ENDOCRINE DISORDERS  The main function of the thyroid hormone is to  Heat intolerance

Review of the Endocrine System control cellular metabolic activity – accelerates  Increase appetite
PHYSIOLOGY: metabolic processes  Diarrhea
 An interconnected network of glands regulating the  T4: relatively weak; maintains the body metabolism in  Weight loss
functions of multiple body organs; work in concert steady  Thin skin
with the nervous system  T3: 5x as potent as T4; has more rapid metabolic  Exophthalmos (Grave’s)
o This regulatory system allows regulation of action  Menstrual changes
functions in response to changes within and outside  Thyroid hormones virtually affect every major organ  Sinus tachycardia and palpitations
the body. system and tissue functions (BMR, thermogenesis,  Arrhythmias
 Works through the release of chemical transmitter cholesterol levels, vascular resistance) Hyperthyroidism
substances known as hormones  Calcitonin/thyrocalcitonin: secreted in response to  Intolerance to heat
 Most of these secreted hormones are released high plasma levels of Ca++; increases deposition of  Fine, straight hair
directly into the bloodstream calcium into bone.  Bulging eyes
 Hormone levels are maintained at a constant level Actions of Thyroid Hormone  Facial flushing
through a negative feedback loop  Enlarged thyroid
ENDOCRIINE SYSTEM:  Tachycardia
 Brain  Increase systolic BP
 Pituitary gland  Breast enlargement
 Pineal gland  Weight loss
 Hypothalamus  Muscle wasting
 Thymus  Localized edema
 Pancreas  Menstrual changes (amenorrhea)
 Thyroid  Increased diarrhea
 Parathyroid gland  Tremors
 Adrenal glands Metabolism
Carbohydrates  Finger clubbing
 Ovaries THYROID STORM
 Testes  Increase glucose uptake by the cells
Thyrotoxic crisis
PHYSIOLOGY:  Increase glycogenolysis
 Hyperpyrexia
 Pituitary Gland – the master gland; secretes  Gluconeogenesis
 Extreme tachycardia
hormones into the bloodstream which affects the  Increase rate of absorption from the GIT
 Exaggerated symptoms of hyperthyroidism with
other endocrine glands Fats
disturbances of a major system altered sensorium
 Hypothalamus – link between the pituitary gland and  Increase lipolysis
Complications
the other endocrine glands  Increase oxidation of free fatty acids
 Myocardial hypertrophy
 Decrease plasma cholesterol by increase loss of feces
 Heart failure
Proteins
Assessment and Diagnostics
 Overall effect is catabolic leading to increase muscle
 Thyroid gland may be enlarged
mass
 Thyroid gland may be soft and may pulsate
Basal Metabolic Rate (BMR) – is the energy requirement
under basal condition (mental and physical rest 12-18  A bruit may be heard over the thyroid arteries
hours after a meal)  Decreased serum TSH
 Increase free T4
HYPERTHYROIDISM  Increase in radioactive iodine uptake
Diagnostic Modalities
Overview  FNAB
 Blood tests
 A common endocrine disorder  Thyroid scan
 Urine tests
 A form of thyrotoxicosis resulting from an excessive Medical Treatment
 Stimulation tests
synthesis and secretion of endogenous or exogenous Depends in the underlying cause
 Suppression tests
thyroid hormones  Treatment is directed towards reducing thyroid
 Imaging: CT, MRI, PET, DXA, radioactive scanning
 Grave’s Disease: an autoimmune disease that results hyperactivity to relieve symptoms and prevent
from an excessive output of thyroid hormones caused complications
ENDOCRINE DISORDERS
by abnormal stimulation of the thyroid gland by  Antithyroid agents
THYROID
circulating immunoglobulins  Beta blockers
Overview:
 8F:M  Radioactive iodine
 Thyroid Gland: the largest endocrine gland; a highly
 Onset: usually 20’s-40’s  Surgery
vascular, butterfly-shaped organ located in the lower
Pathophysiology Nursing Interventions
neck anterior to the trachea;
o Produces T4, T3 and calcitonin
 T3 and T4 are iodine-containing, amino acid
HYPOTHYROIDISM
hormones utilized by all body cells for metabolism;
Overview
bound to proteins for storage and transport
 Result from suboptimal levels of thyroid hormone
 May occur in patients treated for hyperthyroidism
 TSH/THYROTROPIN:
 Hashimoto disease/autoimmune thyroiditis: most
regulates synthesis
common cause of hypothyroidism in adults
of thyroid
hormones through a Most common causes  May occur as primary, secondary or tertiary; may be
negative feedback  Grave’s disease neonatal or congenital
mechanism Rare causes  Myxedema: refers to the accumulation of
 TRH: modulates  TSH-secreting pituitary adenoma mucopolysaccharides in subcutaneous or interstitial
release of TSH Clinical Manifestations tissues; occurs in long-standing hypothyroidism
 Related to increased BMR and O2 consumption o Used to described extreme symptoms of severe
 The goal of this axis
is to maintain a euthyroid state.  Anxiety hypothyroidism
 Restlessness and irritability
 Fine tremors
Pathophysiology  Characterized by bone decalcification and Assessment and Diagnostics
development of calcium-containing kidney stones  Trousseau sign
 2F:M  Chvostek sign
 Half of the diagnosed cases do not have symptoms  S. Ca
 Secondary hyperparathyroidism: occurs in patient of  S. P
have CKD as a result of phosphorus retention  X-rays
Pathophysiology Medical/Surgical Treatment
Goal: increase S. Ca to 9-10mg/dL (2.2 to 2.5 mmol/L and
eliminate s/sx
Clinical Manifestations  Combinations treatment: calcium, magnesium,
 Fatigue ergocalciferol or calcitriol
 Lethargy  Thiazide diuretic
 Weight gain without and increased caloric intake  Calcium gluconate
 Cold intolerance  Calm environment
 Dry skin  Possible tracheostomy/mechanical ventilation
 Deepening of the voice in some patients Clinical manifestations  Bronchodilators
 Bradycardia  May be asymptomatic  Calcium supplements
 Arrythmias  Apathy  Aluminum hydroxide/aluminum carbonate
 Menstrual changes  Fatigue Nursing interventions
 Subnormal body temp and HR  Muscle weakness
 Thickened skin  Nausea POSTERIOR PITUITARY
 Thinning of hair  Vomiting DIABETES INSIPIDUS
 Mask-like facies  Constipation Overview
 Dulled mental processes  Hypertension  A rare disorder that occurs due to injury to the
 Apathy  Cardiac arrhythmias hypothalamus or pituitary gland with deficiency of
 Subdued emotional responses  Psychological changes ADH that results in excretion of large volumes of
 Constipation  Nephrolithiasis dilute urine and extreme thirst
 Tongue enlargement  Benign bone tumors  May be characterized as central, nephrogenic, or
 Deafness  Bone pain dipsogenic as well as gestational
 Peripheral edema  Pathologic fractures
 Pleural effusions  Deformities
 Pericardial effusions Assessment and Diagnostics
 Inadequate ventilation  S. Ca
 Sleep apnea  Radioimmunoassays for parathormone
 Elevated serum cholesterol level  X-rays
 Atherosclerosis  Bone scan
 CAD  Double-antibody PTH test
 Poor LV function  UTZ
 Increased sensitivity to sedative, opioid and  MRI
anesthetic agents  FNAB
 Myxedema coma Medical/Surgical Treatment
Assessment and Diagnostics  Parathyroidectomy
 Serum TSH  Observation may be done for asymptomatic patients
 T3 and T4 levels  Daily fluid intake of 2000mL or more
 UTZ  Mobilization
 FNAB  Restrict calcium in diet
 Thyroid scan Nursing Interventions
Medical/Surgical Treatment
Objective: restore normal metabolic rate HYPOPARATHYROIDISM
 Synthetic levothyroxine Overview
 Prevention of cardiac dysfunction  Caused by anormal parathyroid development,
Pathophysiology
 Supportive therapy destruction of the parathyroid glands, and vitamin D
Nursing intervention deficiency
 Most common cause: near-total removal of the
thyroid gland
PARATHYROID  Results in hyperphosphatemia and hypocalcemia
Overview Pathophysiology:
 Parathyroid glands: situated in the neck and
embedded in the posterior aspect of the thyroid gland Clinical Manifestations
 Parathormone (PTH): regulated calcium and  Hypocalcemia—tetany
 phosphorus metabolism  Numbness, tingling, cramps in the
o Increases calcium absorption from the kidney, extremities Clinical
intestine and resorption from bones with a goal  Bronchospasm Manifestations
to increase serum calcium levels  Laryngeal spasm  Large urine output (>250mL/hr)
o Lower serum phosphorus levels  Carpopedal spasm  Very dilute urine (Specific gravity 1.001 to 1.005)
 Dysphagia  Intense thirst
HYPERPARATHYROIDISM  Photophobia Assessment and Diagnostics
Overview  Cardiac arrhythmias  Fluid deprivation test
 Caused by overproduction of parathormone by the  Seizures  Measurements of plasma levels of ADH
parathyroid glands  Psychological changes  Urine and plasma osmolality
  Desmopressin trial o Regulated by the HPA axis  Imaging: CT, MRI, UTZ, scintigraphy
 IV infusion of hypertonic saline Medical/Surgical Treatment
Medical/Surgical Treatment Goal: control HTN before and during surgery
Objectives: replace ADH, ensure adequate fluid  Bed rest with head of the bed elevated
replacement, and identify and correct the underlying  Volume expansion to prevent a catecholamine storm
pathology  Pre-op: low dose alpha blockers
 Desmopressin  May use beta blockers of CCB
 Chlorpropamide  Adrenalectomy
 Thiazide diuretics*  IV or oral corticosteroids post adrenalectomy
 Mild salt depletion* Adrenal Medulla Nursing Interventions
 Prostaglandin inhibitors*  Functions as a part of the ANS
Nursing Interventions  Located at the center; secretes catecholamines Adrenal Cortex
 Catecholamines regulate metabolic pathways to  Secretions make it possible for the body to adapt to
SYNDROME OF INAPPROPRAITE ADH SECRETION promote catabolism of stored fuel to meet caloric stress of all kinds
Overview needs from endogenous sources  Mineralocorticoids: mainly aldosterone
 Result from a failure of the negative feedback system  90% of its secretion is epinephrine  Zona glomerulosa
that regulates the release and inhibition of ADH  “Fight-or-flight response”  Glucocorticoids: mainly cortisol
 Patients cannot excrete a dilute urine – dilution  Zona fasciculata
hyponatremia PHEOCHROMOCYTOMA  Sex hormones: main androgens
 Often of non-endocrine origin Overview  Zona reticularis
Pathophysiology  A rare tumor that is usually benign and originates  Without the adrenal cortex, severe stress would cause
from the chromaffin cells of the adrenal medulla peripheral circulatory failure, circulatory shock, and
 Cause if high BP in 0.1% of patients with hypertension prostration
 Usually fatal if undetected and untreated  Zona glomerulosa
 Arises in the adrenal medulla in 90%; may occur in  Mineralocorticoids: mainly aldosterone
extra-adrenal chromaffin tissue  Major effects on electrolyte metabolism; increased Na
 10% occurs bilaterally; 10% are malignant absorption in exchange for excretion of K or H ions
 Familial occurrence; may occur as part of MEN type 2  Main hormone for the long-term regulation of Na
 May occur at any age; peaks between 40 to 50 balance
 F=M  Triggers: RAAS, hyperkalemia
Pathophysiology  Zona fasciculata
Clinical Manifestations  Glucocorticoids: mainly cortisol
 Subnormal urine output
 Important influence on glucose metabolism
 Concentrated urine
 Increase cortisol = increase blood glucose levels
 Assessment and Diagnostics
 Secreted in response to ACTH from APG
 Measurements of plasma levels of ADH
 Negative feedback with CRH and ACTH
 Urine and plasma osmolality
 Zona reticularis
Medical/Surgical Treatment
 Sex hormones: mainly androgens
 Generally self-limiting; treatment is focused on
 Exert effects similar to those of male sex hormones
eliminating the underlying cause Clinical Manifestations
 May secrete small amounts of estrogens
 Fluid restriction  Triad: headache, diaphoresis, palpitations
 Controlled by ACTH
 Diuretics  Hypertension and other cardiovascular disturbances
 3% NaCl (severe hyponatremia)  Tremors
PRIMARY ALDOSTERONISM
Nursing Interventions  Flushing
Overview
 Anxiety
 AKA Conn Syndrome
 Hyperglycemia
 The principal action of aldosterone is to conserve S.
 Orthostatic hypotension
Na
 5H’s  More K and H excretion
 Hypertension  Etiologic factors: tumors of the adrenal gland, ovarian
 Headache tumor, family history
 Hyperhidrosis Pathophysiology
 Hypermetabolism
 Hyperglycemia
 Paroxysmal Form
 Acute, unpredictable attacks lasting seconds to
several hours, symptoms usually begin abruptly and
subside slowly
 Extremely anxiety, Tremors, weakness, headache,
vertigo, blurring of visions, tinnitus, air hunger,
dyspnea, polyuria, nausea, vomiting, diarrhea,
abdominal pain, a feeling of impending doom, BP may
exceed 250/150mmHg
ADRENAL DISORDERS Assessment and Diagnostics
Overview  Suspected s/sx of SNS overactivity occur in association Clinical Manifestations
 Each person has 2 adrenal glands, superior to each with marked elevation of BP  Hypertension – most prominent almost universal sign
kidney  Urine and plasma levels of catecholamines and  Hypertension with/without hypokalemia
 Adrenal medulla: center if the gland; secretes metanephrine  Variable muscle weakness
catecholamines  24H urine collection of MN and VMA  Paralysis
 Adrenal cortex: outer portion; secretes steroid  Clonidine suppression test if plasma and urine tests  Cramping
hormones are inconclusive  Fatigue
  Polydipsia
 Hypocalcemia
 Glucose intolerance may occur
Assessment and Diagnostics
 Plasma aldosterone concentration
 Plasma renin activity
 Aldosterone-renin ratio
Medical/Surgical Treatment
Total removal of the tumor through laparoscopic Clinical Manifestations
adrenalectomy  Addisonian Crisis: A life-threatening complications
 Corticosteroids Assessment and Diagnostics  Severe hypotension
 IV  Serum cortisol  Cyanosis
 Weekly postop monitoring of S. K levels  Urinary cortisol (24H urine collection)  Fever
 Spironolactone  Dexamethasone suppression test  Nausea
 Eplerenone  S. Na, S.K  Vomiting
Nursing intervention  Blood Glucose levels  Signs of shock
Medical/Surgical Treatment  Pallor
CUSHING SYNDROME  Surgical removal of the tumor (pituitary tumor)  Headache
 Overview  Radiation of the pituitary gland  Abdominal pain
 Use of corticosteroid medications: the most common  Adrenalectomy (unilateral primary hypertrophy)  Diarrhea
cause of Cushing’s syndrome  Hydrocortisone post-op  Confusion
 AKA Cushing’s Disease  Adrenal enzyme inhibitors (ectopic sources that cannot  Restlessness
 May be due to hyperplasia of the adrenal cortex, be eradicated) Assessment and Diagnostics
pituitary tumor  Reduction/tapering of corticosteroids (if caused by  Early morning serum cortisol and plasma ACTH
 May be from ectopic production of ACTH steroid administration)  S. Na
 Pathophysiology  Insulin therapy and medications for PUD  S. K
 Blood glucose
Nursing Interventions Medical/Surgical Treatment
 Restore circulation: administer fluids and corticosteroids
ADDISON’S DISEASE  Elevate legs
Overview  IV hydrocortisone
 Primary adrenal insufficiency  3-4L of PNSS or D5 containing solutions
 The result of dysfunction of the HPA feedback loop  Vasopressors if hypotension persists
 Autoimmune cause in 70-90% of cases  Antibiotics if with infections
 May be associated with tuberculosis or histoplasmosis  Corticosteroid replacement
 Secondary adrenal insufficiency  Nursing Interventions
Clinical Manifestations  May be the result of sudden cessation of exogenous
 Growth arrest adrenocortical hormonal therapy DIABETES MELLITUS
 Obesity  Pathophysiology Overview
 Glucose intolerance  Diabetes: a group of metabolic diseases characterized
 MSK changes by hyperglycemia resulting from defects in insulin,
 Central obesity insulin action or both (CDC, 2020)
 “Buffalo hump”  Number of people >20y.o diagnosed with diabetes
 Thin, fragile skin increases yearly
 Ecchymoses and striae  Rate of prediabetes is steadily increasing among adults
 Weakness  Can cause: nontraumatic amputations, ESKD, blindness
 Muscle wasting and death
 Osteoporosis Clinical Manifestations  Patients diagnosed with DM who are hospitalized with
 Na and H20 retention  Excretion of Na, Cl and H2O COVID-19 have been found to have a higher rate of
 HTN, HF  Retention of K intubation and mortality
 Moon facies  Decreased CP  Insulin: is a hormone secreted by beta cells which are
 Hyperglycemia/overt diabetes  Hypoglycemia one of the 4 typed of cells in the islets of Langerhans in
 Muscle weakness the pancreas
 Lethargy  An anabolic hormone
 Anorexia  During fasting, the pancreas continuously releases a
 Nausea and vomiting small amount of insulin; glucagon is released when
 Weight loss blood glucose levels decrease, stimulating the liver to
 Hyperpigmentation of skin and mucous membranes release stored glucose.
 Functions of Insulin
 Transports and metabolizes glucose for energy
 Stimulates storage of glucose in the liver and muscle
 Signals the liver to stop the release of glucose
 Enhances storage of dietary fat in adipose tissue
 Accelerates transport of amino acids into cells
 Inhibits breakdown of stored glucose, protein and fats
 DM TYPE 1
 Overview
 Characterized by the destruction of the pancreatic beta
cells
 Combined genetic, immunologic and possibly
environmental factors are thought to contribute to
beta-cell destruction
 Events that lead to destruction are not fully understood
 DKA is a metabolic derangement that occurs most
commonly in persons with DM type 1 and results from a
deficiency of insulin
 Hyperglycemia, ketosis, metabolic acidosis
 Commonly preceded by a day or more of polyuria,
polydipsia, nausea, vomiting and fatigue with eventual
stupor and coma if not treated
 Pathophysiology

  DM TYPE 2
 Overview
 Occurs more commonly among people >30 years old
and who have obesity
 Incidence is rapidly increasing in younger people
 2 main problems: insulin resistance and impaired insulin
secretion
 To overcome insulin resistance and to prevent the
buildup of glucose level at normal or slightly elevated
 Insulin resistance may also lead to metabolic syndrome
 HYPERGLYCEMIC HYPEROSMOLAR SYNDROME
 HHS is a serious condition in which hyperosmolality and
hyperglycemia predominate, with alterations of the
sensorium
 ketosis is usually minimal or absent
 persistent hyperglycemia causes osmotic diuresis, which
results in loses of water and electrolytes
 To maintain an osmotic equilibrium, water shifts from
extracellularly
 Pathophysiology

 Clinical Manifestations
 Depend on the level of hyperglycemia
 Classic 3P’s: Polyuria, polydipsia, and polyphagia
 Fatigue
 Weakness
 Sudden vision changes
 Tingling or numbness in hands or feet
 Skin lessions that are slow to heal
