MISTY
N5315 Advanced Pathophysiology Endocrine
Core Knowledge Objectives with Advanced Organizers
Endocrine
Core Knowledge Objectives with Advanced Organizers
Disorders of the Posterior Pituitary
1. Evaluate the etiologies, clinical manifestations, and the pathophysiology of syndrome of
inappropriate antidiuretic hormone and diabetes insipidus and describe the implications for
clinical practice.
Disease Etiology Clinical Manifestations Pathophysiology Clinical Implications
Syndrome of medications water retention and fluid unregulated, Adenocarcinoma of the
Inappropriate such as overload. Signs and excess secretion of lungs is the most
Antidiuretic barbiturates, symptoms include: antidiuretic common malignancy
Hormone general dilutional hyponatremia, hormone (ADH). which causes SIADH
low plasma osmolality, first five-seven days post-
anesthesia, ADH is one of the
decreased urine output, op, the secretion of ADH
nicotine, high urine specific gravity many factors is increased. Managed
morphine, (concentrated urine), which regulate with free water
antidepressants, urine sodium > 20, urine water balance. restricition. (900ml/day)
antipsychotics, osmolality > 100, weight provides the NO NORMAL SALINE.
and gain, edema is usually necessary signal WORSEN
chemotherapy. absent, thirst, impaired to the kidneys to HYPONATREMIA. USE
taste, anorexia, dyspnea, trigger renal water HYPERTONIC SALINE.
fatigue and abdominal conservation.
cramps may also be
present.
Diabetes Neurogenic POLYURIA decrease in the Neurogenic or central DI-
Insipidus Dispogenic POLYDIPSIA-thirst secretion of ADH. absence of ADH which
nephrogenic dilute urine and an occurs secondary to
The effect of this
increased serum presence of
osmolality. lack of hormone
hypothalamic or
results in
pituitary gland lesion.
Urine output can be characteristics blocks the production of
excessive and over 12 which are ADH nephrogenic DI-
liters daily. opposite of SIADH. secretion of ADH is
sufficient, but the renal
dehydrated and include:
thirst, low urine tubules in the kidneys do
osmolality, high plasma not respond to ADH.
osmolality, urine sodium usually permanent
< 20, and hypernatremia. condition.acquired or
genetic. Acquired =
pyelonephritis. Genetic =
polycystic kidney
disease. Dispogenic-
excess ingestion of water
The over-ingestion of
water suppresses ADH
secretion. often seen
psychiatric diagnosis.
, Thyroid Disorders
2. Differentiate between the etiology, clinical manifestations, pathophysiology and complications of
thyroid disorders.
Thyroid hormone secretion is regulated by TSH which is released from the anterior pituitary.
majority of the hormone released by the thyroid gland is in the form of T4 (90%) and to a much lesser
extent T3 (10%). T4 and T3 have the same functions; however, T3 is more potent, its actions are short-
lived and it is present in the blood in much smaller amounts.
hormones are bound to either albumin or thyroxine-binding globulin (TBG) in the blood. act as
transport proteins for both hormones and release the hormones once they reach their target
Thyroxine is formed with iodine and it takes approximately 1mg per week to produce thyroxine. The
iodides used in the making of thyroxine are trapped by the thyroid gland. The uptake of iodine is
regulated by TSH.
T3 and T4 are stored as thyroglobulin (TG) which is a precursor to both hormones. There is enough
stored hormone to last for two-three months.
A low level of thyroid hormone stimulates the release of thyroid-releasing factor, which in turn
stimulates the release of TSH, which then stimulates the thyroid to release more T3 and T4.
Both hormones function to increase metabolism.
o maintenance of muscle tone, skeletal muscle maturation, antagonization of insulin, regulation
of cellular metabolism, promotion of the production of heat, maintenance of cardiac output,
contraction and rate, maintenance of GI secretion, assistance with calcium mobilization, and
stimulation of lipid metabolism, free fatty acid release and cholesterol synthesis.
a. Analyze the meanings of primary, secondary and subclinical thyroid disorders and
describe the clinical significance this has on the diagnoses of these disorders.
Disease Definition Clinical Significance
Primary Thyroid Results in alterations of thyroid (negative feedback of ^TH and –
Disorders horomone (TH) levels with TSH)
secondary feedback effects on the
pituitary TSH levels.
Subclinical Thyroid disease with no or minimal
Thyroid Disease symptoms but show abnormal lab
values
Secondary Thyroid Related to disorders of the pituitary When there is excessive TSH
Disorders gland’s TSH production. production the TH is elevated due
Caused by TSH secreting pituitary secondary to the primary elevation of
adenomas TSH.
b. Differentiate between the etiology, clinical manifestations, pathophysiology of
thyrotoxicosis, grave’s disease, nodular hyperthyroidism, and thyrotoxic crisis and
describe the implications for clinical practice.
Disease Etiology Clinical Pathophysiology Clinical
Manifestations Implications
Thyrotoxicosis Graves Increase metabolic hypermetabolic Hyperthyroid and
disease, rate, heat intolerance, clinical syndrome thyrotoxicosis are
toxic increased tissue resulting from used
N5315 Advanced Pathophysiology Endocrine
Core Knowledge Objectives with Advanced Organizers
Endocrine
Core Knowledge Objectives with Advanced Organizers
Disorders of the Posterior Pituitary
1. Evaluate the etiologies, clinical manifestations, and the pathophysiology of syndrome of
inappropriate antidiuretic hormone and diabetes insipidus and describe the implications for
clinical practice.
Disease Etiology Clinical Manifestations Pathophysiology Clinical Implications
Syndrome of medications water retention and fluid unregulated, Adenocarcinoma of the
Inappropriate such as overload. Signs and excess secretion of lungs is the most
Antidiuretic barbiturates, symptoms include: antidiuretic common malignancy
Hormone general dilutional hyponatremia, hormone (ADH). which causes SIADH
low plasma osmolality, first five-seven days post-
anesthesia, ADH is one of the
decreased urine output, op, the secretion of ADH
nicotine, high urine specific gravity many factors is increased. Managed
morphine, (concentrated urine), which regulate with free water
antidepressants, urine sodium > 20, urine water balance. restricition. (900ml/day)
antipsychotics, osmolality > 100, weight provides the NO NORMAL SALINE.
and gain, edema is usually necessary signal WORSEN
chemotherapy. absent, thirst, impaired to the kidneys to HYPONATREMIA. USE
taste, anorexia, dyspnea, trigger renal water HYPERTONIC SALINE.
fatigue and abdominal conservation.
cramps may also be
present.
Diabetes Neurogenic POLYURIA decrease in the Neurogenic or central DI-
Insipidus Dispogenic POLYDIPSIA-thirst secretion of ADH. absence of ADH which
nephrogenic dilute urine and an occurs secondary to
The effect of this
increased serum presence of
osmolality. lack of hormone
hypothalamic or
results in
pituitary gland lesion.
Urine output can be characteristics blocks the production of
excessive and over 12 which are ADH nephrogenic DI-
liters daily. opposite of SIADH. secretion of ADH is
sufficient, but the renal
dehydrated and include:
thirst, low urine tubules in the kidneys do
osmolality, high plasma not respond to ADH.
osmolality, urine sodium usually permanent
< 20, and hypernatremia. condition.acquired or
genetic. Acquired =
pyelonephritis. Genetic =
polycystic kidney
disease. Dispogenic-
excess ingestion of water
The over-ingestion of
water suppresses ADH
secretion. often seen
psychiatric diagnosis.
, Thyroid Disorders
2. Differentiate between the etiology, clinical manifestations, pathophysiology and complications of
thyroid disorders.
Thyroid hormone secretion is regulated by TSH which is released from the anterior pituitary.
majority of the hormone released by the thyroid gland is in the form of T4 (90%) and to a much lesser
extent T3 (10%). T4 and T3 have the same functions; however, T3 is more potent, its actions are short-
lived and it is present in the blood in much smaller amounts.
hormones are bound to either albumin or thyroxine-binding globulin (TBG) in the blood. act as
transport proteins for both hormones and release the hormones once they reach their target
Thyroxine is formed with iodine and it takes approximately 1mg per week to produce thyroxine. The
iodides used in the making of thyroxine are trapped by the thyroid gland. The uptake of iodine is
regulated by TSH.
T3 and T4 are stored as thyroglobulin (TG) which is a precursor to both hormones. There is enough
stored hormone to last for two-three months.
A low level of thyroid hormone stimulates the release of thyroid-releasing factor, which in turn
stimulates the release of TSH, which then stimulates the thyroid to release more T3 and T4.
Both hormones function to increase metabolism.
o maintenance of muscle tone, skeletal muscle maturation, antagonization of insulin, regulation
of cellular metabolism, promotion of the production of heat, maintenance of cardiac output,
contraction and rate, maintenance of GI secretion, assistance with calcium mobilization, and
stimulation of lipid metabolism, free fatty acid release and cholesterol synthesis.
a. Analyze the meanings of primary, secondary and subclinical thyroid disorders and
describe the clinical significance this has on the diagnoses of these disorders.
Disease Definition Clinical Significance
Primary Thyroid Results in alterations of thyroid (negative feedback of ^TH and –
Disorders horomone (TH) levels with TSH)
secondary feedback effects on the
pituitary TSH levels.
Subclinical Thyroid disease with no or minimal
Thyroid Disease symptoms but show abnormal lab
values
Secondary Thyroid Related to disorders of the pituitary When there is excessive TSH
Disorders gland’s TSH production. production the TH is elevated due
Caused by TSH secreting pituitary secondary to the primary elevation of
adenomas TSH.
b. Differentiate between the etiology, clinical manifestations, pathophysiology of
thyrotoxicosis, grave’s disease, nodular hyperthyroidism, and thyrotoxic crisis and
describe the implications for clinical practice.
Disease Etiology Clinical Pathophysiology Clinical
Manifestations Implications
Thyrotoxicosis Graves Increase metabolic hypermetabolic Hyperthyroid and
disease, rate, heat intolerance, clinical syndrome thyrotoxicosis are
toxic increased tissue resulting from used
