Endocrine Disorders Flashcards
Pituitary Gland
a small gland located on a stalk hanging from the base of the brain
AKA: “The Master Gland”
Primary function is to control other glands.
Produces many hormones.
Secretion is controlled by the hypothalamus in the base of the brain.
Anterior Pituitary Gland
The hypothalamus controls the release of hormones from the anterior pituitary gland by releasing inhibiting or stimulating hormones
Posterior Pituitary Gland
The hypothalamus controls the release of hormones from the posterior pituitary gland via neural pathways
Releases “effector” hormones
(cause an effect to occur)
Oxytocin (the natural form of Pitocin)
stimulates gravid uterus
causes “let down” of milk from the breast.
ADH
(vasopressin) causes the kidney to retain water/hemostasis
Anterior Pituitary produces:
thyroid-stimulating hormone (TSH) Adrenocorticotropin hormone (ACTH) Growth hormone (GH) follicle-stimulating hormone (FSH) luteinizing hormone (LH)
Anterior Pituitary patho
TSH stimulates the thyroid gland to release its hormones, thus metabolic rate
ACTH stimulates the adrenal cortex to release cortisol, aldosterone, & androgens
Growth hormone (GH)
Stimulates growth & cell reproduction
Maintains or increases Blood Glucose levels
glucose usage by muscles & adipose tissues in prolonged GH excess
Induces insulin resistance in peripheral tissues
consumption of fats as an energy source
FSH
♀: Stimulates ovarian follicle growth & ovulation
♂: Stimulates sperm production
LH
♀: Stimulates corpus luteum development, release of oocyte, and estrogen/progesterone production
♂: Stimulates secretion of testosterone; development of testes
The Thyroid Gland
Lies in the anterior neck just below the larynx.
Two lobes, located on either side of the trachea, connected by a narrow band of tissue called the isthmus.
thyroxine (T4) and triiodothyronine (T3)
Affect growth and maturation of tissues, cell metabolism, heat production, and oxygen consumption
CV function; GI function; Neuromuscular
Parathyroid Glands
small, pea-shaped glands, located in the neck near the thyroid
usually 4 - number can vary
regulate the level of calcium in the body
produce parathyroid hormone - level of calcium in blood
Hypocalcemia can result if parathyroids are removed or destroyed.
Islets of Langerhans
specialized tissues in which the endocrine function of the pancreas occurs
include 3 types of cells: alpha, beta, delta
each secretes an important hormone.
Adrenal Glands
2 small glands that sit atop both kidneys.
Each has 2 divisions, each with different functions.
Adrenal Medulla and Adrenal Cortex
Adrenal Medulla
the Adrenal Medulla secretes the catecholamine hormones norepinephrine and epinephrine
used for stress response
produce vasoconstriction
Adrenal Cortex
The Adrenal Cortex secretes 3 classes of hormones, all steroid hormones:
Glucocorticoids
Mineralocorticoids
Androgenic hormones (not part of this lecture)
Glucocorticoids
accounts for 95% of adrenal cortex hormone production
the level of glucose in the blood
Released in response to stress, injury, or serious infection - like the hormones from the adrenal medulla.
Cortisol
Mobilizes glucose
Stimulates gluconeogenesis
Formation of glucose from proteins in the liver
Promotes protein breakdown (for energy source)
Suppresses inflammation & the immune response
Maintains vascular tone, too much causes hyperglucemia
Mineralcorticoid
Aldosterone: from adrenal gland, response in kidney
Regulated by renin-angiotensin mechanism
work to regulate the concentration of potassium and sodium in the body.
Retains Sodium (and water) and excretes Potassium
Hypersecretion causes Hypokalemia, Hypernatremia depending on situation
Aldosterone
And - if there is an in Aldosterone
Serious electrolyte imbalances can occur:
sodium retention by the kidney, resulting in hypernatremia.
potassium excretion by the kidney, which results in hypokalemia.
Syndrome of inappropriate antidiuretic hormone (SIADH) secretion
Levels of antidiuretic hormone (ADH) are abnormally high.
Ectopic secretion of ADH is the most common cause; is also common after brain surgery and some cancers.
Water retention: Action of ADH on renal collecting ducts increases their permeability to water, thus increasing water reabsorption by the kidneys.
For diagnosis, normal renal, adrenal, and thyroid function must exist.
Results in hypoosmolality, hyponatremia, thirst
Clinical Manifestations of SIADH
Hyponatremia: Sodium <135 mEq/L
Hypoosmolality: <280 mOsm/kg
Urine hyperosmolality: Higher than serum osmolality
Hypervolemia
Weight gain
Serum sodium levels below 110 to 115 mEq/L: Can cause severe and sometimes irreversible neurologic damage
Emergency correction of severe hyponatremia by the administration of hypertonic (0.3) saline
Most important: Fluid restriction between 800 and
1000 mL/day
Diabetes Insipidus
Insufficiency of ADH
Polyuria and polydipsia
Partial or total inability to concentrate the urine
Neurogenic
Insufficient amounts of ADH (head trauma, brain tumors)
Nephrogenic
Insensitivity of the renal collecting tubules to ADH (idiopathic/medications)
Dipsogenic
Excessive fluid intake, lowering plasma osmolarity to the point that it falls below the threshold for ADH secretion
Is characterized by the inability of the kidney to increase permeability to water.
Excretion of large volumes of dilute urine
Increase in plasma osmolality: 300 mOsm or more, depending on adequate water intake
Urine output: 8 to 12 L/day; normal output: 1 to 2 L/day
Clinical Manifestations of Diabetes Insipidus
Polyuria, nocturia, continual thirst
Low urine-specific gravity: <1.010
Low urine osmolality (<200 mOsml/kg)
Hypernatremia
Primary Addison’s Disease: not enough cortisol
Originates within the Adrenal Glands Damage or destruction of Adrenal Gland ↑ACTH d/t lack of feedback inhibition Decreased hormone secretion: Mineralocorticoids Glucocorticoids Androgen
Causes of Primary Addison’s disease
Autoimmune Disease (70%) TB infection (20%) Opportunistic infections Cancer metastasis Surgical removal of Adrenal glands
Secondary Adrenal Insufficiency
Caused by disorder outside of adrenal gland
Hypopituitarism or removal of pituitary gland (leading to decrease of ACTH [corticotrophin] secretion which stimulates the adrenal cortex to produce hormones):
Mineralocorticoids
Glucocorticoids
Androgen
Also caused by RAPID WITHDRAWAL OF STEROIDS
Cushing Syndrome
Too much Cortisol secretion
Primary
Disease of the Adrenal Cortex (tumor)
Secondary
Increased ACTH production from anterior pituitary gland
Iatrogenic
Glucocorticoid therapy
Cushing Syndrome Manifestations
Weight gain (accumulation of adipose tissue in trunk, face, and cervical area)
“Buffalo hump”
“Truncal obesity” with thin extremities
“Moon face”
Hyperglycemia, polyuria
Muscle wasting from catabolic effects of cortisol
Purple striae: loss of collagen
Poor wound healing, infections
Hypokalemia: excess aldosterone
Hypertension
Osteoporosis from loss of protein matrix of bone
Mood changes, memory loss, psychosis: Common, half have this
↑ Androgens: hirsutism, acne, menstrual irregularities
Adrenal Medulla
Secretes the catecholamine hormones norepinephrine and epinephrine
used for stress response
produce vasoconstriction
Hormones that are typically elevated during the acute stress response
Adrenaline, Cortisol, Norepinephrine
Sogomyi Effect
Hypoglycemia in the morning because glycogen is released, counter regulatory hormones (GH, epinephrine, cortisol)
Cushing Syndrome Systemic Complications
Immune system compromise
Slow wound healing from suppressed immune system
Depressed immune system can mask s/s infection
Cardiovascular
Increased blood pressure due to increased sodium/water retention (↑Aldosterone) & vascular sensitivity to catecholamines
Sexual/Psychological Disturbances
Menstrual disturbances, mood swings, psychosis
Dawn Effect
Rising glucose between 2-8 AM in diabetic people
Hypoglycemia S/S
Heart palpitations Fatigue Pale skin Shakiness Anxiety Sweating Hunger Irritability Tingling sensation around the mouth Crying out during sleep
Type 1 Diabetes Patho
Beta Cells (which produce insulin) in pancreas destroyed or suppressed
Can be idiopathic or immune mediated
Genetic activated by an environmental trigger (virus?)
Insulinitis
Inflammatory response resulting from auto-immune attack on Beta cells
By the time s/s develop, 80% of Beta cell are destroyed
Type 2 Diabetes Patho
Resistance to insulin action in target cells
Relative insulin deficiency from beta cell dysfunction
As a consequence of obesity
Over production of glucose (gluconeogenesis) by the liver
Genetic predisposition
Hyperthyroidism/Graves Disease Manifestations/Labs
Autoimmune disorder
Trigger for autoimmune response is unclear:
Possible genetic and immunological factor
Thyroid stimulating antibodies bind to and stimulate the TSH receptors of the thyroid gland
Leads to increased production of T4 and T3 hormones
Increased metabolism, increased SNS activity, & increased oxygen consumption
Everything elevated EXCEPT (decrease)
Weight
Sex drive
Fluid volume
Hypothyroidism Manifestations/Labs
Too little thyroid hormone (too little T3 and T4)
Hypometabolic state
Primary
Destruction or dysfunction of the thyroid gland itself
Secondary
Failure of the pituitary to produce TSH
Inability to synthesize thyroid hormones due to iodine deficiency
Use of antithyroid medications
Myxedema: Generalized Hypometabolic state: can’t metabolize medication well
non-pitting edema, Cardiac dilation, Thickening of facial features, Skin indurations, Enlarged tongue, Hoarse voice
PTH, Vitamin D, Calcitonin
PTH: increase calcium in blood when levels are low
Calcitonin: decrease calcium in blood when levels are high and store on bone
Vitamin D: Increase calcium in blood
