ofthe hormone assess patient notify HP

significant weight changes indicates ineffectiveness of medication

Hypothyroid Pl fiber
must increase
7314 monitoring monthlyuntil seable then 6month
Medication on
empty stomach
 Myxedema extreme
hypothyroidism
hyperthypo
hyper
extremehyper

risk also stay away from soybeans t cabbage

hypothyroidism
T3 TY TSH
eldation
Parathyroid
of cholesterol triglycerides

Pangffany
kidney

Hypothyroidism has dec S S

a Patient already is an
b They are already tired
d Patient is constipated
 It decreases the edema
around the eyes
Due to the bulging of theeyes
the patient sometimes cannot
properly closetheir eyes which

can cause corneal abrasion

It is also good to decrease
salt intake for exopthalmos

storm

They wouldbein deficit

hyperthermignitability
delirium
1st priority medical emergency

hypothyroidism
chihthyroidism
418yo only
safefor
notforchildren
hyperthyroidism
Themedication canworktoowell
 Nodule agrowth

growth painless suspect cancer

hyperthyroidism
enlargement of no
extremehyperthyroidism

PostOPThyroid Surgery
L suspect the parathyroids
L Worryabout
hypokalemia

Hypocalcemia s s
Tetany
musclenerve irritation
BPcuff thingy
Tingly extremities
The cheekthing

Patient can have possible

laryngeal nerve damage edema
accumulation which can cause
airway obstruction
stethoscope

BP
Pillows wehave to make
them stay in position
 1stpriority

Hyperparathyroidism
Calcium

If Hypercalcemia Urinaryimpairment

serum calcium
dehydration

renalcalculi

soweWANT toforcefluids
a Pt is already dehydrated
c Wemust administerfluid at all times
d Acidic helps prevent cat to dump up the bacteria sticking
in the bladder
Hyperparathyroidism
HyperKalcemia
serumcalcium whichmeans
calcium depositto bone
2ndpriority
2nd risk for osteoporosis fractures
and
Patient w Dl What s s is indicative of the disorder
Polydipsia

Patient does not have enough ADH polydipsia

Pt in myxedema coma What is priority

Maintain patient armay

Myxedema extreme hypothyroidism

HR BP cognition RR

Patient w hyperthyroidism is prescribed propylthiouracil PTU

What is priority assessment
Symptoms of hypothyroidism

Hyperthyroidism
exaggerated 55
If medication workstoo well hypothyroidism

IV KCI is ordered for dehydrated Px what is priority assessment

Check urine output

Dehydrated kidney function

L Potassium should be excreted accordingly
L Build up toxicity then checkBP
 what is NOT a complication of DM
Increased perfusion these are good things
gas exchange
not a complication

DM affects most all organ structures

CV changes
Hyperglycemia
Slow wound healing due to serum glucose bacteria glucose

Microvascular changes
kidney eye changes

Pt w Phenyketonuria
PKU What are the clinical manifestations

Digestive problems
seizures PKU missinggene that
Cognitive disturbances breaks down PW
Eczema L they get toxic levels
Musty odor in arive I mostly affectsCNS

Hyperactivity

Dehydrated Pt What sts wouldyou expect to assess for

Tachycardia

Flatjugular veins Tachycardia heat willtry to compensate

230me her
Urine OP
bypushing funids
Thirst

Ratjugular due to 1 IN
Urine kidney compensatingby
retention forproper organ perfusion
Pediatric Pt w fever Nsg intervention
Remove extra clothing d blankets
provide IV fluids as ordered
Adminster acetaminophen
eyelenol

Px Pop thyroidectomy voice is hoarse d weak Nsgintervention

Teach px that this is temporary

signs of bleeding gulping frequent swallowing

labs RBC
THR IBP urineup

We only administer calcium gluconate if patient is HYPOKALEMIA

serumcalcium

tetany
BPcuff
irritation
Nene muscle

Weonly notify HCP if

Ptis in crisis
Complete assessment data
L if problem cannotbe fully resolved w Nsg interventions

DKA pt What are expected assessment findings

Fruity breath 101