Hypopituitarism
Etiology o Congenital, genetic
disease
o Destruction of the gland (surgery/ radiation)
o Tumor/ mass lesions o Pituitary
... [Show More] infection
o Deficiency of hypothalamic hormones
Disorders of the posterior pituitary
ADH
• ADH: peptide synthesized by cells in the hypothalamus -> transported along a neural
pathway -> store in pituitary
• Nerve impulses causes stored ADH to be released into circulation based on serum
osmolality (so based on what your body needs) o Too much concentration – you
hold pee to balance
Very sweet juice, you dilute it with water so you hold it in o Too little
concentration- you let it out
Unsweetened juice, you pee it out to make it sweet
Exerts effects on tubular cells of the kidney to cause reabsorption of water
Osmolality is how concentrated or diluted the serum is
Sensitive changes in blood pressure and can lead to the release of ADH
Abnormal synthesis of ADH because of trauma, stress, severe pain, nausea and certain
medications
You can check for osmolality on a blood test
Usually 280-310 osm/L
Isotonic – 300
Lactate ringers, normal saline 0.9%
Hypertonic – above 300
Hypotonic- less than 300
Trigger is higher the osmolality the higher the concentration
Secretes ADH and ADH vasoconstricts and keeps fluid on board
Comes from posterior pituitary
SIADH vs DI
Diabetes insipidus
Insipidus –no flavor
SIADH
(syndrome of inappropriate ADH)
Super increased ADH
ADH (regulates H2O) and
vasoconstriction
Deficiency Excessive secretion
Serum osmolality ↑blood very concentrated ↓blood very diluted
Urine osmolality ↓ ↑
Urine output High urine output
(diluted) 5-24 L per day
Low urine output
Fluid volume status Deficit Overload
Sodium level Hypernatremia Hyponatremia
• Diabetes insipidus is a disorder of the posterior lobe of the pituitary
• Vasodepressor
• Diabetes insipidus are unable to concentrate their urine and excretes large volumes of
urine o CNS component to it because of something in the ADH ex: head trauma,
surgery
• When kidneys don’t respond to ADH
• Drugs that cause DI- electrolyte disorders…
• We can evaluate antidiuretic hormone levels along with osmolality of the urine
• If you can’t excrete urine it stays in the tissue o Polyuria: lots of urine o Sodium is low
because there is a lot of fluid o Syndrome of ADH is a result of brain tumors
• Brain tumors can start secreting hormones
o -surgery o
-temperature changes
Disorders of the thyroid
• Thyroid releases T3 and T4
• Both are carried by binding proteins
• T3 stimulates metabolism
• T4 is inactive until converted into T3 in the tissues o Needs iodine to activate
• Both exert negative feedback on the hypothalamus
• Located in the larynx
• TSH is very important in hypo and hyperthyroidism and how we measure thyroid
function
Actions of the thyroid hormone
• Most major organs are affected by altered levels of thyroid hormone
o Metabolic rate
Glucose, fat, and protein usage
Lipids mobilized from adipose tissue
Catabolism of cholesterol by the liver
Muscle protein is broken down and used as fuel o Cardiovascular function
Increase in oxygen consumption
Increase in vasodilation
Increase in heart rate and contractility, BP
Tachycardia o GI function
Absorption is increased
GI secretions
Hungry
Hyperactive bowel sounds o Neuromuscular effects
React more vigorously
• Hypereflexsive
Clinical manifestations
• Metabolic rate o Basal metabolic rate can increase by 60-100% above normal
with the large amounts of T4 are present o Increase use of protein, glucose and
fat
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Muscle proteins broken down and used as fuel
o Changes in cholesterol
• Cardiovascular function o With increase metabolism= rise in oxygen
consumption, production of end products
o Vasodilation
o Increase blood volume, cardiac output, HR and contractility
• GI Function
o Increase in motility and production of GI secretions (diarrhea) o Increase in
appetite o Weight loss
• Neuromuscular effects o Changes in skeletal muscle reaction
Hyperthyroid: fine muscle tremor, extreme nervousness, anxiety
Increased HR, palpitations
Diagnostics
• T3
o Low in primary hypothyroidism
• T4
o Measures unbound portion (produces effects) o Free T4 decreased in primary
hyperthyroidism
• TSH
o Differentiates between primary and secondary thyroid disorders
• Radioiodine uptake test
• Ultrasound o Cysts or lesions
• CT/MRI
• Needle biopsy o Done with guided ultrasound
Will tell if benign or malignant
We really look at TSH and is important in the negative feedback loop
Hypothyroidism is elevated TSH because it keeps sending the signal to increase T3 and T4
We monitor medication therapy through this
TSH increased, T3 and T4 decreased
Hyperthyroidism
• Excessively high levels of circulating thyroid hormone
• Common causes o Graves disease
Enlarged thyroid
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B cells make antibodies against TSH receptors and the antibodies
stimulate TSH
o Adenoma
tumor o Thyroid
storm o Iodine- containing
agents
Autoantibodies get produced
Low TSH levels because of negative feedback loop
Negative feedback loop would close off anterior pituitary
Goiter- can involve entire gland and can develop nodules and may produce signs of thyroidtoxosis
Glands can be so enlarged that it puts pressure on other organs or masses
Signs and symptoms
• Increase in oxygen consumption
• Use of metabolic fuels
• Tissues exposed to high level of circulating thyroid hormone
• Increase SNS activity o Increased HR, palpitations o Shortness of breath, fine muscle
tremor
o Heat intolerance o Excessive sweating
o Muscle gramps in the GI tract
Diarrhea
Listen for hyperactive bowel sounds o Thin
hair/ skin o Nervousness, anxiety
Hyperthyroidism: Graves Disease
• Autoimmune disorder
• Abnormal stimulation of thyroid by thyroid-stimulating antibodies
• Cytokine-mediated responses causes o Exophthalmos
Results in cytokine and develop abnormal tissue in the eyes that push the
eyeballs out and corneal ulcerations
o Goiter
Weight loss o Anxiety o
S/S hyperthyroid o Seen in
ages 20-40 years old
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Hyperthyroidism: thyroid storm
• Thyroid crisis
• Life threatening
• Rare: seen in undiagnosed cases or inadequate treatment
methods
• Precipitated by stress, (infection, DKA –precipitation of
stress and infection, physical/emotional trauma,
thyroidectomy)
Clinical manifestations
• Very high fever
• Extreme CV effects o Tachycardia, CHF, angina o High
cardiac output that can decrease cardiac output
• Severe CNS effects o Agitation o Restlessness
o Delirium – acute changes in mental status
Hypothyroidism
• Congenital (at birth) o Can lead to cognitive delays
• Acquired (primary or secondary disease) o Causes a
slowing down of metabolic processes
o Myxedema
Presence of nonpitting edema
o Myxedema coma (life threatening)
Severe life threatening form of
hypothyroidism
Causes
• Thyroidectomy
• Radiation (causes ablation) o When radiation kills the cells
• Iodine
• Hashimoto thyroiditis (autoimmune disease)
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o
Increased in women
o Thyroid is destroyed
o Can develop goiter because of immune mediated destruction of the thyroid
gland
Clinical manifestations
• Hypometabolic state o Weakness, fatigue,
weight gain o Cold intolerance / dry skin o
Mental sluggishness o Puffy face, edema o
Brittle hair o Slowed GI motility
Constipation o Mental dullness,
lethargy o Hoarse voice o Bradycardia,
decreased CO
Hypothyroidism: myxedema coma
Pathophysiology
• Carbon dioxide retention
• Fluid and electrolyte imbalance
• Hypothermia
Clinical manifestations
• Coma, cardio vascular collapse
• Hypoventilation
• Hyponatremia
• Hypoglycemia Lactic acidosis
• Unable to metabolize sedatives
• Hypothermia
Disorders of the adrenal gland
HPA Axis
• Aldosterone: retention of water and sodium and excretes
potassium
• Adrenal medulla makes epi and norepi
Disorders of adrenal function
• Control of adrenal cortical function
Aldosterone (principal mineralocorticoid)
Function in sodium, potassium, and
water balance
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Cortisol (hydrocortisone [major glucocorticoid])
Aid in regulating the metabolic functions of the body and in controlling
the inflammatory response
Essential for survival in stress situations
• If you don’t have it you can’t respond to stress and die
Regulated by negative feedback loop by ACTH o Androgens (chief sex
hormone)
Disorders of adrenal cortex: adrenal insufficiency
• Primary
o Patho: disorder caused by destruction of adrenal gland
o Addisons disease
• Secondary o Patho: disorder of the HPA system [Show Less]