Hypothalamus & Pituitary:
○ Hypothalamus - MASTER GLAND
■ Located above base of pituitary gland and controls everything
● Located in an area with poor blood-brain barrier protection, allowing it to
sense electrolytes, hormones and chemicals in the bloodstream
■ It is the link between the nervous system and endocrine system
■ Controls signals from brain into hormonal responses
■ Regulates the CNS, autonomic nervous system (parasympathetic &
sympathetic) and endocrine system to maintain homeostasis
■ Controls hormone production and regulation called “neuroendocrine link”
■ Helps to maintain homeostasis - regulates vital functions of body
● Hunger, thirst, sleep (autonomic functions)
■ Controls circadian rhythm (sleep-rhythm, sleep-wake cycles)
■ Control pituitary gland
■ Release TRH to signal pituitary
■ Produces inhibiting hormone such as somatostatin and
prolactin inhibiting factor (dopamine), which suppress
pituitary hormone release
■ Produces ADH and oxytocin which are transported and stored
in pituitary for later release
○ Pituitary -
■ Anterior pituitary
● Releases GH (growth and metabolism), ACTH (stress response -
cortisol), FSH, LH (both reproductive regulation), PRL (lactation) TSH
(thyroid function)
■ Posterior pituitary -
● ADH (vasopressin) - water retention, osmolarity control
○ Release is triggered by increased plasma osmolarity (higher
concentration of solutes; sodium, glucose in blood plasma
triggered by dehydration, hyperglycemia, hypernatremia)
○ Decreased blood volume
● Oxytocin - uterine contraction, milk let-down
■ Intermediate Lobe -
● produce endorphins and enkephalins to block pain perception
○ Disorders caused by PITUITARY DYSFUNCTION:
■ GH deficiency → dwarfism
■ GH excess → acromegaly
■ ADH deficiency → Diabetes Insipidus (DI)
■ ADH excess → SIADH (syndrome of inappropriate ADH)
○ Hypothalamic disorders:
■ Reproductive disorders
■ Thyroid disorders ; TRH imbalance → affects TSH
■ Growth abnormalities
■ Prolactin excess (dopamine inhibition blocked) leads to galactorrhea
(spontaneous flow of milk from nipples in men or women who
are breastfeeding) ○ Nursing priorities:
■ Monitor growth, development and metabolism
■ Monitor thyroid function
■ For DI - monitor urine output, specific gravity, dehydration signs
■ SIADH - monitor fluid overload, serum sodium, mental status
■ Assess for CNS effects - dizziness, confusion, headache
● Thyroid
○ Lab values for T3-T4
■ Normal VS abnormal T3-T4 levels
○ Produces T3 & T4 calcitonin
○ These hormones regulate - basal metabolic rate, thermoregulation,
cardiovascular output, oxygen consumption, growth and development,
carbohydrate, fat and protein metabolism ○ When thyroid hormone levels
rise it suppresses TRH and TSH
○ Helps to regulate serum calcium by lowering calcium levels
○ Disorders:
■ Hypothyroidism
■ Myxedema
■ Hyperthyroidism
■ Goiter
○ Nursing priorities:
■ Hormone replacement therapy - Levothyroxine
● Medication increases metabolism, heart rate and oxygen demand
● Start low and go slow
● Monitor cardiac status - angina, arrhythmias
● Monitor for hypothyroid storms
■ Hyperthyroidism -
● Monitor cardiovascular status - thyroid hormones raise metabolic rate
○ Assess for tachycardia, palpitations, hypertension, arrhythmias
● Provide calm environment, reduce heat exposure
● Medication management - methimazole, PTU
○ Block thyroid hormone production
○ Monitor for liver toxicity - PTU
■ Side effect of PTU - can cause acute liver failure
○ Monitor for iodine toxicity
○ Teach patient to avoid foods high in iodine
● Parathyroid
○ Produces PTH
○ Regulates serum calcium
○ PTH raises serum calcium by ;
■ Increasing calcium reabsorption in the kidneys
■ Increasing calcium reabsorption in the GI tract
■ Increasing bone resorption (release of calcium from bone)
○ When serum calcium falls → PTH is released
○ When serum calcium rises → PTH is inhibited
○ Magnesium affects PTH secretion – increased phosphate indirectly
stimulates PTH by suppressing
○ Disorders:
■ Hypoparathyroidism - low PTH → low calcium
● Cause - usually from accidental removal or damage to the parathyroid
glands during thyroid surgery
● Leads to hypocalcemia
● Clinical manifestations - tetany, muscle cramps,
paresthesias, seizures, bronchospasm, laryngospasm,
prolonged QT interval
● Assess for: chvostek’s sign, trousseau’s sign, numbness, tingling,
seizures, laryngospasm (airway risk)
● Treatment - calcium and vitamin D therapy to increase serum calcium
levels
○ Monitor ECG during IV calcium
○ Avoid phosphorus-rich foods (worsens hypocalcemia)
○ Monitor magnesium levels: high magnesium levels suppress
PTH and low magnesium stimulates PTH secretion
■ Low magnesium initially mimics a drop in calcium
and signals the parathyroid to increase PTH
production
■ When magnesium levels are high, they inhibit
parathyroid glands from secreting PTH
■ Hyperparathyroidism - high PTH → high calcium
● Can occur as a result of a parathyroid tumor or certain genetic disorders
● Primary hyperparathyroidism occurs most often in women 60-70 years
old
● Clinical manifestations - hypercalcemia, bone pain, kidney stones, GI
symptoms (nausea, constipation), fatigue, muscle weakness, cardiac
dysrhythmias
● Assess for: muscle weakness, fatigue, confusion, constipation,
nausea/vomiting, bone pain, polyuria/polydipsia, kidney stones, cardiac
arrhythmias
● Promote hydration - due to increase kidney stone risk (2-3L/day fluids)
● Maintain mobility - to reduce bone resorption
● Monitor ECG → for shortened QT interval and dysrhythmias
● Prevent injury - bone fragility caused by PTH-induced bone breakdown
● Treatment - bisphosphonates, calcitonin (decreases calcium levels),
diuretics (NOT thiazides), phosphate therapy
● Adrenal Cortex
○ Controlled by the hypothalamus
○ 1. CRH is released from the hypothalamus is used to stimulate the
pituitary’s release of ACTH which in turn tells the adrenal cortex to
produce cortisol and androgens ○ 2. The RAAS system uses angiotensin
II, influenced by the kidneys to stimulate the outer layer of the adrenal
cortex to produce aldosterone
○ Work in a negative feedback loop - high levels of cortisol or
aldosterone signal the hypothalamus and pituitary to reduce CRH
and ACTH production
○ Produces hormones ; corticosteroids
■ Androgens, glucocorticoids, mineralocorticoids
○ Glucocorticoids also known as cortisol
■ Increases glucose production, stimulates fat deposition and
protein breakdown, inhibits protein formation
■ Role: maintain metabolism, increase blood glucose, support
stress response, provides anti-inflammatory and
immunosuppressive effects, part of sympathetic
“fight-or-flight” response
○ Mineralocorticioids also known as Aldosterone
■ Stimulates retention of sodium and water and excretion of potassium
■ Role: maintain fluid balance, maintain electrolyte balance,
regulates blood pressure and vascular volume
○ Androgens
■ Affect electrolytes, stimulate protein production and
decreases protein breakdown
■ Affect muscle mass and red blood cell formation
○ Disorders:
■ Adrenocortical Insufficiency - Addison’s disease
● Causes -
○ Damage to glands
○ Pituitary ACTH deficiency
○ Prolonged corticosteroid use causing adrenal atrophy
● Effects - hypotension, fluid loss, low sodium, high
potassium, fatigue, weakness, risk of adrenal crisis
(life-threatening)
● Adrenal crisis - hypotension, fluid shift, shock and death
if patients under stress cannot increase cortisol or
steroids are stopped abruptly after long-term use
● Priority - continuous BP, HR monitoring
○ Treat hypotension immediately
○ Administer IV corticosteroids
○ Because adrenal cortex cannot respond to ACTH, administer
prescribed hydrocortisone/fludrocortisone
○ Teach patient corticosteroid replacement is lifelong
○ Aldosterone normally retains sodium and water and excretes
K;
■ Expect hyponatremia, hyperkalemia, dehydration
■ Monitor Na, K, glucose
■ Assess for arrhythmias
■ Hypercortisolism - Cushing’s Syndrome
● Endogenous - Can be caused by tumors on pituitary gland which
produces excess ACTH or tumors on adrenal glands that produce too
much cortisol
● Exogenous - long term corticosteroid medication
use (prednisone, dexamethasone)
● Excess corticosteroids leads to:
○ Immunosuppression
○ Peptic ulcers
○ Fluid retention
○ Hyperglycemia
○ Osteoporosis
○ Frail skin
● Signs - weight gain, crackles, edema, hypertension
● Priority -
○ Infection prevention - due to immunosuppression
○ Monitor glucose levels - steroids increase glucose production
○ Monitor fluid retention and BP - steroids cause sodium/water
retention
○ Monitor for GI bleeding - due to peptic ulcers
○ Bone protection - osteoporosis and fractures
○ Do not stop steroids abruptly - can cause adrenal crisis due to
adrenal atrophy
○ Taper slowly and educate patient not to stop on their own
● Adrenal Medulla
○ Produces epinephrine, norepinephrine (amine hormones)
■ Catecholamines - responsible for activating the sympathetic
“fight or flight” response
■ Cause - increased HR, BP, bronchodilation, increased blood
glucose, increased metabolic rate, peripheral vasoconstriction,
heightened alertness
■ Medulla releases catecholamines rapidly in response to: stress, danger,
hypotension, hypoglycemia
○ Disorders:
■ Pheochromocytoma - Catecholamine-Secreting Tumor
● Overproduction of catecholamines causes
○ Severe hypertension
○ Tachycardia
○ Headaches
○ Sweating
○ Anxiety
○ Hyperglycemia
● Priority - monitor BP closely
○ Assess for hypertensive emergencies
○ Avoid triggers - stress, physical strain
○ Monitor HR - risk of arrhythmias
○ BG monitoring
■ Adrenal Medullary Insufficiency
● Leads to lack of epinephrine/norepinephrine causing:
○ Inability to adequately respond to stress
○ Hypotension
○ Orthostatic changes
○ At risk for shock
● Priority - patients may not tolerate illness, hypoglycemia,
injury, surgery ○ Maintain adequate hydration
○ Loss may lead to hypoglycemia - monitor BG
● Pancreas:
○ ENDOCRINE ROLE:
■ Produces insulin; beta cells
■ Contains Alpha cells - produces and secretes hormone glucagon
■ Our body regulates glucose in the pancreas
■ Beta cells & Alpha cells work in conjunction
■ Based on hormones, pancreas decides what to send out
■ After you eat something, glucose level goes up and beta cells
in pancreas will release insulin
● Insulin decides what goes into the cell
● Insulin will escort glucose into the cell. This will
prevent blood sugar glucose levels from getting too
high
● If there is too much glucose into the bloodstream it gets
stored in adipose tissue
○ Initial storage - excess glucose is first stored as glycogen in the
liver and muscles
○ Conversion to fat - when these glycogen stores are full, the liver
converts the remaining excess glucose into fat (triglycerides)
○ Fat storage - this fat is then transported and stored in adipose
tissue (fat cells) for long-term energy reserves
● Disruption to this system will lead to diabetes
○ EXOCRINE ROLE:
■ Production and secretion of digestive enzymes
● Lipase - for fat digestion
● Amylase - for carbohydrate digestion
● Without functional exocrine secretion, nutrients (proteins, fats,
carbohydrates) cannot be properly broken down leading to
malabsorption, steatorrhea (presence of excess fat in stool –pale,
greasy, oily, foul-smelling), malnutrition
■ Disorders:
● Type 1 Diabetes Mellitus
● Type 2 Diabetes Mellitus
● Secondary Diabetes - caused by diseases of exocrine
pancreases (ex: cystic fibrosis or pancreatitis)
■ Priorities for DM Type 1:
● Insulin therapy management
● Ensure correct insulin type, dose, timing
● Monitor blood glucose before meals and at bedtime
● Prone to DKA if insulin is missed
■ Priorities for DM Type 2:
● Promote lifestyle interventions - diet, exercise, weight reduction
● Manage oral antidiabetic drugs - many drugs act on the pancreas,
stimulating it to release insulin
● Administer 30 minutes before meals
● Monitor liver and renal function for drug metabolism/excretion
● Risk of pancreatitis
○ Monitor for severe abdominal pain
■ Priorities for Secondary Diabetes -
● Monitor for pancreatic enzyme insufficiency
● Manage glucose with insulin if endocrine function is impaired
● Provide pain management - especially with pancreatitis
● Ensure hydration
● Monitor triglycerides - pancreatitis risk factor