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319 Cards in this Set

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Define hormone.
The endocrine's chemical messenger.

A blood-borne chemical messenger (ligand) that has an effect on target cells anatomically distant from the secreting cell.

Initiates or regulates the activity of an organ or group of cells.

"first messengers"
What are the two major classifications of hormones?
1. Water-soluble amino acid derivatives or peptide hormones (most endocrine hormones) (travel easily in plasma)
2. Lipid-soluble steroid hormones: adrenal & sex glands (require protein transport to travel in blood circulation)
Describe endocrine action.
The hormone is distributed in blood and bind to DISTANT target cells.
Describe paracrine action.
The hormone acts locally (short distance) by diffusing from its source to target cells in the neighborhood; travels in ECF.
Describe autocrine action.
The hormone acts on the same cell that produced it (very short distance); acts on itself.
Describe receptors for water soluble hormones.
Receptors for water soluble hormones are found on the surface of the target cell, on the plasma cell membrane.

These type of receptors are couple to various second messenger systems which mediate the action of the hormone in the target cell.
Describe the receptors for lipid soluble hormones.
Receptors for the lipid soluble hormones reside in the nucleus (and sometimes the cytoplasm) of the target cell.

Because these hormones can diffuse through the lipid bilayer of the plasma membrane, their receptors are located on the interior of the target cell.
What is the job(s) of the endocrine system?
Job one: maintain the optimum biochemical environment (maintain homeostasis and balance)
-controls via negative feedback
-regulates by excreting or inactivating hormones

-Takes care of the metabolic process
(1) Energy production
(2) Growth
(3) Fluid and electrolyte balance
(4) Response to stress
(5) Reproduction
(
The three endocrine system components
The CELL in which the chemical message originates in the form of a hormone.

The ENVIRONMENT in which the chemical (hormone) is transported. (Usually the bloodstream.)

The TARGET CELL which receives the chemical message (hormone). -> Goes back to original messaging cell to say, "That's enough."
Physiologic vs. Pharmacologic Hormones
Physiologic hormone concentrations are extremely low in most cases, and pharmacologic levels of hormones are usually several-fold greater than would normally be secreted by endocrine tissues.
Hormone Metabolism and Excretion
The plasma concentration of a hormone depends not only on the rate of synthesis and release of the hormone but also on how rapidly the hormone is metabolized and excreted.

Water-soluble hormones may be excrete in the urinary filtrate. Lipid-soluble hormones, which are bound to plasma proteins and stored in adipose tissues, are less readily metabolized and remain in the circulation for a more prolonged period of time.
Receptor Specificity
Refers to a molecular "fit" of a hormone within a receptor binding pocket.
Receptor Affinity
Affinity describes the degree of "tightness" of the hormone-receptor bond, or the inclination of the hormone to remain bound to the receptor. The higher the affinity of the receptor of the hormone, the lesser the amount of hormone needed to produce a response.
Down-regulation
When cells are exposed to high concentrations of hormone for a prolonged period of time, a common result is that the cell decreases the number of receptors, thus decreases the sensitivity to the hormone (i.e., insulin in obese people).

Down-regulation probably serves a protective function: the cells are protected against excessive activity despite pathologic processes that cause excessive hormone levels.
Up-regulation
An increase in the number of receptors in response to a chronically low hormone concentrations. This would make the cell more sensitive to the hormone, and hormone-dependent cellular activity would occur at normal or nearly normal levels despite a lower than normal hormone concentration.
Permissiveness
An effect that hormones have may on target cells is to increase the number of receptors for other hormones, thus enhancing the effect of the second hormone.
What are the big nine endocrine glands?
-Gonads: ovaries, testes
-Pancreas
-Thymus
-Hypothalamus
-Pituitary
-Thyroid
-Parathyroid
-Pineal
-Adrenals
Describe the anatomical location of the pituitary gland.
Connected to the hypothalamus by the pituitary stalk and sits in a bony pocket called the sella turnica.
Describe the pituitary gland.
Also called the hypophysis.
Anterior - adenohypophysis secretes 6 hormones
Posterior - neurohypophysis secretes 2 hormones
What hormones are secreted by the anterior pituitary gland?
The anterior lobe has 5 endocrine cell types that secrete 6 peptide hormones:
(1) Growth hormone [GH]
(2) Luteinizing hormone [LH]
(3) follicle-stimulating hormone [FSH]
(4) Thyroid-stimulating hormone [TSH]
(5) Adrenocorticotropic hormone [ACTH]
(6) Prolactin [PRL]
What hormones are secreted by the posterior pituitary gland?
(1) antidiuretic hormone (vasopressin)
(2) oxytocin
Describe the antidiuretic hormone.
It is secreted by the posterior pituitary gland (neurohypophysis).

It is released in response to altered serum osmolality, hypotension and when body fluid become too concentrated. It causes water retention by increasing water reabsorption by the renal collecting duct.
Describe the oxytocin hormone.
It is secreted by the posterior pituitary gland (neurohypophysis).

It is released during sexual activity, childbirth, and breast-feeding and causes uterine and milk duct contractions.
Trophic Hormones
A hormone released by the anterior pituitary gland that stimulates the release of other hormones, which then act on target organs.
Anatomical Feedback Loop of Endocrine System
CNS (+) or Input (-)
Hypothalamus
Releasing or Inhibiting Hormones
Anterior Pituitary
Trophic Hormones
Target Organs
Hormones
Physiologic Effect
What would happen to the growth hormone (GH) without the negative feedback loop?
Too much GH; can lead to giants.
What would happen to the gonadotropin hormone
without the negative feedback loop?
Sexual characteristics would appear too soon, leading to precocious puberty.
What would happen to the antidiuretic hormone (ADH) without the negative feedback loop?
If too much ADH, would lead to Syndrome of Inappropriate Antidiuretic Hormone (SIADH).

If too little ADH, would lead to diabetes insipidus.
What controls the secretion of growth hormone (GH)?
Growth hormone-releasing hormone (GHRH) and growth hormone-inhibiting hormone (somatostatin).
What controls the secretion of the prolactin (PRL) hormone?
The lactotropes secrete prolactin. Prolactin is best known for its trophic effects on breast tissue development and lactation and its ability to suppress reproductive function in both me and women.
What controls the secretion of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH)?
They are both secreted by the gonadotropin-releasing hormone. FSH and LH can also be called gonadotropins.

In general, FSH and LH stimulate testosterone production in men and estrogen and progesterone production in women.
What controls the secretion of the thyroid stimulating hormone (TSH)?
Thyrotropes release TSH in response to hypothalamic thyrotropin releasing hormone (TRH).

TSH regulates all aspects of thyroid function, including growth of the gland, hormone synthesis, and hormone secretion.
What controls the secretion of the adrenocorticotropic hormone (ACTH)?
ACTH is produced by corticotropes in the anterior pituitary gland in response to hypothalamic corticotropin-releasing hormone (CRH).

ACTH binds to the adrenal cortex and stimulates the production of cortisol and adrenal androgens. It also have trophic effects on the adrenal cortex and supports the structure and synthetic enzymes of the gland.
What type of steroids does the adrenal cortex produce?
(1) Glucocorticosteroids (cortisol)
(2) Mineralocorticoids (aldosterone)
(3) Sex steroids (androgen)

Synthesis and secretion of these hormones are considered essential for life, regulating the body's response to normal and abnormal levels of physiologic and psychological stress. The activities can be known as the "three S's": sugar, salt, and sex.
What controls the secretion of triiodothyronine (T3) and thyroxine (T4)?
The thyroid glandd secretes the thyroid hormones T3 and T4. Approximately 90% of the thyroid hormone is in the form of T4 and 10% is in the form of T3.
What controls the secretion of epinephrine and norepinephrine?
The adrenal glands are composed of an inner medulla and outer cortex. The adrenal medulla secrete epinephrine and norepinephrine in response to sympathetic nervous system stimulation.
Name the three zones of the adrenal glands.
(1) Outer zona glomerulosa
(2) Middle zona fasciculata
(3) Inner zona reticularis
What does the zona glomerulosa of the adrenal glands produce?
The outer zona glomerulosa produces the mineralocorticoid, aldosterone, in response to stimulation by angiotension II (AII).
What does the zona fasciculata of the adrenal glands produce?
The middle zona fasciculata produces the glucocorticoid, cortisol, in response to stimulation of (adrenocorticotropic hormone) ACTH from the pituitary gland.
What does the zona reticularis of the adrenal glands produce?
The inner zona reticularis is adjacent to the adrenal medulla and produces the androgen. It is stimulated by adrenocorticotropic hormone (ACT).
Describe glucocorticoids.
Glucocorticoids, principally cortisol, are named for their primary effect on glucose metabolism. Glucocorticoids oppose the effects of insulin and raise blood sugar. This is accomplished by decreasing glucose uptake by many body cells (decreased glycogenesis), increasing glucose synthesis in the liver from glycogen and amino acid and glycerol substrates in protein and fat stores (glycogenolysis, gluconeogenesis). Glucocorticoids also contribute to protein catabolism by releasing muscle stores of proteins, providing amino acids for glucose production in the liver.
Describe mineralocorticoids.
Mineralocorticoids, principally aldosterone, function to maintain normal salt and water balance by promoting sodium retention and potassium excretion at the distal renal tubules.
Where do endocrine disorders results from?
-Hormone deficiency (hyposecretion)
-Hormone excess (hypersecretion) (usually caused by exogenous ingestion of hormone such as anabolic steroid abuse)
-Hormone resistance

Hyporesponsiveness is similar to hyposecretion and is due to hormone receptor dysfunction; this phenomenon is called tissue resistance.

Almost without exception, hormone deficiency causes disease. EXCEPT for calcitonin deficiency.
The is the etiology of endocrine disorders?
It may be congenital, infectious, autoimmune, neoplastic, idiopathic, or iatrogenic.

Endocrine disorders involving control by the anterior pituitary gland common are classified as primary (intrinsic malfunction of the hormone-producing target gland) or secondary (malfunction of the hypothalamus/pituitary cells that control the hormone-producing target gland).
What are the three ways that pharmacological hormones are used?
(1) Replacement therapy (for deficiency) - insulin/DM, steroids/Addison's disease
(2) Interventional therapy (to stop disease) - steroids/inflammation (i.e., asthma)
(3) Endocrine diagnostic testing - cortisol testing for levels
What are the signs and symptoms of growth hormone excess in children?
Increased linear growth and tall stature
What are the signs and symptoms of growth hormone excess in adults?
-Soft tissue hyperplasia
-Increased bone density
-Large hands, feets
-Coarse facial features
-Thick, leathery skin
-Weight gain
-Glucose intolerance or hyperglycemia (GH is diabetogenic)
-Pts usually notice increased ring or shoe size
-enlargement of frontal sinuses cause a prominent brow
-Growth of mandible results in progressive underbite (prognathism)
-Organ enlagement (goiter, cardiomegaly); may cause arrythmia
-Deepening of voice due to vocal cord thickening and enlargement of tongue, which also results in sleep apnea
What are the signs and symptoms of growth hormone deficiency in children?
-Delayed growth
-Fine features
-Short stature, proportionate
What are the signs and symptoms of growth hormone deficiency in adults?
-May be associated with hyposecretion of other pituitary hormones
What are the clinical manifestations of growth hormone deficiency?
GH-deficient children fall below the third percentile of growth in comparison to their peers: dwarfism. Dental eruption is delayed, and the development and setting of teeth are irregular. (Overcrowded, malpositional teeth may affect nutrition.) The hair is thin, and nail growth is poor.

This does not affect intelligence, cognition, and they are able to produce normal offspring (unlike achrondoplasia).
Describe achrondoplasia.
Achrondoplasia is a common cause of dwarfism due to a mutated gene.

Children with GH deficiency are not achrondoplasic and can have produce normal offspring.
What are the clinical manifestations of growth hormone excess?
-Overgrowth of long bones, viscera and muscles: acromegaly in adults or prepubertal gigantism in kids.
-Separation of teeth and malocclusion.
What is the therapeutic management for growth hormone deficiency?
-Surgical intervention: removal (via nares) or irradiation (shrink or cause damage) of craniopharyngioma (tumor at junction of anterior and posterior pituitary gland).
-Endocrine: replacement of GH with recombinant DNA GH
-Stop GH replacement when epiphyseal closes (or will lead to acromegaly)
What is the therapeutic management for growth hormone excress?
-Surgical removal of lesion.
-Endocrine replacement of all hormones affected. (will need to replace all 8 hormones if surgically remove half of pituitary gland.)
What is the diagnosis for precocious puberty?
- Gonads (sex hormones) in excess from gonadotropin
- Very rare to see this in the U.S.
- Hypothalamic-pituitary-gonadal Axis
- Caucasian females < 7 y/o
- African American females < 6 y/o
What is the therapeutic management for precocious puberty?
- Family support and instructions on IM drug therapy
- Leuprolide acetate IM q 4 weeks. Stopped at chronologically appropriate time (use Tanner scale).
- May need GH therapy.
What is the nursing care management for precocious puberty?
- Family support. Child is chronologically age appropriate
- When child reaches puberty, care must be taken with estrogen based therapy (still have mind of child by looks attractive to others).
What can cause growth hormone deficiency?
GH deficiency may be idiopathic or related to tumors, radiation, or trauma. The Dx is confirmed by a finding of decreased GH levels in the blood or deficient GH release in response to hypoglycemia or other stimulants.
What can cause growth hormone excess?
Excessive GH production is usually due to a pituitary adenoma.
Describe the thyroid gland.
-located in middle anterior part of neck, below larynx and in front of trachea
-butterfly-shaped
-2 lobes connected by isthmus
-increase in size during puberty and pregnancy
-has rich blood supply; able to deliver high levels of hormones in short period of time
-produces Thyroxin (T4) & Tri-iodothyronine (T3)
-Calcitonin: involved in calcium and phosphate homeostasis
Describe regulation and negative feedback loop of the thyroid.
Thyrotropin hormone (TRH) in the hypothalamus stimulates thyroid-stimulating hormone (TSH) in the anterior pituitary gland. TSH stimulates all aspects of thyroid function, including the growth of the thyroid.

After some growth, TSH stimulates the thyroid to release T3 & T4.

Rising plasma levels of T3 and T4 tell the anterior pituitary gland to suppress TSH. With less TSH, the thyroid shrinks and releases less T3 & T4.
Describe T3 and T4.
Tri-iodothyronine (T3) and thyroxine (T4) are lipid-soluble and can cross the cell membrane by simple diffusion. T3 is the active form; T4 is the storage form.

T4 is converted to T3 inside all of the cells in the body to become active. Need iodine to make this occur.
What happens to the thyroid without iodine?
Iodine is necessary for the body to convert T4 to T3. Without it, the thyroid will grow bigger and bigger trying to make T3 and T4. (We do not see signs of iodine insufficiency for a while. We can store up to 1 month of T4.)
What are the major type of hypothyroidism?
(1) Congenital hypothyroidism (cretinism)
(2) Lymphocytic thyroiditis (Hashimoto thyroiditis, or autoimmune thyroiditis) is the most common cause of acquired hypothyroidism
(3) Irradiation of the thyroid gland, surgical removal of thyroid tissue, and iodine deficiency
What is primary and secondary hypothyroidism?
The majority of cases of hypothyroidism are primary, due to intrinsic dysfunction of the thyroid gland (i.e., congenital cretinism, lymphocytic thyroiditis, radiation or surgery).

Secondary hypothyroidism is caused by defects in TSH production. This includes individuals who have been exposed to severe head trauma, cranial neoplasms, brain infections, cranial irradiation, and neurosurgery.
Describe congenital hypothyroidism.
Also called cretinism. Thyroid dysgenesis (lack of thyroid gland development) accounts for most congenital hypothyroidism. Abnormal TSH receptors and defective synthesis of thyroid hormone are other mechanisms causing congenital hypothyroidism.
Describe lymphocytic thyroiditis.
Also called Hashimoto thyroiditis or auto-immune thyroiditis. Characterized by an enlarged thyroid gland caused by lymphocytic infiltration. Thyroid hormone production decreases, stimulating the release of TSH from the pituitary gland, indicating a hypoactive thyroid gland.
Describe hypothyroidism.
Primary hypothyroidism will manifest as elevated TSH. Low levels of T3 & T4 may not occur until later in the disease course (we store up to a month of T4 in body). In rare cases of hypothalamic-pituitary dysfunction results in low levels of TSH and T4.
What is myxedema?
Myxedema occurs in severe or prolonged thyroid deficiency. The term myxedema refers to the generalized, non-pitting edema that patients with long-term hypothyroidism tend to demonstrate.

These pts typically have facial puffiness and dull expressions; the edematous-looking skin is from the accumulation of glycosaminoglycans in the interstitial spaces, which then retain fluid.

Without medical intervention, pts may lapse into myxemeda coma, a medical emergency with upward of 60% mortality.
What are the clinical manifestations of hypothyroidism?
-Lethargy
-Weakness
-Dry, pale, cool, coarse skin
-Cold intolerance
-Weight gain
-Constipation
-Bradycardia
-Dyspnea, chest pain
-Sluggish return on reflexes
-Facial edema
-Heavy, prolonged menses
What diagnostic test can be utilized to discover if a pt has hypothyroidism?
We can measure TSH levels. Pts with hypothyroidism will have elevated TSH levels because of the lack of feedback exerted by the T3 & T4.
What is the etiology and pathogenesis for hyperthyroidism?
(1) Thyroid follicular cell hyperfunction with increased synthesis and secretion of T4 and T3 (Graves disease)
(2) Thyroid follicular cell destruction with release of preformed T4 and T3 (Hashimoto thyroiditis)
(3) Ingestion of excessive thyroid hormone (thyroid med/supplement) or iodide preparations (salt)
What is primary and secondary hyperthyroidism?
(1) Primary - autonomous (could be dysfunction of thyroid itself)
(2) Secondary - mediated through stimulus of TSH receptors by substances such as TSH (negative feedback loop not working)
(3) Autoimmune - related to TSH receptor antibodies
What is Graves disease?
The most common etiology of hyperthyroidism is from autoantibodies that bind and stimulate TSH receptors on the thyroid gland. This stimulation leads to a diffuse toxic goiter and a type of primary hyperthyroidism called Graves disease.
What are the clinical manifestations of hyperthyroidism?
-Changes in behavior
-Insomnia
-Restlessness
-Tremor
-Irritability
-Palpitations
-Heat Intolerance (can tolerate heat or not)
-Diaphoresis
-Inability to concentrate that interferes with work performance
-Increased basal metabolic rate leads to weight loss, although appetite and dietary intake increases
-Amenorrhea/scant menses
-Thyroid storm
What are the clinical manifestations of Graves disease?
-thyromegaly (diffused enlarged thyroid, goiter)
-thyrotoxicosis
-exophthalmos (enlargement of retro-orbital muscles causing protrusion of the eyes)

Spasm and retraction of the eyelids leads to widening of the palpebral fissure, resulting in exposed sclera. Lid lag develops, and severe, progressive exophthalmos may occur. Eye complaints may include vision changes and photophobia.
What is a thyroid storm?
It is a form of life-threatening thyrotoxicosis that occurs when excessive amounts of thyroid hormones are acutely released into the circulation. This may occur under conditions of psychological pr physiological stress or wih physical manipulation o the gland during diagnostic or surgical procedures.

It presents with the clinical features of elevated temperatures, significant tachycardia, cardiac arrythmias, and congestive heart failure. Extreme restlessness, agitation, and psychosis may occur. The pt may also experience vomiting, nausea and diarrhea; jaundice may develop due to hepatic dysfunction. Prompt Tx is required.
What is the treatment for hyperthyroidism?
Propylthiouracil (PTU), radioactive iodione, surgery
Describe the adrenal glands.
-located superiorly to the kidneys
-divided into two anatomical sections: adrenal medulla (inner) and adrenal cortex (outer)
-regulates the three "S" salt, sugar, sex
What does the adrenal cortex synthesize?
-glucocorticoids: cortisol is primary glucocorticoid and negative feedback suppresses adrenocorticotropic hormone (ACTH) release
-mineralcorticoids - aldosterone
-androgens: regulated by angiotensin II
What hormone secreted from the adrenal cortex provides negative feedback and suppresses ACTH release from the anterior pituitary gland?
Cortisol, which is the primary glucocorticoid and is synthesized in the adrenal cortex.
What is CRH?
Cortisol releasing hormone
Is adrenocortical hormone insufficiency (or Addison disease) a medical emergency?
Yes!
What is the primary etiology or pathogenesis of adrenocortical hormone insufficiency?
Hyposecretion due to disease of adrenal cortex (Addison disease).

Primary adrenal insufficiency (Addison disease) is caused by destruction of the adrenal gland through idiopathic or autoimmune mechanisms, TB, trauma or hemorrhage of the adrenals, fungal disease, and neoplasia.
Name the outer layer of the adrenal gland.
Adrenal cortex
Name the inner layer of the adrenal gland.
Adrenal medulla
What is the secondary etiology or pathogenesis of adrenocortical hormone insufficiency?
Inadequate secretion of ACTH from the anterior pituitary gland.

Secondary adrenal insufficiency (hypothalamic-pituitary dysfunction) is usually iatrogenic in origin because of the large number of patients receiving corticosteroid therapy for chronic illnesses (i.e., asthma, chronic inflammation).

Related to corticosteroid therapy can suppress ACTH, CRH. Need to gradually take pt off of steroids slowly.

May also occur due to damage of the anterior pituitary pituitary or hypothalamus by tumors, infection, radiation, postpartum necrosis (hormones go out of whack due to pregnancy), trauma, or surgery.
What is ACTH?
Adrenocorticotropic hormone, secreted from the anterior pituitary gland.
What is the tertiary etiology or pathogenesis of adrenocortical hormone insufficiency?
Lack of corticol releasing hormone (CRH) secretion from the hypothalamus due to hypothalamic malfunction or injury (i.e., croup, vascular bleed, car crash).
What is glucose intolerance and impaired glucose tolerance?
Glucose intolerance is diabetes mellitus (all types). Impaired glucose tolerance is pre-diabetes.
What is the method for diagnosing and evaluating a pt with acute adrenocortical insufficiency?
Pt history and physical exam. Decreased plasma cortisol levels -> low VS, if really bad then pt will go into shock. Acute decompensation can progress to death so rapidly that levels are drawn and therapy is initiated presumptively.
What is the method for diagnosing and evaluating a pt with chronic adrenocortical insufficiency?
ACTH provocation test may be given. Abdominal CT or MRI can be performed to determine size of adrenal glands. (Small adrenal glands occur with autoimmune destruction, whereas TB glans are large and calcified, and hemorrhagic glands are large smooth).
What is the treatment for adrenocortical insufficiency?
We need to replace the absent or deficient hormones in a manner that mimics natural production. About 2/3 of the dose will be given in the morning and 1/3 given in the evening to closely mimic the physiologic adrenal cortical function.
What is the treatment for adrenal crisis, a life-threatening situation?
IV glucocorticoids given intermittently until Sx (hypotension, hypoglycemia) resolve. IV glucocorticoids will help with cortisol replacement. This is used via a large bore needle.

In addition, volume replacement is needed to replace the increased urine output associated with renal sodium excretion.
What is the treatment for stress situations of adrenocortical insufficiency?
May need to double or triple the needed daily corticosteroid dose needs. This includes acute illness, injury (trauma, burns, surgery), and psychological episodes (psychosis).
What are the signs and symptoms of Cushing Syndrome (an adrenocortical hormone imbalance)?
-Truncal obesity
-Moon face
-Buffalo hump
-Hirsutism (abnormal growth of hair on a person's face and body, esp. on a woman)
*-Muscle wasting
*-Striae
*-Petechiae
*-Glucose intolerance (DM)
*-Hypertension
*-Hypokalemia
What are the signs and symptoms of Adrenocortical insufficiency (an adrenocortical hormone imbalance)?
-weakness
*-hypotension
*-hypoglycemia
*-hyperpigmentation (Addison disease)
*-Hyperkalemia
-weight loss
What is congenital adrenal hyperplasia?
Also called adrenogenital syndome. Occurs when an enzyme needed for cortisol production is lacking due to gene defect. Thus, circulating cortisol level is inadequate to provide negative feedback. Anterior pituitary gland continues to secrete ACTH and leads to renal hypertrophy and overproduction of androgen. Can happen at any age.

If occurs to female infant, she may have enlarged clitoris and fused labia, resembling a scrotal sac.

If occurs in female adult, she may develop lower voice, facial hair, baldness, and growth of clitoris to resemble penis.
What is hypercortisolism?
Hyperfunction of the adrenal cortex to secrete cortisol (glucocorticoid).

Also called Cushing syndrome, regardless of cause.
What is the primary etiology of hypercortisolism or adrenocortical hyperfunction?
Disease of the adrenal cortex, adrenal adenoma. (Tumor in the adrenal cortex.)
What is the secondary etiology of hypercortisolism or adrenocortical hyperfunction?
Caused by hyper function of the anterior pituitary ACTH-secreting-cells.
What is the tertiary etiology of hypercortisolism or adrenocortical hyper function?
Caused by hypothalamic dysfunction or injury.
Differentiate between Cushing syndrome and Cushing disease.
The term Cushing syndrome is used to describe the clinical features of hypercortisolism, regardless of cause.

Cushing disease is the Dx reserved for pituitary dependent conditions.
What causes hyperaldosteronism?
Excessive aldosterone production may be from primary hyperaldosteronism (Conn syndrome) or secondary to conditions associated with poor kidney perfusion, heart failure, and liver cirrhosis.
What is Conn syndrome?
Primary hyperaldosteronism, usually due to aldosterone-secreting tumors.
Is aldosterone under pituitary control?
Nope!
What does aldosterone facilitate?
Aldosterone facilitates salt and water retention by the kidney.
What happens to salt and potassium in hyperaldosteronism?
There is a high retention rate of water and salt (hypernatremia) in hyperaldosteronism; thus these pts would have decreased levels of potassium (hypokalemia).
What is the treatment for hyperaldosteronism?
The drug spironolactone is an aldosterone antagonist; it increases sodium excretion and potassium retention.

Also dietary sodium restriction (retained sodium by kidneys can lead to HTN) and potassium replacement may be necessary.
What is the function of the parathyroid glands?
The parathyroid glands detect serum calcium concentration and help maintain constant levels through the regulation of calcium absorption and resorption from bone.

The absorption of calcium from intestine and renal tubules is dependent on vitamin D and is impaired in conditions such as renal failure, where active vitamin D is deficient. (Just like thyroid being iodine dependent.)
What is PTH?
Parathyroid hormone. Serum calcium levels provide the feedback necessary to regulate PTH secretion.
Is PTH regulated by the hypothalamic-pituitary system?
Nope! It's regulated by the calcium serum levels in the body.
What causes a release of PTH?
A decrease in serum calcium causes a release of PTH. PTH increases osteoclastic activity, resulting in release of calcium from bone into extracellular fluid.
What cases a suppression of PTH?
An increase of serum calcium leads to a suppression of PTH secretion.
What are the signs and symptoms of hyperparathyroidism?
"Stones, bones, abdominal groans with psychiatric moans"

-kidney stones, nephrocalcinosis, DI, can all lead to renal failure
-bone-related complications and diseases
-GI constipation, indigestion, nausea, and vomiting
-CNS effects include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma
Describe vasopressin.
Also called antidiuretic hormone and is responsible for retaining and resorption of water (vs. diuretic drugs).

It is secreted by the posterior pituitary gland in response to changes in blood osmolality. It acts directly on the renal collecting ducts and distal tubules, increasing membrane permeability to and reabsorption of water.
What is osmolarity?
The concentration of an osmotic solution, especially when measured in osmols or milliosmols per liter of solution
What is osmolality?
The concentration of an osmotic solution, especially when measured in osmols or milliosmols per 1,000 grams of solvent
Define diabetes insipidus.
The actual term means "a large diuresis of inappropriately dilute urine."

Diabetes insipidus is a disorder of insufficient ADH activity characterized by excessive loss of water in the urine, the inability to concentrate urine, and rapid development of dehydration.
What is central DI or neurogenic DI?
There is damage to the posterior pituitary gland and may cause temporary or permanent deficiency of ADH. Thus, urine cannot be concentrated and free water is lost, causing hyperosmolality and hypernatremia.

It is the most common.
What is nephrogenic DI?
This occurs when the kidney is unable to respond to ADH because of chronic renal disease, serum electrolyte abnormalities, or drugs (i.e., lithium).
What is the hallmark signs of diabetes insipidus?
The "2 P's." Polyuria and polydispia.
Name the clinical manifestations of diabetes insipidus.
-polyuria
-polydipsia
-dehydration
-imbalance
-hypernatremia
-decrease in specific gravity of urine
-azotemia (urea in blood due to kidney insufficiency) or azothemia (nothing in urine, passing water, dilute urine?)
-possible circulatory collapse
A patient with diabetes insipidus will urinate how much?
The patient may void as much as 15L of urine daily.
How can a patient get diabetes insipid us?
-closed head trauma
-brain tumor
-hypothalamus tumor
What tests are administered to diagnose diabetes insipidus?
Individuals presenting with the sudden onset of polyuria and polydipsia should undergo laboratory studies, including tests for glucose, urine and serum electrolytes, cerum creatinine, and BUN levels.
What is the treatment for diabetes insipidus?
-restrict oral intake and observe urine output
-vasopressin SQ or IM
-CT brain scan
-kidney function tests- renal failure
-DDAVP (synthetic ADH)
-nasal spray q 8-12 hrs
What is the nursing care management for diabetes insipidus?
-early identification: enuresis (involuntary urination) with thirst
-strict i&O pre and post surgery
-instruct parents on life long therapy for SQ, IM, or nasal spray
-attach a med tag alert on pt
Differentiate between "Strict I&O" and "Restrict I&O."
Strict I&O: you need to count every amount that the pt intakes.

Restrict I&O: you can only give the pt a certain amount to intake.
What does SIADH stand for?
Syndrome of Inappropriate Antidiuretic Hormone Secretion.
Name predisposing conditions for SIADH.
-infections
-tumors
-CNS disease or trauma
Describe the clinical manifestations for SIADH.
SIADH results in hyponatremia (low sodium) because free water is retained and dilutes the serum sodium level.

Osmolality: Blood serum low and urine is high because of increased water retention. Low Na! (When you mess with gradient concentration = Sz precautions, LOC.)
What laboratory tests are used to diagnose SIADH?
Laboratory findings include low serum sodium, hematocrit, and BUN levels as a results of expansion of extracellular fluid volume.
What is the therapeutic management of SIADH?
-restrict fluids to 1/4-1/2 maintenance
-monitor electrolytes
-observe for neurologic deterioration (i.e., LOC, mentation)
What is the nursing care management for SIADH?
-early identification of at risk patients
-strick I&O
-daily weights
-Sz precautions
-instruct family/pt on fluid restrictions.
How do you tell the difference between diabetes insipidus and SIADH?
DI: polyuria, polydipsia, hypernatremia
SIADH: hyponatremia, water retention
Does a patient with diabetes insipidus have sweet smelling breath?
Nope! Don't confuse DI with diabetes mellitus.
What is the hallmark sign of SIADH?
Water retention

Also hyponatremia, hypoosmolarity with urine, hyperosmolarity
If normal daily output is 1500 mL, what is the expected output for 1 hour? For an 8 hour shift? For a 12 hour shift?
1 hr: 62.5 mL
8 hr: 500 mL
12 hr: 750 mL

We will go 1/2 of a shift and observe a patient's I&O. Then we decide whether it's insufficient and if so, call a physician for an order.
What antidiuretic hormone meds do we administer?
-Hormone extract posterior pituitary: Pitressin (vasopressin)
-Synthetic DDAVP (desmopressin)
Which ADH med is synthetic?
DDAVP (desmopressin)
Which ADH med is a hormone extract?
Pitressin (vasopressin)

*Davis's Drug Guide 13 Ed. Page 1269, Pitressin is discontinued.
What is the route administration for Pitressin (vasopressin)?
SQ and IM
What is the route administration for DDAVP (desmopressin)?
SQ, IV, PO, intranasal
What is the mechanism of action for ADH meds?
Natural (vasopressin) and synthetic (desmopressin) antidiuretics. They produce concentrated urine by increasing tubular reabsorption of water. (Make sure the pt has functional kidneys. Thus, contraindication would be renal failure, kidney disease, etc.)
ADH meds are used for what disorders?
-Diabetes Insipidus
-SIADH caused by trauma, surgery, etc.
-Bedwetting
How should we monitor the administration of ADH med therapy?
-blood pressure (because of vasopressin stimulates contraction of vascular smooth muscle and smooth muscle of the GI tract; causes vasoconstriction)
-I&O
-weight
-urine specific gravity
What is the brand name for vasopressin (ADH med)?
Pitressin
What is the brand name for desmopressin (ADH med)?
DDAVP
What is the brand name for oxytocin?
Pitocin
How is Pitocin (oxytocin) administered?
IV (add drug to IV bag after IV is started)
What is the mechanism of action in Pitocin (oxytocin)?
It enhances contractile activity of the uterine smooth muscle.
What are the uses for Pitocin (oxytocin)?
-induce or stimulate labor
-control post partum hemorrhage
-milk ejection during breastfeeding (milk ejection will not occur without oxytocin)
When administering Pitocin (oxytocin), what should we monitor for during therapy?
-accurate dose
-close monitoring of contractions (uterine may rupture)
-fetal heart monitoring during labor
What does somatostatin (in the hypothalamus) do?
It acts on the pituitary gland and inhibits growth hormone release in the anterior pituitary gland.
What human growth hormone do we administer for pts with deficient GH?
somatropin
What is the route for somatropin administration therapy?
SQ preferred because it's less painful; Im for obese pts
What is the mechanism of action for somatropin?
It promotes growth in children whose growth has been impaired by a deficiency of GH.
What do we use somatropin for?
-children with deficiency of growth hormone
-adults with deficiency of growth hormone from disease
What do we monitor for during somatropin therapy?
-Monitor for epiphyseal plate closure in children
-Monitor height and weight
How do we obtain baseline data for assessing whether a patient should receive somatropin therapy?
Assess developmental status (height, weight, etc.) and obtain laboratory data on thyroid function and GH levels.
What are the contraindications for somatropin or growth hormone therapy?
GH is contraindicated during and after epiphyseal closure, and in children with Prader-Willis syndrome (PWS) (a genetic disorder characterized by short stature, mental impairment, incomplete sexual development, behavior problems, low muscle tone, and the urge to eat constantly, which promotes obesity) who are obese or have severe respiratory impairment.

Also, use with caution in children with DM and hypothyroidism.
Name the adverse effects of somatropin (GH) therapy.
-Hyperglycemia: GH can elevate plasma glucose levels in diabetes. Increase insulin dosage as needed.
-Hypothyroidism: GH may suppress thyroid function. Assess thyroid function before treatment and periodically thereafter. If levels of thyroid hormone fall, institute replacement therapy.
-Fatality with PWS patients: Do not give to children with PWS who are severely obese or have severe respiratory impairment.
-Interaction with Glucocorticoids: Glucocorticoids can oppose the growth-stimulating effects of GH. Carefully adjust glucocorticoid replacement dosage to avoid growth inhibition.
-Neutralizing Antibodies: Antibodies that neutralize exogenous GH can develop over the course of treatment. If this happens, mecasermin (recombinant IGF-1) may be an effective alternative to GH.
Differentiate among hypothyroidism, myxedema, and cretinism.
Hypothyroidism: mild deficiency of thyroid hormone in adults.
Myxedema: severe deficiency of thyroid hormone in adults.
Cretinism: hypothyroidism in infants.
What drugs are administered for hypothyroidism?
-levothyroxine (synthetic thyroxine T4): Synthroid, Leothroid
By what route is levothyroxine administered?
-PO and IV

Levothyroxine is almost always administered by mouth; oral doses should be taken on an empty stomach because absorption is reduced by food. IV is used for myxedema coma and pts who cannot take levothyroxine orally.
What is the mechanism of action for levothyroxine?
It increases the metabolic activity of the body.
What are the uses of levothyroxine?
It is the drug of choice for all forms of hypothyroidism, regardless of cause: simple goiter, myxedema coma, cretinism, etc.
What should we monitory for when administering levothyroxine therapy?
Signs and symptoms of hyperthyroidism:
-tachycardia
-sweating
-intolerance to heat
-diarrhea
-abdominal cramping
-weight loss
-decreased bone density in the hip and spine

*You always monitor for the opposite disorder during therapy: hypo becomes hyper and vice versa.
What are the treatment options for Graves' disease?
1. surgical removal of thyroid tissue
2. destruction of thyroid tissue with radioactive iodine
3. suppression of thyroid hormone synthesis with an antithyroid drug (methimazole or propylthiouracil)

Radiation is the preferred treatment for adults, whereas antithyroid drugs are preferred for younger patients.
What drugs do we administer for hyperthyroidism?
-Methimazole (Tapazole) is the first line drug
-PTU (propylthiouracil) prototype (thyrotoxic crisis)
-Lugol's solution (strong iodine solution thyroid storm)
What is the route for methimazole, PTU, and Lugol's solution (hyperthyroid drugs)?
Oral
What is the mechanism of action for hyperthyroid meds?
PUT and Tapazole (methimazole) interfere with the synthesis of thyroid hormone and inhibits conversion of T4 to the more active T3.

Lugol's solution inhibits the release of thyroid hormones, causing them to accumulate in the thyroid gland (causes T4 to store)
What are the uses of hyperthyroid drugs?
-Short-term treatment of hyperthyroid to bring patient to euthyroid pre-op
-Decrease size and vascularity of thyroid pre-op
What should we monitor for when administering hyperthyroid drug therapy?
Monitor for hypothyroidism.

*You always monitor for the opposite disorder during therapy: hypo becomes hyper and vice versa.
Why is methimazole the first line drug for hyperthyroidism?
It is safer and more convenient than PTU, except for pregnant or breast-feeding women, or pts in thyrotoxic crisis.
What are adverse reactions to methimazole?
-Agranulocytosis is the most dangerous toxicity.
-It can convert the pt to hypothyroidism.
-Can cause neonatal hypothyroidism, goiter, and cretinism; should not be used during pregnancy.
If PTU (propylthiouracil) is the second-line drug for hyperthyroidism as compared to methimazole, when would you use PTU (propylthiouracil)?
-pregnant women, but only during the 1st trimester (methimazole is preferred during the 2nd and 3rd trimester)
-women who are breast-feeding
-pts experiencing thyroid storm
-pts who are intolerant for methimazole
What are the adverse reactions to PTU (propylthiouracil)?
As with methimazole, adverse effects are relatively rare. Nonetheless, severe adverse effects can occur, especially liver injury and agranulocytosis. The most common undesired effect is rash. PTU may also cause nausea, arthralgia, headache, dizziness, and parethesias.
What is the therapeutic goal for using Lugol's Solution?
Suppression of thyroid hormone production in preparation for subtotal thyroidectomy. Also used to suppress thyroid hormone release in patients experiencing thyroid storm.
What do mineralocorticoids do?
They influence renal processing of sodium, potassium, and hydrogen. They also have direct effects on the heart and blood vessels.

Aldosterone is the most important mineralocorticoid hormone.
What does aldosterone promote?
Aldosterone acts on the collecting ducts of the nephron to promote sodium (and water) reabsorption in exchange for secretion of potassium and hydrogen. It also helps maintain intravascular volume.
What happens in the absence of aldosterone?
Renal excretion of sodium and water is great increased, whereas excretion of potassium and hydrogen is reduced. As a result, adolsterone insufficiency causes hyponatremia, hyperkalemia, acidosis, cellular dehydration, and reduction of ECF.

If left uncorrected, can lead to renal failure, circulatory collapse, and death.
What drug do we administer for mineralocorticoid replacement?
Fludrocortisone (Florinef) is the only mineralocorticoid available and is the drug of choice for chronic mineralocorticoid replacement.
What is the route of fludrocortisone?
Oral
What is the mechanism of action for fludrocortisone?
-promotes NA and water retention
-help maintain fluid and electrolyte imbalance
What are the uses of fludrocortisone?
-primary adrenocortical insufficiency
-primary hypoaldosteronism
What should we monitory for during fludrocortisone therapy?
-hypokalemia
-fluid retention/edema/weight gain
-hypertension/cardiomegaly
What does water intoxication look like?
-hyperkalemia
-hyponatremia
-fluid retention leads to edema and weight gain
-drowsiness, listlessness, headache
-severe intoxication = convulsions, coma
What are the adverse reactions of fludrocortisone?
When dose is too high, salt and water are retained in excess and excessive amounts of potassium are lost. These effects on salt and water can result in expansion of blood volume, hypertension, edema, cardiac enlargement, and hypokalemia.
What are the effects of glucocorticoids on the body?
-promote glucose availability
-promote protein catabolism
-promote lipolysis (high levels produce Cushing's Syndrome, "moon face" and "buffalo hump")
-required to maintain the functional integrity of the vascular system
-support function of striated muscle, primarily by maintaining circulatory competence
-affect mood, CNS excitability, and the electroencephalogram
-responds to stress
Describe the feedback loop of glucocorticoids.
The loops begins with the release of corticotropin-releasing hormone (CRH) from the hypothalamus. CRH acts on the anterior pituitary to promote release of adrenocorticotropic hormone (ACTH), which stimulates the zona fasciculata of the adrenal cortex, causing synthesis and release of cortisol and other glucocorticoids.
What drugs are administered for adrenal insufficiency (corticosteroids glucocorticoids)?
-Decadron (dexamethasone) - long-acting corticosteroids
-Solu-Medrol (mthylprednisolone) -intermediate-acting corticosteroid
-Prelone (prednisone) - intermediate-acting corticosteroid
What is the route for glucocorticoid drugs?
Oral.
What is the mechanism of action for glucorcoticoid drugs?
It is a corticoid replacement therapy: so think about how cortisol works.
What are the uses of glucocorticoid drugs?
Replacement therapy in deficiency states of glucocorticoid hormones (especially cortisol).
What should we monitor for when administering glucocorticoid replacement therapy?
-edema
-hyperglycemia
-hypokalemia
-muscle wasting
-peptic ulcer
-hypertension
-immunosuppression
-increased WBC
-masks signs of infection
-thin skin
What are the nursing measures when administering glucocorticoid replacement therapy?
Give PO with food. Give at 9am to mimic normal corticosteroid levels and minimize adrenal suppression. Weight daily. Monitor BP, blood sugars, and electrolytes.
(Giving with food prevents peptic ulcer disease, mimics cortisol which is usually secreted during the day and very little at night.)
Define glycolysis.
Glucose being oxidized for the energy needs of the cell.

The breakdown of glucose by enzymes, releasing energy and pyruvic acid.
Define glycogenesis.
The formation and storage of glycogen from sugar and stored in muscle and liver. Opposite of glycogenolysis.
Define glycogenolysis.
Breakdown of stored glycogen to glucose. Opposite of glycogenesis.
Define gluconeogenesis.
Production of glucose from amino acids and other substrates. This happens when insulin falls to basal level.
How much do we normally pee per day and how much does a diabetic normally pee per day?
Normal output is 1-2 L/day
DM output is 2-3 L/day
If a DM exhibits polyuria, what should we be concerned about?
Polyuria can lead to dehydration, hemoconcentration, increase in viscosity, hyperkalemia (can lead to arrythmia), and stroke from increased viscosity.
What the "3 P's" that are hallmark signs of diabetes mellitus?
-polyuria
-polyphagia
-plolydipsia
What does "Diabetes Mellitus" mean?
The disease of foundatin or syphon water
Diabetes = drawing out from body
Mellitus = sweet kind, taste like honey
What pancreatic cells produce insulin?
Beta cells in the islets of Langerhans in response to increased levels of glucose in the blood.

The hormone insulin requires zinc for storage in the pancreatic tissue.
Pancreas affects carbohydrate metabolism along with the pituitary, adrenal and thyroid glands.
What do the alpha cells in the pancreas do?
The alpha cells in the islets of Langerhans produce glucagon, and is though to oppose the action of insulin.
What is glucagon?
A hormone formed in the pancreas that promotes the breakdown of glycogen to glucose in the liver. It is responsible for most glucose production in a fasting state.
What does glucose release in the body?
In reaction with oxygen, glucose releases water and carbon dioxide.
Name the classifications of glucose intolerance.
1. Type 1 Diabetes Mellitus
2. Type 2 Diabetes Mellitus
3. Gestational Diabetes Mellitus
Is prediabetes a classification of glucose intolerance?
Nope! Prediabetes classes are impaired glucose tolerance and impaired fasting glucose tolerance.
How often should we screen for people with diabetes?
Because of the high prevalence of undiagnosed type 2 diabetes mellitus, current recommendations are to screen all adults over the age of 45 for diabetes at least every 3 years.
Describe diabetes mellitus.
-disorder of carbohydrate metabolism
-deficient of insulin
-resistance to action of insulin
What are the clinical manifestations of diabetes mellitus?
-sustained hyperglycemia
-polyuria
-polydipsia
-polyphagia (in presence of weight loss)
-ketonuria (no glucose to pull from, so pulls from protein)
-weight loss
What is the general public concern regarding diabetes mellitus?
-21 million people have DM and will increase to 366 million by 2015 (DM people having DM babies)
-6th leading cause of death (heart attack, stroke)
-increases risk for: heart disease/stroke, blindness, end stage renal disease
What is the glucose transporter necessary for glucose to be absorbed into the cells?
Active glucose transporters, GLUT-4, are inside the cells and assist in the diffusion of the glucose molecule to the mitochondria. Without GLUT-4, the cells are resistant to glucose.
What is the pathology of Type 1 DM?
Primary defect is destruction of pancreatic beta-cells; absolute insulin deficiency, ketosis is common. Also called IDDM.
What is the prevalence of Type 1 DM?
5%-10% of all DM cases are Type 1.
What is the pathology of Type 2 DM?
-obesity is almost always present
-insulin resistance and impaired insulin secretion
-most prevalent form of DM
-about 19 million Americans have it
-NIDDM
-adult-onset DM (but it can actually happen at any age)

Impaired pancreatic insulin secretion leads to hyperglycemia.

Decreased peripheral glucose uptake in muscles leads to taking energy from protein, or gluconeogenesis.

Increased hepatic glucose production leads to hyperglycemia. Not good for liver to keep doing this for a long period of time, only meant to provide during times of stress.
What is IDDM and NIDDM?
IDDM = Insulin-Dependent Diabetes Mellitus (Type 1)
DIDDM = NonInsulin-Dependent Diabetes Mellitus (Type 2)
How do you diagnose DM? Labs?
-A1c Hemoglobin, oral glucose tolerance test (if 7 or above, then glucose level is 154 mg/dL+) (Pt must be tested on 2 days in case of error or not fasting)
-Three tests: fasting plasma glucose (FPG), causal plasma glucose, oral glucose tolerance test (OGTT)
What is FPG?
Fasting Plasma Glucose - sees how much glucose is left in bloodstream after the body takes what it needs for energy
What is OGTT?
Oral Glucose Tolerance Test
What is IGT?
Impaired Glucose Tolerance, or pre diabetes.
What is IFGT?
Impaired Fasting Glucose Tolerance, or pre diabetes.
What is pre diabetes?
Impaired glucose tolerance or impaired fasting glucose tolerance.

IFGT is 100-125 mg/dL.

Increased risk for developing DM Type 2. May reduce risk with diet and exercise and possibly certain oral anti diabetic drugs.
What is normal fasting blood glucose?
80-90 mg/dL
What are the possible complications of Diabetes Mellitus?
-macrovascular (damage to large blood vessels providing circulation to heart, brain, and extremities)
-microvascular (retinopathy, nephropathy)
-neuropathy (interruption in nerve transmission)
-amputations
-complications in pregnancy
What are the treatment priority for an incoming DM patient?
-#1 is to replace fluid loss!
-Treat s/s of three Ps and concomitant metabolic and fluid problems
-also important to control BP (hemoconcentration, renin control @ kidneys) and blood lipids (body converts lipids to energy when no glucose available)
What can cause postprandial hyperglycemia in DM Type 2?
-delayed and inadequate postprandial insulin secretion
-decreased peripheral glucose uptake and failure to suppress hepatic glucose output
What can cause fasting hyperglycemia in DM Type 2?
-progressive lost of Beta-cell function
-"insulinopenic" by the time fasting plasma glucose FPG > 200
Define insulinopenic.
Diminishing, or pertaining to a decrease in, the level of circulating insulin.
What are the hypoglycemia symptoms?
-trembling
-tachycardia
-sweating
-headache
-irritability
-stupor (when the patients show up in ER)

This all leads to brain starvation with no energy! All these s/s are red flags before going into coma.
What is gestational diabetes mellitus?
-disorder of glucose intolerance of variable severity with onset during pregnancy
-closely resembles DM Type 2
-most likely precipitated by the presence of placental hormones
-increased likelihood with obese mom
-management through dietary counseling, exercise, and blood glucose/ketone monitoring
What are the two types of hyperglycemic crises?
Diabetic ketoacidosis (DKA) and Hyperglycemic hyperosmotic nonketotic syndrome (HHNS)
What is DKA?
Diabetic ketoacidosis is a severe manifestation of insulin deficiency.
What happens during DKA?
Body burns protein and fats for energy, pH drops to 7.2, destructive to brain because no glucose is going there.

Characterizations include hyperglycemia, production of ketoacids, water loss which leads to hemoconcentration, acidosis, and coma.

Altered fat metabolism: production of ketoacids leads to acidosis leads to coma.
What is HHNS?
Hyperglycemic hyperosmotic nonketotic syndrome. Also known as hyperglycemic hyperosmolar syndrome (HHS)
How is HHNS different from DKA?
-no ketoacidosis (there is little or no change in ketoacid levels in blood, thus no change in blood pH)
-no sweet or acetone smell in urine or breath
-usually occurs with DM Type 2 and evolves slowly
How are DKA and HHNS similar?
-severe hyperglycemia brought on by insulin deficiency
-large amount of glucose excrete in urine, carrying large volume of water with it
-results in dehydration and loss of blood volume, which greatly increases the blood concentrations of electrolytes and non electrolytes, hence hyperosmolar
-loss of blood volume also increases hemotocrit
How is DKA different from HHNS?
-blood levels of ketoacids rise dramatically in DKA, causing blood pH to fall
-sweet or acetone smell in urine or breath
-usually occurs with DM Type 1 and develops quickly
-most common complication in pediatric patients and leading cause of death
Which hyperglycemic crisis involves a drop in pH?
DKA
Which hyperglycemic crisis involves sweet and acetone smelling urine and breath?
DKA
Which is more severe? DKA or HHNS?
HHNS
What is the treatment for DKA?
-must replace fluids quickly
-correct hyperglycemia with IV insulin (do it slowly or incur neuro damage), check replacement with sliding scale (increase or decrease over time)
-correct hemoconcentration - IV 1.9% saline (sodium left body with water)
-correct acidosis - IV Na HCO3 (if pH < 7 after 1 hour of above Tx)
-correct hypokalemia - serum K is ≤ 3.3 mEq/L which is detrimental, K leaves cell but stays in plasma
How can insulin overdose (hyperglycemia) be reversed?
The preferred treatment is IV glucose; it raises blood glucose immediately. However if that option is not available, glucagon can be used.
How will glucagon help reverse insulin overdose (hyperglycemia)?
Glucagon is produced by the alpha cells in the pancreas and has opposite effects of insulin. It promotes the breakdown of glycogen to glucose, reduces conversion of glucose to glycogen, and stimulates biosynthesis of glucose.

Basically, it raises plasma glucose level.
When will glucagon not work to reverse insulin overdose (hyperglycemia)?
Glucagon will not correct hypoglycemia resulting from starvation because glucagon acts by promoting glycogen breakdown, and people who are starved have little or no glycogen left.
What is the glycemic index and why is it important?
The glycemic index is an indicatory of how a particular carbohydrate will affect blood glucose levels.

Specifically, eating food that have a high glycemic index (i.e., white bread, unprocessed white rice) will raise glucose levels more rapidly and to a higher peak than will eating foods that have a low glycemic index (i.e., roll oats, 100% whole wheat break, lentils and legumes, most fruits and non starchy vegetables).

Eating foods in a low glycemic index should permit better glycemic control because when glucose levels rise slowly after eating, the body has more time to process the glucose load.
If DM Type 1 patients don't receive insulin replacement, what happens?
They'll die from ketoacidosis.
What is right glycemic control?
The process of maintaining glucose levels within a normal range, around-the-clock (ATC).
What is SMBG?
Self-Monitoring of Blood Glucose
Is the metabolic action of insulin called anabolic or catabolic?
Anabolic because insulin promotes the conservation of energy and buildup of energy stores, such as glycogen.
Is insulin deficiency called anabolic or catabolic?
Catabolic (a metabolic state that favors the breakdown of complex molecules into their simpler constituents)

In the absence of insulin, glycogen is converted into glucose, proteins are degraded into amino acids, and fats are converted to glycerol and free fatty acids.
Differentiate between human insulin and human insulin analogs.
Human insulin = products identical to natural insulin produced by human pancreas

Human insulin analog = modified forms of human insulin
If a patient is taking an oral hypoglycemic, what three sites in the body must be functioning?
-pancreas
-liver
-small intestine
How many types of insulin are there?
7 types: one "natural" and six modified insulins. The six are modified by a protein and zinc to prolong the effect.
What is the drug of choice for DKA?
IV insulin - it is reserved for emergencies that require a rapid reduction in blood glucose.
What are the benefits of tight glycemic control in DM Type 1?
It reduces microvascular and macrovascular complications.
What are the drawbacks of tight glycemic control in DM Type 1?
The greatest concern is hypoglycemia. Because glucose levels are kept relatively low, the possibility of hypoglycemia increases.
What are the benefits of tight glycemic control in DM Type 2?
Benefits include microvascular complications. Also, benefits accrue more to younger adults with recent-onset disease, than to older adults with well-established disease.
What are the drawbacks of tight glycemic control in DM Type 2?
Same as DM Type 1, tight glycemic control poses a significant risk of hypoglycemia and weight gain. It also increases the risk of death.
What are the therapeutic indications for using insulin?
-primary indication is DM
-IV insulin is for DKA
-because if its ability to promote cellular uptake of potassium and thereby lower plasma potassium levels, insulin infusion is employed to treat hyperkalemia
-can aid in the diagnosis of growth hormone (GH) deficiency
How can insulin aid in the diagnosis of growth hormone (GH) deficiency?
The insulin hypoglycemia test can aid dx of suspected GH deficiency in preadolescent children who are not growing as fast as their peers. The test is based on the fact that even modest insulin-induced hypoglycemia can trigger GH release, causing blood levels of GH to rise. In children with GH deficiency, the rise in blood GH will be lower than in children with normal pituitary function.
How does insulin promote the uptake of potassium?
Insulin works on the sodium-potassium pumps on the cell membrane, thus helps reduce hyperkalemia.
What are the adverse effects of insulin?
1. Hypoglycemia from insulin overdose, insufficient caloric intake, ETOH consumption promotes hypoglycemic response.
2. Hypokalemia: insulin draws K into cell with glucose
3. Anaphylaxis
4. Lipohypertrophy at injection site: if you always inject same spot, insulin stimulates fat synthesis
5. Weigh gain
6. Injection complications
What are the different time categories of insulin?
1. Rapid-acting
2. Short-acting
3. Intermediate
4. Long-acting
5. Long-acting combination
Name the rapid-acting insulin drugs.
-lispro (Humalog)*
-aspart (Novolog)*
-glulisine (Apidra)

*"log" means log rhythmically faster than short-acting
Name the short-acting insulin drugs.
-regular "natural" (Humulin R, Novolin R)*
Name the intermediate insulin drugs.
Neutral Protamine Hagedorn NPH
(Humulin N, Novolin N)*
Lente
Name the long-acting insulin drug.
Glargine (Lantus)
Name the long-acting combination insulin drug.
Lantus + Humulin 70/30 or 50/50
What is the time category for lispro (Humalog) insulin?
Rapid-acting. Make sure to give 15 minutes prior to or after eating (because onset is 15-30 min).
What is the time category for regular "natural" insulin (Humulin R, Novolin R)?
Short-acting. Give these 30-60 minutes prior to eating because the onset is 30-60 minutes.
What is the time category for NPH (Neutral Protamine Hagedorn) or Lente insulin (Humulin N, Novolin N)?
Intermediate acting. The onset is delayed and cannot be administered at meal time; rather the drug is injected twice daily to provide glycemic control between meals and during the night.

*N = intermediate acting
What is the time category for glargine (Lantus) insulin?
Long-acting. This lasts about 24 hours. Do not mix with any other insulin; give at night. Used to decrease risk of nocturnal hyperglycemia.
Can you mix glargine (Lantus) with other insulin?
No way! Don't mix with other insulin; it will precipitate and form crystals.
What is the one insulin that doesn't peak?
Glargine (Lantus)!
What are the most common sites for insulin subcut injection?
The most common sites of subQ injection are the upper arm, thigh, and abdomen. Absorption is fastest and most consistent following abdominal injection, and slowly following injection in the thigh.
Tell me about inhaled insulin.
-recombinant DNA human insulin
-dry powder delivered to lungs
-a first in pharmacology
-proved to be just as effective as subQ insulin
-great in combination with existing therapies
-contraindicated in smokers (poor functioning alveoli)

The lungs are an excellent option because of the large vascular absorption area with high permeability of the alveolar surface.
What signs do we monitor for when administering insulin?
Hypoglycemia!
-trembling
-tachycardia
-sweating
-headache
-irritability
-stupor (ER at this point)

=brain starvation!
Brain starvation occurs at what number?
Brain starvation occurs at hypoglycemic status. This is > 60 mg/dL.
For DM Type 2 meds, what organs of the body must be functional?
Liver, small intestines, pancreas
What is unique about DM Type 2?
DM Type 2 changes over time, thus the treatment changes over time.
A newly diagnosed DM Type 2 is considered how many years?
5 years
With a progressive decline of beta-cells from the pancreas, does that convert a DM Type 2 patient to a Type 1?
Nope! There is still some functionality in the pancreas.
Which pancreatic cells produce glucagon?
Alpha cells
Which pancreatic cells product insulin?
Beta cells
How many groups of DM Type 2 oral meds are there?
Six groups of oral medications
Name the six groups of DM Type 2 oral meds.
-Meglitinides
-Sulfonylureas
-Dipeptidy peptidase-4 (DPP-4 inhibitors)
-Biguanides
-Thiazolidinediones
-Alpha-glucosidase Inhibitors
What is the action of the Meglitinides?
They stimulate the release of insulin.
What is the advantage of using Meglitinides?
They work quickly.
What is the possible side effects of Meglitinides?
SEVERELY LOW BLOOD SUGAR (hypoglycemia)
Name the Sulfonylureas meds.
-Glipizide (Glucotrol)*
-Glimepiride (Amaryl)
-Glyburide (DiaBeta, Glynase)
all 2nd generation drugs

First oral hypoglycemics
What the action of the Sulfonylureas meds?
They stimulate the beta cells to release insulin.
What is the advantage of using Sulfonylureas in DM Type 2?
They work quickly.

-1st generation controversy: cardiovascular toxicity (we don't use them now due to heart damage)
-2nd generation agents: more potent and less drug-drug interactions
What are the possible side effects of using Sulfonylureas in DM Type 2?
-hypoglycemia
-weight gain
-nausea
-skin rash

-drug interactions: alcohol, NSAIDs, Sulfonamides, Cimetidine, beta-adrenergic blocking agents
What is the action of DDP-4 inhibitors?
They stimulate the release of insulin, INHIBIT THE RELEASE OF GLUCOSE FROM THE LIVER.
What is the advantage of using DDP-4 inhibitors?
They don't cause weight gain.
What are the possible side effects of using DDP-4 inhibitors?
-upper respiratory tract infection
-sore throat
-headache
-inflammation of the pancreas (sitagliptin)
Name the Biguanide meds for DM Type 2.
-Metformin (Fortamet, Glocophage, others)*

Go to drug for DM Type 2 or gestational diabetes
What is the action of Biguanide meds for DM Type 2?
Inhibit the release of glucose from the liver, improve sensitivity to insulin.

May be used as monotherapy or with a sulfonylurea, a glitazone, or exenatide

more effective in combination, well suited for patients who skip meals

gestational diabetes
What are the advantages of using Biguanides for DM Type 2?
May promote modest weight loss and modest decline in low-density lipoprotein (LDL) or "bad" cholesterol.
What are the possible side effects of using Biguanides for DM Type 2?
Nausea, diarrhea, rarely the harmful buildup of lactic acid (lactic acidosis)*

polycystic ovary syndrome (PCOS)
What is the action of Thiazolidinediones?
Improve sensitivity to insulin, inhibit the release of glucose from the liver.
What is the advantage of using Thiazolidinediones in DM Type 2?
May slightly increase HDL, or "good" cholesterol.
What is the disadvantage of using Thiazolidinediones in DM Type 2?
HEART FAILURE, HEART ATTACK, STROKE, LIVER DISEASE.
What is the action of alpha-glucosidase inhibitors?
Slows the breakdown of starches and some sugars.
What is the advantage of using alpha-glucosidase inhibitors in DM Type 2?
Doesn't cause weight gain.
What are the possible side effects of using alpha-glucosidase inhibitors in DM Type 2?
Stomach pain, flatulence*, diarrhea
How many injectable meds are there for DM Type 2?
Two.
Name the two injectable meds for DM Type 2.
-Amylin mimetics - Pramlintide (Symlin)
-Incretin mimetics - Exenatide (Byetta), Liraglutide (Victoza)
What is the action of Amylin mimetics?
Stimulate the release of insulin, used with insulin injections
What are the advantages of using Amylin mimetics for DM Type 2?
May suppress hunger, may promote modest weight loss
What are the possible side effects of using Amylin mimetics for DM Type 2?
-hypoglycemia
-nausea or vomiting
-headache
-redness and irritation at injection site
What is the action of incretin mimetics?
Stimulate the release of insulin, used with metformin and sulfonylurea.
What are the advantages of using incretin mimetics?
May suppress hunger, may promote modest weight loss.
What are the possible side effects of using incretin mimetics?
-nausea or vomiting
-headache
-dizziness
-kidney damage or failure