MED SURG EXAM 3 - Comprehensive review of the material covered A+
lOMoAR cPSD| 30878495
MED SURG EXAM 3 - Comprehensive review of the
materialcovered A+
MED SURG EXAM 3
ENDOCRINE DISORDERS (CH 52)
ADRENAL + PITUITARY DISORDERS
PITUITARY GLAND
-Abnormalities of the anterior and posterior portion of the gland may occur independently
-Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland
itself or of the hypothalamus (result is essentially the same)
-hypopituitarism can result from radiation therapy to the head + neck
-Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid,
gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair
loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not
replaced
ANTERIOR PITUITARY
-TSH, ACTH, FSH, and LH release hormones from other endocrine glands
-Prolactin acts on the breast to stimulate milk production
-GH protein hormone that increases protein synthesis in many tissues, increases the breakdown of
fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are
essential for normal growth)
Oversecretion:
• ACTH (Cushing’s)
• “Cushing’s syndrome – elevated cortisol level; blood sugar may be high”
• Basophilic tumors giv
• rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and
amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia
• GH (acromegaly)
• Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height
• Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall
• “Acromegaly – hypersecretion of GH; everything will be overdeveloped
1|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
– a lot of cardiac complications *
– sometimes they cannot see properly
– enlarged extremities, forehead
– female – might have issues with periods, anuria, or unable to have babies”
•
• Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all
proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the
excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin,
giving rise to ACROMEGALY.
Insufficient secretion:
– GH (dwarfism)
• Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth
• “Dwarfism – undersecretion of GH; other glands will be underdeveloped”
– Panhypopituitarism undersecretion commonly involving all of the anterior pituitary hormones
• Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropic-
stimulating hormones)
• “everything is going to be decreased/diminished as a result”
POSTERIOR PITUITARY
- vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the
post. pit. but synthesized in the hypothalamus
- ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in
osmolality of the blood or be a decrease in BP
- Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during
lactation & increases contractions during labor + delivery
Diabetes Insipidus (DI) ➔ LOW ADH
• “DI = posterior pituitary is not producing enough ADH (vasopressin); patient will be eliminating a
lot of diluted urine (about 250 mL of urine an hour) so you need to give the vasopressin”
• too little ADH = will eliminate a lot of fluid
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion ➔ HIGH ADH
• “a lot of fluid accumulation”
• too much ADH = will retain a lot of fluid
DIABETES INSIPIDUS
• Patho: Deficiency of ADH decreases the collecting and distal renal tubules ability
to concentrate urine excessive diluted urine, excessive thirst, & excessive fluid intake
• “kidney is going to be affected by this lack of vasopressin
2|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
• patients will be very thirsty + require a lot of water b/c losing a lot of urine
• Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain
tumors, traumatic brain injury, infections of the nervous system, post hypophysectomy,
failure of renal tubules to respond to ADH, and use of specific meds
• Risk Factors:
o Head injuries and infections
o Lithium* or demeclocycline use
▪ *TQ: Lithium affects vasopressin, has a relationship with this hormone
▪ Google: Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium
therapy
▪ Another cause of DI is failure of the renal tubules to respond to ADH; this Nephrogenic form may
be related to hypokalemia, hypercalcemia, and a variety of medications (ex. lithium or
demeclocycline)
• Clinical manifestations
o Enormous daily urine output (greater than 250 mL/hr)
o Very dilute urine (specific gravity of 1.001-1.005) inability to increase the specific gravity + osmolality of
urine is characteristic of DI
o Intense thirst (pt. tends to drink 2-20 L of fluid daily – craves cold water)
o Urine does not contain abnormal substances like glucose or albumin
o Weight loss
o Increasing serum osmolality
o Elevated sodium levels
• Medical Management
o ADH replacement (Vasopressin, DDAVP) usually a long-term therapeutic program
▪ DDAVP = Desmopressin a synthetic vasopressin w/o the vascular effects of natural ADH; admin.
intranasal
▪ Vasopressin causes vasoconstriction (use cautiously w/ CAD pts)
o Administer diuretic
▪ “ONLY if the patient is compromised with CHF…this issue is not related to diuretic; it is
related to vasopressin so give vasopressin to control elimination of the diluted urine!”
o Low Na diet
▪ there is a lot of sodium accumulation – (action of ADH is on the distal tubule (not
proximal) so only water leaves) give low sodium diet for DI patients!
▪ IF DI is renal in origin, the other TXs are ineffective – thiazide diuretics, mild salt prep, and prostaglandin
inhibitors are used to treat the Nephrogenic form of DI
o Increase fluid intake (ensure adequate fluid replacement)
▪ *Disease cannot be controlled by limiting fluid intake b/c high-volume fluid loss of urine continues even
without fluid replacement. Attempts to restrict fluids cause patient to have insatiable craving for fluid and
development of hypernatremia and severe dehydration
• Nursing Management
o I & O and daily weights
o Monitor neuro status, VS
o No caffeine “caffeine triggers more fluid elimination”
o Monitor and manage fluid & electrolyte balance (retaining Na)
SIADH
Excessive ADH secretion from the pituitary gland even in the face of subnormal serum osmolality. These pts cannot excrete a dilute
urine, retain fluids a develop a sodium deficiency known as “dilutional hyponatremia”
• Patho: Excessive release of ADH renal absorption of water and suppresses renin-angiotensin
mechanism renal excretion of Na+ water intoxication, cellular edema, and dilutional
hyponatremia fluid shifts within compartments decreased serum osmolarity
• “losing a lot of sodium dilutional hyponatremia”; edema?
• Risk Factors:
o Malignancies may occur in pts w/ bronchogenic carcinoma in which malignant lung cells
synthesize + release ADH (non-endocrine origin)
o Head injury and infections disorders of the CNS (head injury, brain surgery or
tumor, and infection thought to produce SIADH by direct stimulation of pituitary gland
3|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
o CVA
o Medications
o Pain
o Stress
• Medical Management
o IVF NS to replace Na “losing the Na+ b/c a lot of ADH holding the fluid”
o Treat underlying cause
o Restricting fluid intake!
o Diuretics (Lasix) may be used along with fluid restriction if severe hyponatremia
• Nursing Management
o I & O and daily weights
o Monitor neuro status
o Monitor VS
o Monitor and manage fluid & electrolyte balance (losing Na)
ADRENAL GLANDS
ADRENAL MEDULLA – center portion of the gland
– Functions as part of the autonomic nervous system (ANS)
– Secretes catecholamine hormones (epinephrine and norepinephrine)
– ~90% of secretion is epinephrine (adrenaline)
– catecholamines regulate metabolic pathways to promote catabolism of stored fuels to meet
caloric needs from endogenous sources. Major effect of epinephrine release = prepare to meet
a challenge (fight or flight response); it causes blood flow to decrease in areas not needed in
emergency situations (ex. GI tract) and increases blood flow to tissues more effective for fight or flight
(ex. cardiac or skeletal muscle). They also increase BMR + blood glucose level.
ADRENAL CORTEX – outer portion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would
cause peripheral circulatory failure, circulatory shock, and prostration)
– Secretes steroid hormones:
– Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels
– Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act principally on
renal tubular and GI epithelium to increase Na+ ion absorption in exchange for excretion of K+ or H+ ions
– Sex hormones (mainly androgens)
– Secretion of hormones from adrenal cortex is regulated by the hypothalamic-pituitary-adrenal axis (hypothalamus secretes CRH, which
stimulates the pituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of
negative feedback mechanism– increased levels of the adrenal hormone then inhibit the production or secretion of CRH and ACTH.
– Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory response
to tissue injury and to suppress allergic manifestations
– Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hyperkalemia). ACTH only minimally
influences aldosterone secretion (primarily it is secretion in response to presence of angiotensin II in the bloodstream)
“Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon”
“Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland
is not functioning properly”
Phenochromocytoma
• Benign tumor of the adrenal medulla causes high blood pressure
• Clinical Manifestations
– Typical triad = headache, diaphoresis, and palpitations with hypertension –
– “fight or flight symptoms” …HTN, headache, hyperhidrosis, hypermetabolism, hyperglycemia (“the 5 H’s”)
4|Page
lOMoAR cPSD| 30878495
MED SURG EXAM 3 - Comprehensive review of the
materialcovered A+
MED SURG EXAM 3
ENDOCRINE DISORDERS (CH 52)
ADRENAL + PITUITARY DISORDERS
PITUITARY GLAND
-Abnormalities of the anterior and posterior portion of the gland may occur independently
-Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland
itself or of the hypothalamus (result is essentially the same)
-hypopituitarism can result from radiation therapy to the head + neck
-Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid,
gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair
loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not
replaced
ANTERIOR PITUITARY
-TSH, ACTH, FSH, and LH release hormones from other endocrine glands
-Prolactin acts on the breast to stimulate milk production
-GH protein hormone that increases protein synthesis in many tissues, increases the breakdown of
fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are
essential for normal growth)
Oversecretion:
• ACTH (Cushing’s)
• “Cushing’s syndrome – elevated cortisol level; blood sugar may be high”
• Basophilic tumors giv
• rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and
amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia
• GH (acromegaly)
• Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height
• Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall
• “Acromegaly – hypersecretion of GH; everything will be overdeveloped
1|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
– a lot of cardiac complications *
– sometimes they cannot see properly
– enlarged extremities, forehead
– female – might have issues with periods, anuria, or unable to have babies”
•
• Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all
proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the
excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin,
giving rise to ACROMEGALY.
Insufficient secretion:
– GH (dwarfism)
• Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth
• “Dwarfism – undersecretion of GH; other glands will be underdeveloped”
– Panhypopituitarism undersecretion commonly involving all of the anterior pituitary hormones
• Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropic-
stimulating hormones)
• “everything is going to be decreased/diminished as a result”
POSTERIOR PITUITARY
- vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the
post. pit. but synthesized in the hypothalamus
- ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in
osmolality of the blood or be a decrease in BP
- Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during
lactation & increases contractions during labor + delivery
Diabetes Insipidus (DI) ➔ LOW ADH
• “DI = posterior pituitary is not producing enough ADH (vasopressin); patient will be eliminating a
lot of diluted urine (about 250 mL of urine an hour) so you need to give the vasopressin”
• too little ADH = will eliminate a lot of fluid
Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion ➔ HIGH ADH
• “a lot of fluid accumulation”
• too much ADH = will retain a lot of fluid
DIABETES INSIPIDUS
• Patho: Deficiency of ADH decreases the collecting and distal renal tubules ability
to concentrate urine excessive diluted urine, excessive thirst, & excessive fluid intake
• “kidney is going to be affected by this lack of vasopressin
2|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
• patients will be very thirsty + require a lot of water b/c losing a lot of urine
• Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain
tumors, traumatic brain injury, infections of the nervous system, post hypophysectomy,
failure of renal tubules to respond to ADH, and use of specific meds
• Risk Factors:
o Head injuries and infections
o Lithium* or demeclocycline use
▪ *TQ: Lithium affects vasopressin, has a relationship with this hormone
▪ Google: Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium
therapy
▪ Another cause of DI is failure of the renal tubules to respond to ADH; this Nephrogenic form may
be related to hypokalemia, hypercalcemia, and a variety of medications (ex. lithium or
demeclocycline)
• Clinical manifestations
o Enormous daily urine output (greater than 250 mL/hr)
o Very dilute urine (specific gravity of 1.001-1.005) inability to increase the specific gravity + osmolality of
urine is characteristic of DI
o Intense thirst (pt. tends to drink 2-20 L of fluid daily – craves cold water)
o Urine does not contain abnormal substances like glucose or albumin
o Weight loss
o Increasing serum osmolality
o Elevated sodium levels
• Medical Management
o ADH replacement (Vasopressin, DDAVP) usually a long-term therapeutic program
▪ DDAVP = Desmopressin a synthetic vasopressin w/o the vascular effects of natural ADH; admin.
intranasal
▪ Vasopressin causes vasoconstriction (use cautiously w/ CAD pts)
o Administer diuretic
▪ “ONLY if the patient is compromised with CHF…this issue is not related to diuretic; it is
related to vasopressin so give vasopressin to control elimination of the diluted urine!”
o Low Na diet
▪ there is a lot of sodium accumulation – (action of ADH is on the distal tubule (not
proximal) so only water leaves) give low sodium diet for DI patients!
▪ IF DI is renal in origin, the other TXs are ineffective – thiazide diuretics, mild salt prep, and prostaglandin
inhibitors are used to treat the Nephrogenic form of DI
o Increase fluid intake (ensure adequate fluid replacement)
▪ *Disease cannot be controlled by limiting fluid intake b/c high-volume fluid loss of urine continues even
without fluid replacement. Attempts to restrict fluids cause patient to have insatiable craving for fluid and
development of hypernatremia and severe dehydration
• Nursing Management
o I & O and daily weights
o Monitor neuro status, VS
o No caffeine “caffeine triggers more fluid elimination”
o Monitor and manage fluid & electrolyte balance (retaining Na)
SIADH
Excessive ADH secretion from the pituitary gland even in the face of subnormal serum osmolality. These pts cannot excrete a dilute
urine, retain fluids a develop a sodium deficiency known as “dilutional hyponatremia”
• Patho: Excessive release of ADH renal absorption of water and suppresses renin-angiotensin
mechanism renal excretion of Na+ water intoxication, cellular edema, and dilutional
hyponatremia fluid shifts within compartments decreased serum osmolarity
• “losing a lot of sodium dilutional hyponatremia”; edema?
• Risk Factors:
o Malignancies may occur in pts w/ bronchogenic carcinoma in which malignant lung cells
synthesize + release ADH (non-endocrine origin)
o Head injury and infections disorders of the CNS (head injury, brain surgery or
tumor, and infection thought to produce SIADH by direct stimulation of pituitary gland
3|Page
, MED SURG EXAM 3 - Comprehensive review of the material covered A+
o CVA
o Medications
o Pain
o Stress
• Medical Management
o IVF NS to replace Na “losing the Na+ b/c a lot of ADH holding the fluid”
o Treat underlying cause
o Restricting fluid intake!
o Diuretics (Lasix) may be used along with fluid restriction if severe hyponatremia
• Nursing Management
o I & O and daily weights
o Monitor neuro status
o Monitor VS
o Monitor and manage fluid & electrolyte balance (losing Na)
ADRENAL GLANDS
ADRENAL MEDULLA – center portion of the gland
– Functions as part of the autonomic nervous system (ANS)
– Secretes catecholamine hormones (epinephrine and norepinephrine)
– ~90% of secretion is epinephrine (adrenaline)
– catecholamines regulate metabolic pathways to promote catabolism of stored fuels to meet
caloric needs from endogenous sources. Major effect of epinephrine release = prepare to meet
a challenge (fight or flight response); it causes blood flow to decrease in areas not needed in
emergency situations (ex. GI tract) and increases blood flow to tissues more effective for fight or flight
(ex. cardiac or skeletal muscle). They also increase BMR + blood glucose level.
ADRENAL CORTEX – outer portion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would
cause peripheral circulatory failure, circulatory shock, and prostration)
– Secretes steroid hormones:
– Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels
– Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act principally on
renal tubular and GI epithelium to increase Na+ ion absorption in exchange for excretion of K+ or H+ ions
– Sex hormones (mainly androgens)
– Secretion of hormones from adrenal cortex is regulated by the hypothalamic-pituitary-adrenal axis (hypothalamus secretes CRH, which
stimulates the pituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of
negative feedback mechanism– increased levels of the adrenal hormone then inhibit the production or secretion of CRH and ACTH.
– Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory response
to tissue injury and to suppress allergic manifestations
– Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hyperkalemia). ACTH only minimally
influences aldosterone secretion (primarily it is secretion in response to presence of angiotensin II in the bloodstream)
“Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon”
“Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland
is not functioning properly”
Phenochromocytoma
• Benign tumor of the adrenal medulla causes high blood pressure
• Clinical Manifestations
– Typical triad = headache, diaphoresis, and palpitations with hypertension –
– “fight or flight symptoms” …HTN, headache, hyperhidrosis, hypermetabolism, hyperglycemia (“the 5 H’s”)
4|Page
