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Pathophysiology Final Exam
Review
Hypopituitarism
Etiology o Congenital, geneticdisease
o Destruction of the gland (surgery/ radiation)
o Tumor/ mass lesions o Pituitary 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
, 2
Secretes ADH and ADH vasoconstricts and keeps fluid on board
Comes from posterior pituitary
SIADH vs DI
Diabetes insipidus SIADH
(syndrome of inappropriate ADH)
Insipidus –no flavor Super increased ADH
ADH (regulates H2O) and Deficiency Excessive secretion
vasoconstriction
Serum osmolality ↑blood very concentrated ↓blood very diluted
Urine osmolality ↓ ↑
Urine output High urine output Low urine output
(diluted) 5-24 L per day
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
, 3
• 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
, 4
lOMoAR cPSD| 4971631
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
Pathophysiology Final Exam
Review
Hypopituitarism
Etiology o Congenital, geneticdisease
o Destruction of the gland (surgery/ radiation)
o Tumor/ mass lesions o Pituitary 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
, 2
Secretes ADH and ADH vasoconstricts and keeps fluid on board
Comes from posterior pituitary
SIADH vs DI
Diabetes insipidus SIADH
(syndrome of inappropriate ADH)
Insipidus –no flavor Super increased ADH
ADH (regulates H2O) and Deficiency Excessive secretion
vasoconstriction
Serum osmolality ↑blood very concentrated ↓blood very diluted
Urine osmolality ↓ ↑
Urine output High urine output Low urine output
(diluted) 5-24 L per day
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
, 3
• 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
, 4
lOMoAR cPSD| 4971631
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
