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Types of Hormonal and Metabolic Dysfunctions - Coggle Diagram
Types of Hormonal and Metabolic Dysfunctions
Syndrome of Inappropriate Antidiuretic Hormone Secretion
Hypothalamus
Antidiuretic hormone (vasopressin)
posterior pituitary gland
released to circulation
controls fluid balance by regulating thirst
secretion rate based on serum osmolality and ECF volume
Low levels
water loss through urination
high levels
water retention
promotes fluid retention
increases permeability of the nephrons in the kidneys
senses changes in serum osmolality, adjusts thirst senstation
excessive production and release of ADH despite changes in serum osmolality and blood volume
CNS is most sensitive to changes
excess circulating fluid in cells increases total body water concentration
dilutes sodium concentration in EC space
Diagnostic Criteria
hyponatremia
hypotonicity
high urine concentration with elevated sodium content
absence of renal, adrenal, or thyroid abnormalities
clinical manifestations
anorexia
nausea/vomiting
headache
irritablility
treatments
water restriction
hypertonic IV solution
Diabetes Insipidus
condition of insufficient ADH
body's inability to concentrate or retain water
Causes
insufficient production of ADH
inadequate kidney response to presence of ADH
nephrogenic DI
chronic renal insufficiency
lithium (treats manic-depressive disorder)
toxicity
hypercalcemia
hypokalemia
disease of renal tubules
ingestion of extremely large volumes of fluid
decrease ADH levels
clinical manifestations
polyuria (large volume urine output)
polydipsia (excessive thrist)
diagnostic criteria
laboratory measurements
urine specific gravity of <1.005
urine osmolality <200 mOsm/kg
treatment
drink enough fluids
IV hydration w/ hypotonic solution
pharmacological
desmopressin
synthetic vasopressin analog
potent antidiuretic
Hyperthyroidism
excessive thyroid hormone
causes
excessive stimulation of thyroid gland
disease of the thyroid gland
excess production of TSH by a pituitary adenoma
hypothalamus releases TRH
TSH released from anterior pituitary
production and release of thyroid hormones from thyroid gland
thyroxine (T4)
triiodothyronine (T3)
suppressed or activated depending on thyroid hormone levels
Graves Disease
most common autoimmune condition
IgG antibodies bind to TSH receptors on thyrocytes
stimulates excessive thyroid hormone secretion
thyrotoxicosis
thyroid gland undergoes hyperplasia
thyrotoxic crisis (thyroid storm)
sudden, severe worsening of hyperthyroidism
Clinical Manifestations
enlargement of thyroid gland
goiter
excessive metabolic rate
weight loss
tachycardia
protrusion of eyeballs
exophthalmos
Diagnostic Criteria
patient history and physical examination
autoimmune disease
thyroid disease
emigration from an iodine-deficient location
measure thyroxine in serum
treatment
radioactive iodine
gland destruction
medication to block thyroid hormone production
ablasion
removal of thyroid gland
lifetime oral thyroid hormone will be required post-op
Cushing Syndrome
condition of prolonged exposure to elevated levels of glucocorticoids
endogenous glucocorticoids
from adrenal cortex or cortisol-producing tumors
exogenous glucocorticoids
when taking glucocorticoid drugs
suppression of cortisol production
suppresses inflammatory and immune responses
decrease the deleterious effects of chronic inflammation
glucocorticoids contribute to metabolic function, the inflammatory and immune responses, and stress responses
four major processes
long-term administration of corticosteroid medication (i.e. prednisone)
tumors of pituitary gland
stimulate excess ACTH production
adrenal hyperplasia
excess cortisol production
tumors of adrenal gland
stimulate excess cortisol production
ectopic production of ACTH or CRH from a tumor at a distant site
clinical manifestations
metabolic alterations
excessive circulating glucose and subsequent glucose intolerance
suppression of the inflammatory and immune responses
mobilization of fats and changes in fat metabolism
obesity
diagnostic criteria
based on 24-hour urine collection
elevated cortisol excretion
Treatment
surgery or radiation to remove tumor
gradually withdraw from corticosteroid medications
Hypothyroidism
deficient thyroid hormone
congenital
during fetal development
congenital hypothyroidism
intellectual disability and impaired growth
untreated after birth
lack of thyroid hormone production and secretion
acquired
deficient thyroid sythesis
destruction of thyroid gland
impaired TSH or TRH secretion
autoimmune hypothyroidism
attacks the thyroid gland
block TSH or TSH receptor
Hashimoto Thyroiditis
total destruction of thyroid gland
clinical manifestations
gradual onset
fatigue
cold intolerance
weight gain
goiter
myxedma
swelling of skin and underlying tissue
diagnostic criteria
laboratory studies
sensitive TSH assay
free T4, T4, T3 uptake
thyroid autoantibodies and antithyroglobin
decreased serum thyroid levels; elevated TSH
treatment
lifelong thyroid hormone replacement therapy
levothyroxine
synthetic form of T4
Addison Disease
primary adrenocortical insufficiency
insufficient production of cortisol and aldosterone from adrenal cortex
clinical manifestations
hormone deficiency
glucocorticoids
hypoglycemia
weakness
nausea/vomiting
weight loss
personality change
mineralocorticoids
dehydration
hyponatremia
hyperkalemia
hypotension
shock
androgens
sparse axillary and pubic hair
diagnostic criteria
electrolyte levels
hyponatremia
hyperkalemia
serum corticosteroid levels
remains depressed after ACTH administration
treatment
isotonic IV fluid replacement
infused with hydrocortisone sodium succinate or sodium phosphate