Endocrine Disorders Flashcards
Mechanisms of hormone alterations
Alterations:
1. Feedback system failure: Dysfunction or response to inappropriate signals
- Gland dysfunction: (1) Inability to produce hormones/acquire hormone precursors/or convert precursors into active hormones or (2) excessive/inadequate hormone production
- Altered hormone
- Ectopic hormone release: Non-endocrine sites out of feedback loop
Target cell dysfunction
- Hormone insensitivity
- Receptor-associated disorders: (1) Decreased number/impaired function, (2) presence of antibodies against receptors/blocking receptor sites, or (3) unusual receptor expression
- Intracellular disorders: (1) Inadequate synthesis of second messenger or (2) failure of target cell to produce anticipated hormonal response
Hypothalamus disorders
Hyperactive hypothalamus: No known diseases
Hypoactive hypothalamus: Often leads to hypopituitarism (s/t CA, radiation damage, infections, TBI)
Anterior pituitary: HYPERFUNCTION (s/t Adenoma)
Third most common brain tumor (most are benign) after meningiomas and gliomas
Most common types of adenomas:
- Prolactinomas (40%)
- GH-secreting tumors (Acromegaly; 20%)
- ACTH-secreting tumors (Cushing’s disease; 10%)
S/S (dependent on hormones being produced and size of tumor): HA, vision issues, bleeding
Acromegaly
Disorder that results from excess GH after the growth plates have closed
Usually diagnosed in adults aged 30 to 50, but it can affect people of any age (Gigantism = Abnormal growth in children)
Tx: Surgical removal, GH-blocking medications, and radiation
Anterior pituitary: HYPOFUNCTION
Caused by:
- Congenital conditions
- Acquired: Tumors, infections (TB meningitis, syphilis), surgery (s/t acromegaly surgery), TBI, radiation damage, and chemotherapy
S/S: Fatigue, weight loss or gain, generalized weakness, low mood, difficulty concentrating, reduced appetite, postural hypotension
Posterior pituitary: HYPERFUNCTION (SIADH)
Excess ADH that causes the body to retain too much water = Dilutional hyponatremia and low urine output
Caused by: Meds. (for seizures, DM, anti-depressants, heart/BP, CA), general anesthesia, brain disorders (stroke, injury, infection), lung disease/CA, and pituitary disorder
Tx: Treat underlying cause, fluid restriction (most common approach), salt intake, vasopressin-receptor antagonists, hypertonic saline
Hyponatremia
Potentially life threatening if <125 mEq/L
S/S ("Saltloss"):
Stupor/confusion/coma
Anorexia
Lethargy (d/t cerebral edema)
Tendon reflexes decreased
Limp muscles
Orthostatic hypotension
Seizures/HA
Stomach issues: N/V/
Posterior pituitary: HYPOFUNCTION (Diabetes insipidus)
Low ADH that causes the body to excrete large amounts of water = Hypernatremia and high urine output
Caused by:
- Central: Head trauma/pituitary injury, idiopathic, tumors, infections, and toxins (snake venom, puffer fish)
- Nephrogenic: Kidneys are insensitivity to ADH (d/t renal disease, meds.)
S/S: Polydipsia, polyuria (4-18 L/day; normally 0.8-2 L/day), low urine specific gravity (very dilute), weight loss, insomnia, change in mentation, tachycardia, and signs of dehydration
Tx: DDAVP (ADH)
Thyroid gland alterations
PRIMARY thyroid alterations:
- Thyroid issues: Altered T3/T4 production
- Hyperthyroidism: Graves’ disease, nodular thyroid disease, and thyrotoxic crisis
- Hypothyroidism: Hashimoto disease, endemic goiter, and congenital hypothyroidism
SECONDARY thyroid alterations:
- Hypothalamus or pituitary issues (downstream effect)
- Exogenous thyroid hormone taken in excess
Hyperthyroidism
S/S: Intolerance to HEAT, fine/straight hair, bulging eyes, enlarged thyroid, TACHYCARDIA, increased systolic BP, breast enlargement, weight LOSS, muscle wasting, localized edema, finger clubbing, tremors, D/, and amenorrhea (menstrual changes)
Primary hyperthyroidism: GRAVES’ disease
Autoimmune disease that causes antibodies to bind to TSH receptors on the thyroid = Stimulate continuous release of T3 and T4 (Type II hypersensitivity reaction)
Risk factors: FHX, stress, infection, giving birth, other autoimmune diseases (T1DM, rheumatoid arthritis), and smoking
Diagnosed by: Elevated thyroid levels, and radioactive iodine and uptake scan (iodine is an essential building block for T3/T4)
Hallmark:
- Graves’ opthalmopathy: exophthalmos (eye protrusion), periorbital edema, orbital fat accumulation, upper eyelid retraction, lid lag, redness, conjunctivitis, and diplopia
- Pretibial myxedema: thickening/edema of skin on shins
Tx: Anti-thyroid agents, beta blockers, thyroid removal, and radiation therapy
Primary hyperthyroidism: Nodular thyroid disease
Not always associated with disease (nodules can be non-functioning); cause is largely unknown, but increases risk for thyroid CA and hyperthyroidism
Hyper-functioning nodules = Hyper-secrete thyroid hormones
Types:
- Toxic multinodular goiter: one or more nodules
- Solitary toxic adenoma: only one nodule
Primary hyperthyroidism: Thyrotoxic crisis (“Thyroid storm”)
Rare, acute, life-threatening, hyper-metabolic state induced by excessive release of thyroid hormones that is characterized by a sudden, multi-system involvement (s/t Graves’ disease or excess thyroid hormone replacement therapy)
Unclear patho, however it is caused by:
- A precipitating factor (such as abruptly stopping anti-thyroid hormone meds., thyroid surgery, trauma, stress, acute illness, giving birth, and recent iodine contrast use)
- Rapid increase in T3/T4 OR increased cell sensitivity to T3/T4 with SNS hyperactivity
S/S: Fever (>104° F), HR >140, HF, delirium, N/V/, acute liver failure, and death (there is up to 30% mortality)
Hypothyroidism
S/S: Intolerance to COLD, receding hairline, facial/eyelid edema, dull/blank expression, extreme fatigue, macroglossia, slow speech, anorexia, brittle nails/hair, amenorrhea, hair loss, apathy, lethargy, dry/coarse/scaly skin, muscle aches/weakness, and CONSTIPATION
Late clinical manifestations: Subnormal temp., BRADYCARDIA, weight GAIN, decreased LOC, thickened skin, and cardiac complications
Primary hypothyroidism: HASHIMOTO’S disease
Autoimmune disease involving thyroid gland destruction, preventing the production of thyroid hormones (Type IV hypersensitivity reaction)
Most common cause of hypothyroidism in the U.S.; affects women more than men
Risk factors: 30-60 y/o, FHX, other autoimmune diseases, and radiation exposure
Primary hypothyroidism: Endemic goiter
An iodine-deficiency disease that prevents synthesis of thyroid hormones; leads to constant TSH stimulation and thyroid hyperplasia
Most common cause of hypothyroidism worldwide (2.7% of the world population)
Tx: Thyroid hyperplasia can be reversed with iodine-rich diet and replacement hormones if treated within 5 years
Primary hypothyroidism: Congenital hypothyroidism
Present at birth (and evident at 2-6 months of age) d/t lack of/dysfunction of thyroid gland
S/S: Hoarse cry, distended abdomen, dry skin/hair, macroglossia, slow responses, poor growth and development, and mental deficits
Thyroid CA
Largely treatable; ~100% 5-year survival rate if localized
Types of thyroid CA:
- Papillary: Typically affects 30-50 y/o
- Follicular: Typically affects >50 y/o
- Medullary: C-cells produce excess calcitonin (severe hypocalcemia)
- Anaplastic: Rare, aggressive, poor prognosis; 30% 5-year survival rate
Tx: Lobectomy or thyroidectomy, radioactive iodine, and chemotherapy
Thyroid levels
Primary hyperthyroidism:
High T3/T4; Low TSH
Secondary hyperthyroidism:
High T3/T4; High TSH or Low TSH (Excess thyroid meds.)
Primary hypothyroidism:
Low T3/T4; High TSH
Secondary hypothyroidism:
Low T3/T4; Low TSH
Hyperparathyroidism
Abnormally HIGH PTH levels = Hypercalcemia (increased risk for renal calculi) and hypophosphatemia
Typically caused by: Benign adenoma
Risk factors: Female (3x more likely than men), >50 y/o, ionizing radiation, lithium ingestion, and FHX
Hypoparathyroidism
Abnormally LOW PTH levels = Hypocalcemia and hyperphosphatemia
Typically caused by: Thyroid surgery, autoimmune diseases, and genetics
S/S: Confusion, muscle spams/cramps, numbness in hands/feet/face, itchy skin, and rash
Adrenal medulla
HYPER-FUNCTION is typically caused by: Pheochromocytoma (rare tumor that hyper-secretes catecholamines); S/S: HTN, tachycardia, diaphoresis, HA
HYPO-FUNCTION: No known conditions
Adrenal cortex: HYPERFUNCTION (CUSHING’S)
Cushing’s SYNDROME: PRIMARY adrenal cortex condition; increased cortisol d/t adrenal cortex dysfunction (i.e. adrenal adenoma or exogenous glucocorticoid use)
Cushing’s DISEASE: SECONDARY adrenal cortex condition; increased cortisol d/t increases in ACTH (i.e. anterior pituitary adenoma or ectopic ACTH)
Results in:
- Loss of the diurnal release of cortisol (and chronically elevated cortisol levels)
- Inability to produce cortisol in response to stressors
S/S: Hyperglycemia, personality changes, moon face, increased susceptibility to infection, gynecomastia (males), fat deposits on face/back/shoulders, osteoporosis, CNS irritability, sodium and water retention (edema), thin extremities, GI distress (increased acid), amenorrhea/hirsutism (females), thin skin, purple striae, and bruises/petechiae
Adrenal cortex: HYPERFUNCTION (Hyperaldosteronism)
Excess aldosterone that causes the body to retain too much sodium = Increased water retention, blood volume, and BP
Caused by:
- Primary: Adrenal adenoma, CA, or hyperplasia
- Secondary: Diet or other disorders of the heart/liver/kidneys
S/S: HA, blurred vision, dizziness, hypokalemia
Adrenal cortex: PRIMARY HYPOFUNCTION (Addison’s disease)
Insufficient amounts of cortisol, and sometimes aldosterone
Caused by: Autoimmune diseases (75%), infections (TB), CA metastasis, hemorrhagic injury to adrenal glands
S/S: Weakness, N/, loss of appetite, weight loss, hyperpigmentation, vitiligo (lose of skin color), hyperkalemia/hyponatremia, hypotension
Tx: Replacement hormones
Adrenal cortex: SECONDARY HYPOFUNCTION
Failure of the pituitary to stimulate adrenal cortex hormone production
Caused by:
- Lack of ACTH from anterior pituitary
- Chronic exogenous corticosteroids use (gradually reduce corticosteroid dose to encourage the adrenal cortex to produce its own cortisol and prevent hypofunction)
Adrenal crisis
Life-threatening condition characterized by severe acute adrenal insufficiency of cortisol, and sometimes aldosterone
Caused by: Trauma, Addison’s disease, pituitary injury, severe dehydration, physiological infection/emotional stress, strenuous physical activity; or sudden discontinuation of chronic glucocorticoid use (most common cause)
S/S: Acute shock, HYPOTENSION, tachycardia, weakness, fatigue, decreased appetite/weight, orthostatic hypotension, and electrolyte imbalances
Insulin
Hormone that regulates BG; it is produced by beta cells of the islets of Langerhans within the pancreas
Functions:
1. Attaches to insulin receptors on cell membranes to help absorb glucose
- Stores glucose in the liver as glycogen
- Cellular intake of potassium
T1DM
Autoimmune destruction of pancreatic beta cells = Severe insulin deficiency resulting in elevated BG
Younger onset; can affect any age
Risk factors: FHX and viral exposure
T2DM
Chronically elevated BG = Increased insulin resistance, resulting in impaired insulin production and secretion
Elevated triglycerides further exacerbate the destruction of pancreatic beta cells
Risk factors: >45 y/o, physically active <3 times/week, FHX (DM), HTN, gestational diabetes, overweight
Diagnostic criteria for T2DM
Diagnostic testing:
1. Fasting blood glucose (FBG); Normal: <100 mg/dL, Diabetic: >126 mg/dL
- Hemoglobin AIC (HgbA1C): measures the % of Hgb that are glycated over time; Normal: <5.7%, Diabetic: >6.5%
- Oral glucose tolerance test: ability to decrease BG (measured 2 hrs. after drinking syrup); Normal: <140 mg/dL, Diabetic: >200 mg/dL
- Random plasma glucose test (RPG); Diabetic: >200 mg/dL
DM: Clinical manifestations
Both T1DM and T2DM: (“Polys”) Polyuria, polydipsia, and polyphagia; and blurred vision
T1DM: Weight LOSS and fatigue
T2DM: Parasthesia and frequent infections
Long-term complications: Vascular and nerve-related conditions (hyperglycemia decreases the elasticity of blood vessels, causing them to narrow and impede blood flow, resulting in high BP and nerve damage)
Diabetic ketoacidosis (DKA)
“Starving cells” turn to fat for energy = Ketone (acidic) byproduct excreted in urine
S/S: Fruity-scented breath, N/V/, polyuria/polydipsia, fatigue, confusion, Kussmaul respirations, coma/death
At risk: DM (Missed insulin dose/insulin pump obstruction), BG > 250 mg/dL, infections, and stress
