Ch. 54 Flashcards
major endocrine glands
- hypothalamus
- pituitary
- thyroid
- parathyroid
- pancreas
- adrenals
hypothalamus: location
lower middle of the brain
hypothalamus: function
- link between endocrine and nervous system
- “master” gland that stimulates pituitary
hypothalamus: selected hormones
- corticotropin-releasing hormone
- growth hormone- releasing hormone
- vasopressin (ADH)
- thyrotropin-releasing hormone
pituitary: location
below the hypothalamus
pituitary: function
- also called a master gland or “executive” hypothalamus
- anterior or posterior pituitary are different; both are connected to the hypothalamus
pituitary: selected hormones
- anterior pituitary: TSH
- ## adrenocorticotropic hormone (ACTH)
- posterior pituitary: vasopressin
thyroid: location
in front and to the sides of the trachea
thyroid: function
- controls metabolic rate- how fast cells create energy from food
- helps regulate calcium
thyroid: selected hormones
- thyroxine (T4)
- triiodothyronine (T3), Calcitonin
parathyroid: location
behind or next to the thyroid
parathyroid: function
regulates blood calcium
parathyroid: selected hormones
parathyroid hormone (PTH)
pancreas: location
behind the stomach
pancreas: function
controls glucose levels and produces digestive enzymes
pancreas: selected hormones
- insulin
- glucagon
- somatostatin
adrenals: location
on top of each kidney
adrenals: function
medulla: fight-or-flight response; blood pressure regulation
adrenals: selected hormones
- glucocorticoids (cortisol)
- mineralocorticoids (aldosterone)
- ## androgens (testosterone)
- adrenalin (epinephrine)
- noradrenalin
anterior pituitary hormones
- Adrenocorticotropic (ACTH)
- Thyroid-stimulating (TSH)
- Growth hormone
- Gonadotropic hormones
-Follicle-stimulating (FSH)
-Lutenizing (LH)
-Prolactin
posterior pituitary hormones
- oxytocin
- ADH (vasopressin)
Arginine Vasopressin Deficiency/Resistance
(AVP-D or AVP-R) aka Diabetes Insipidus
- Posterior pituitary does not secrete ADH, so kidneys start excreting more water and ECF decreases to the point of shock.
- OR—inability of kidney to respond to ADH (as in drug induced)
Blood becomes concentrated and urine output increases and it is very dilute
primary AVP-D
(neurogenic) disorder in pituitary or hypothalamus
- e.g. tumor
secondary AVP-D is caused by
(neurogenic) craniotomy, trauma, or surgery
- e.g. skull trauma, CVA can get AVP-D or SIADH
drug induced AVP-R
i.e. lithium, alcohol, general anesthesia interfere with kidney’s response to ADH
s/sx of AVP-D or AVP-R
Urine output >4L in 24 hours(polyuria)
Sudden onset thirst(polydipsia)
Dehydration (because of excess UO)
Hypotension and tachycardia (hypovolemia)
Changes in LOC: lethargy to possible coma
Vision changes
Weight loss
Headache
AVP-D or AVP-R: labs
- *Serum Na+ ↑ (blood is concentrated)
- *urine Na+ ↓ (dilute urine)
- *Specific Gravity ↓ (dilute urine)
- Hematocrit and hemoglobin↑
- BUN↑
- Serum vasopressin↓ (ADH- AP isnt producing enough: cause of AVP-D)
AVP-D or AVP-R: interventions
- Administer ADH like medications- Desmopressin acetate or vasopressin (works to decrease UO; increase USG)
- Maintain fluid volume
- Monitor I&O
- Assess VS
- Daily Weight
- Check labs (electrolytes)
- Encourage PO fluids
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
- Too much ADH is produced resulting in FVE
- ECF becomes very dilute due to water retention resulting in hyponatremia
causes of SIADH
- Drugs increase action or production of ADH; e.g. morphine, metoclopramide, anti-depressants
- Tumors in lungs, pancreas, prostate, brain secrete ADH or vasopressin like substance
- Infections –meningitis, encephalitis can affect pituitary
- Head injury affecting pituitary
- Cancer in kidney decreasing response to ADH
s/sx of SIADH
Decreased urine output
Hyponatremia
HTN, tachycardia
↓hematocrit, serum Na+, BUN
Weight gain and edema
Altered LOC because brain doesn’t like low Na+
SIADH labs
- Serum Na+ ↓
- Urine Na ↑
- ADH ↑
SIADH interventions
Treat underlying cause (stop drugs, treat infection)
Diuretics
Hypertonic saline (to treat low serum Na, increase IV FV)
Fluid restriction
Monitor daily weights
Monitor I&O
pathophysiology of adrenal glands
- Two adrenal glands sit on top of the kidneys
- Pituitary secretes ACTH which stimulates adrenal glands to release hormones.
adrenal medulla is the ___ layer
inner layer of the kidneys
adrenal cortex is the __ layer
outer layer of the kidneys
adrenal medulla hormones
- epinephrine and norepinephrine (fight or flight)
adrenal cortex hormones
- Glucocorticoids (cortisol)
- Mineralocorticoids (aldosterone)
- Sex hormones (testosterone, estradiol, progesterone)
glucocorticoids (cortisol): fx
- Essential for life
- Stimulate gluconeogenesis (production of cortisol in the liver)
- Provide amino acids and glucose during stress
- Suppress immune system and anti-inflammatory properties
- Stimulate fat breakdown
causes of increased cortisol
Trauma, burns, infection, shock, pain, fear, emotional upset, hypoxia, exercise
mineralcorticoids (aldosterone)
Control body sodium and potassium content
- Promotes Na and H2O reabsorption and potassium excretion in renal tubules
major adrenal cortex diseases
- addison’s diseas
- cushing’s disease
addison’s disease
- not enough steroids
cushing’s disease
- too many steroids
adrenal gland hypofunction
Adrenocortical steroids may decrease from inadequate secretion of ACTH.
Dysfunction of hypothalamic-pituitary control mechanism
Direct dysfunction of adrenal tissue
Addisonian crisis vs. Addison’s disease
addisonian crisis: definition, sx, treatment
someone with Addison’s who is not adequately controlled
(not enough cortisol or aldosterone)
s/sx
- severe hypotension (ie 70/40)
- severe hypoglycemia
- hypovolemic
RX: rapid infusion of IV fluids (ie 500mL/hr); IV glucose (dextrose), IV steroids (corticosteroid)
addison’s disease
- not enough steroids- cortisol, aldosterone
causes of addison’s disease
primary:
- Autoimmune antibodies attack adrenal tissue
- metastatic cancer
secondary:
pituitary tumors
Hypopituitarism if pituitary isn’t working can’t trigger adrenals
Sudden withdrawal of steroid medication (tapering medication of chronic steroid causes addison’s)
s/sx of addison’s disease
- bronzing pigmentation of the skin
- vascular collapse
- hyperkalemia
- hyponatremia
- hypoglycemia
- hypotension
- GI involvement
- progressive weakness
- confusion
- apathy
- psychosis
treatment of addison’s disease
IVFs
Monitor for arrhythmias due to hyperkalemia
Correct hyperkalemia
IV glucocorticoids or mineralocorticoids
addison’s disease labs
Serum cortisol level <10 µg/dL in the morning
Urine decreased corticosteroid concentrations
Serum Na+ (low) and K+ levels (high)
Blood glucose (low)
Serum ACTH –depends on cause
addison’s crisis sx/tx
Hypotension, shock, coma
- Requires rapid fluid and steroid replacement
adrenal gland hypofunction: goals
Promote fluid balance
Monitor for fluid deficit
Prevent hypoglycemia
addison’s disease: teaching for steroids
Take with food
Never stop taking abruptly
Watch for weight gain
Increase dose in times of stress
Anticoagulants and insulin decrease
effectiveness
will take this medication for life
addison’s disease: diet
intervention to treat low Na+ and high K+
- follow a high salt diet (french fries, hot dogs, chicken nuggets)
- avoid foods high in potassium (bananas, leafy greens, citrus)
addison’s disease: interventions
- teaching for steroids
- diet
- steroid use makes you more susceptible to infection
adrenal gland hyperfunction
- hypersecretion by adrenal cortex results in Cushing’s syndrome/disease, hypercortisolism, or excessive androgen production.
hypercortisolism (cushing’s disease): causes
Caused by an excess of cortisol
Can be caused by drug therapy for another health problem
pituitary or adrenal tumor
s/sx of cushing’s disease
Mood changes (depression, euphoria, irritability)
Skinny arms and legs
Muscle weakness
Poor wound healing
Buffalo hump (posterior neck fat pad) and truncal obesity (thin arms and legs)
Hyperglycemia and Glycosuria
Osteoporosis
Fluid volume excess
HTN
Hypokalemia
Sodium imbalances
Voice deepening, beard growth, menstrual irregularities, thinning hair, ruddy complexion
hypercortisolism (cushing’s disease): incidence and prevalence
Most common non-drug cause – pituitary adenoma
Women are affected more than men
More commonly caused by exogenous corticosteroids
cushing’s manifestations
- pear-shape (gynecomastia), truncal obesity, skinny legs and arms
- edema, no spots
- slow wound healing
- moon-face
- higher risk for osteoporosis
cushing’s labs
Serum cortisol (high)
Serum ACTH (depends on the cause)
High Na, Low K
High blood sugar
cushing’s treatment
Depends on cause- need to reduce cortisol levels
- pituitary adenoma: remove tumor
- steroids: decrease dose
cushing’s interventions
Daily weights
I&O
VS
Assess for hypervolemia s/sx
Restrict fluids and Na in diet
Monitor blood sugar
Help patient cope with body image (psychosocial)
cushing’s evaluation
Maintain fluid and electrolyte balance
Remain free from injury
Remain free from infection
Not experience acute adrenal insufficiency
ADH
antidiuretic hormone
- fluid volume balance
