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Endocrinology > Posterior Pituitary > Flashcards

Posterior Pituitary Flashcards

1
Q

Describe the pathway of ADH/Oxytocin release

A

1) Hypothalamic neurons synthesize oxytocin or ADH
2) Transported down axons of hypothalamic-hypophyseal tract to posterior pituitary
3) Oxytocin/ADH are stored in axon terminals in posterior pituitary
4) Hypothalamic neurons firing causing releasing of oxytocin/ADH to blood

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2
Q

What is the function of oxytocin?

A

Releases milk and uterus muscle contractions during labor, dilation of cervix

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3
Q

What are the actions of vasopressin?

A

Adjust water permeability of collecting duct in kidneys
Electrolyte handling: mild increase in reabsorption of Na and secretion of K
Vascular resistance: increase vascular resistance —> increase BP
Association with cortisol: cortisol has inhibitory effect on CRH and ADH, adrenal insufficiency leads to a persistent rise in ADH
Factor VIII and vWF release from vascular endothelium

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4
Q

What are the major stimuli for ADH secretion?

A

Hyper osmolality and effective circulating volume depletion

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5
Q

How is osmolality and volume sensed to release ADH?

A

Osmoreceptors in the hypothalamus sense sodium concentration or glucose in uncontrolled diabetes

Baroreceptors also sense volume in aortic arch and carotid sinus

Cause release of ADH —> increased water reabsorption —> increased blood volume and pressure

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6
Q

What factors can increase circulating ADH?

A

Nausea (500 fold rise)
Surgery (elevated ADH for several days after operation due to stress response)

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7
Q

What is the action of ADH on the kidneys?

A

Adds aquaporins to the collecting duct leading to dilute blood (concentrated urine)

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8
Q

What happens to ADH when you drink a glass of water?

A

Water is absorbed into blood, plasma osmolality drops—> hypothalamus sees drop and signals pituitary gland to slow release of ADH —> low ADH leads to diluted urine —> plasma osmolality is back to normal

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9
Q

When extracellular fluid sodium concentration rises, plasma osmolality will ___

A

Increase

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10
Q

When plasma osmolality increases, all of the following occur except:

Thirst mechanism in hypothalamus is activated, anterior pituitary decreases release of ADH, ADH causes increased water absorption in collecting ducts, ADH causes vasoconstriction to increase BP

A

Anterior pituitary decreases release of ADH

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11
Q

Based on what you know about ADH, high levels of ADH will cause

Large Volume of dilute urine, small volume of concentrated urine

A

Small volume of concentrated urine

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12
Q

Based on what you know about ADH, high levels of ADH will cause

Large volume of dilute urine, small volume of concentrated urine

A

Small volume of concentrated urine (high urine osmolality)

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13
Q

Condition defined by hyponatremia and hypo-osmolality resulting from continued secretion or action of ADH despite normal or increased plasma volume

A

Syndrome of Inappropriate Antidiuretic Hormone secretion

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14
Q

What is the most common cause of euvolemic hyponatremia in hospitalized patients?

A

Syndrome of Inappropriate Antidiuretic Hormone secretion

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15
Q

SIADH consists of __________

A

Hyponatremia, inappropriately elevated urine osmolality, and decreased serum osmolality in a euvolemic patient, urine sodium >30-40 mmol/L (normal is 20 on random sample)

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16
Q

What setting does SIADH need to be diagnosed in?

A

Setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function in absence of diuretic therapy

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17
Q

What is the etiology of SIADH?

A

Inappropriate hypersecretion from hypothalamus/pituitary or ectopic production

4 categories that stimulate ADH release, potentiate ADH action, or have uncertain mechanism:
-nervous system disorders: acute psychosis, hemorrhage, inflammatory and demyelinating diseases, mass lesions, stroke, trauma
-Neoplasms: extra thoracic, mediastinal, pulmonary
-Pulmonary diseases: hypercapnia can stimulate ADH release
Drug-induced: can stimulate release of ADH or potentiate

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18
Q

What is the general clinical presentation of SIADH/early symptoms?

A

Based on severity of hyponatremia and rate of progression (slower=less symptoms)

Anorexia, nausea, and malaise are early symptoms and may be seen when serum Na is less than 125

Further decrease in Na: headache, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, and coma as osmotic fluid shift results in cerebral edema and increased ICP

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19
Q

What are the 3 key mild-moderate symptoms of SIADH?

A

Headache, disorientation/confusion, impaired memory

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20
Q

What are the 5 advanced symptoms of SIADH?

A

Confusion, disorientation, somnolence, hallucinations, acute psychosis

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21
Q

What are the 3 key symptoms of grave SIADH?

A

Seizures, severe somnolence, coma

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22
Q

In SIADH, the patient is normally ____ and _____ presenting as

A

Euvolemic, normotensive; peripheral and pulmonary edema, dry mucous membranes, reduced skin turgor, and orthostatic hypotension are usually absent

Edema in a hyponatremia patient warrants consideration of CHF, cirrhosis, or CKD

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23
Q

What is diagnostic criteria for SIADH?

A

Hyponatremia with corresponding serum hypo osmolality
Continued renal excretion of Na
Urine osmolality is increased
Absence of clinical evidence of volume depletion- normal skin turgor, blood pressure
Absence of other causes of hyponatremia ie adrenal insufficiency, hypothyroidism, cardiac failure, pituitary insufficiency, renal disease with salt wastage, hepatic disease, or drugs that impair renal water excretion
Correction of hyponatremia by fluid restriction

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24
Q

What labs should be ordered to diagnose SIADH and rule out other causes?

A

Serum Na+, potassium, chloride, and bicarbonate
Plasma osmolality
Serum creatinine
Blood urea nitrogen
Blood glucose
Urine osmolality
Serum cortisol
Thyroid-stimulating hormone

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25
What diagnostic tests should be ordered to help in diagnosis of SIADH and rule out other causes?
Serum Na+, potassium, chloride, bicarbonate Plasma osmolality Serum creatinine Blood urea nitrogen Blood glucose Urine osmolality Serum cortisol Thyroid-stimulating hormone
26
How is SIADH treated?
Depends on degree of hyponatremia, symptoms, and whether acute (<48 hours) or chronic Consult with nephrologist for difficult cases
27
What can correcting hyponatremia too rapidly in SIADH cause?
Central pontine myelin ply’s is with permanent neurologic deficits
28
Neurological disease caused by severe damage of the myelin sheath of nerve cells in the brain stem, specifically the pons, and characterized by acute paralysis, dysphagia, and dysarthria, and other neurological symptoms.
Central pontine myelinolysis
29
What is treatment of SIADH in an emergency setting?
Aggressive management if seizures, stupor, coma, respiratory arrest: Raise serum Na+ levels (by .5-1 mEq/h and not more than 10-12 mEq in first 24 hours) 3% hypertonic saline = fluid of choice Neurological symptoms and serum Na+ monitoring Furosemide increases excretion of free water and has been used along with hypertonic saline
30
How is SIADH treated in an acute setting?
3% hypertonic saline Loop diuretics with saline (furosemide) Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan) Water restriction
31
What is the MOA of vasopressin receptor antagonists?
Inhibition of AVP V2 receptor reduces number of aquaporins-2 water channels in the renal collecting duct and decreases water permeability of collecting duct
32
What are the aquaretics (agents that competitively block ADH action and increase water excretion)?
Vaptans: conivaptan (Vaprisol), IV Tolvaptan (Samsca), oral
33
What is the MOA of conivaptan?
Parenteral dual V1a and V2-receptor antagonist
34
What is the mechanism of action of tolvaptan?
Selective oral V2 receptor antagonist approved for use in hospitalized patients for hypervolemic and euvolemic hyponatremia
35
What should you keep in mind when using vaptans?
Have profound effect on serum Na Should be avoided in hypovolemic hyponatremia Benefit of prompt serum Na correction Risk of excessively rapid rate of correction of serum Na More effective than fluid restriction alone
36
How is SIADH treated in chronic setting?
Fluid restriction and V2 receptor antagonists, referral to nephrologist for chronic vaptan use
37
Condition characterized by increase in thirst and passage of large quantities of urine of low specific gravity, caused by a deficiency of vasopressin or resistance to vasopressin
Diabetes insipidus
38
What are the causes of primary central diabetes insipidus
Something is wrong with ADH release: no lesion of pituitary or hypothalamus Autoimmunity against hypothalamic AVP-secreting cells Genetic: familial diabetes insipidus -dominant genetic trait
39
What is the cause of secondary central diabetes insipidus?
Damage to hypothalamus or pituitary stalk by tumor, hypophysitis, infarction, hemorrhage, anoxic encephalopathy, surgical or accidental trauma, infection, or granulomas
40
What are causes of nephrogenic diabetes insipidus?
Defect in kidney tubules that interferes with water reabsorption Normal secretion of vasopressin and polyuria is unresponsive to it Congenital nephrogenic diabetes insipidus is present from birth due to defective expression of renal vasopressin V2 receptors or vasopressin-sensitive water channels (X-linked trait) Acquired: usually less severe, pyelonephritis, renal amyloidosis, myeloma, Sjogren syndrome
41
What is the cause of vasopressinase-induced diabetes insipidus?
Last trimester of pregnancy and puerperium, circulating enzyme destroys native vasopressin but synthetic desmopressin unaffected
42
What is the clinical presentation of diabetes insipidus?
Intense thirst Craving for ice water Polyuria: large urine volumes High volume of ingested fluid: 2 L to 20 L Partial diabetes insipidus = less intense symptoms, enuresis May present with hypernatremia and dehydration if no free access to water or altered thirst mechanism Aggravated by administration of high-dose corticosteroids, which increases renal free water clearance
43
How is diabetes insipidus diagnosed?
Clinical judgement, no single diagnostic test 24-hour urine collection for volume and creatinine (volume <2 L/24 hr rules out DI) Serum glucose, urea nitrogen, calcium, potassium, sodium, and uric acid levels Restrict water intake and pt with central DI = dilute urine Supervised vasopressin challenge test: desmopressin acetate IN with measurement of urine volume before and after admin —> if central DI, reduction in thirst and polyuria
44
In nonfamilial central DI, what should be done?
MRI of pituitary and hypothalamus to look for mass lesions
45
If nephrogenic DI is a diagnostic consideration, what diagnostic test should be done?
Measurement of serum vasopressin during mild fluid restriction
46
Central diabetes insipidus myst be distinguished from polyuria caused by _______
Psychogenic polydipsia, diabetes mellitus, Cushing syndrome, corticosteroid treatment, lithium, hypercalcemia, hypokalemia, and nocturnal polyuria of Parkinson’s disease
47
Central diabetes insipidus must be distinguished from polyuria caused by _____
Psychogenic polydipsia, diabetes mellitus, Cushing syndrome, or corticosteroid treatment, lithium, hypercalcemia, hypokalemia, and nocturnal polyuria of Parkinson’s disease
48
How is DI treated?
Mild: no treatment other than adequate fluid intake Desmopressin acetate for central and vasopressinase-induced DI
49
What is the MOA of desmopressin acetate?
Synthetic analogue of vasopressin with prompt onset and longer, more specific Antidiuretic action; increases water permeability in renal tubular cells, which decreases urine volume and increases urine osmolality
50
What can desmopressin acetate cause?
Agitation, emotional changes, and depression with increased risk of suicide, hyponatremia
51
A 26 year old female presents with signs and symptoms of diabetes insipidus. After a 24 hour fluid restriction, her urine osmolality normalizes. Which form of DI does this likely represent?
Psychogenic
52
A 51 year old male presents with signs and symptoms of diabetes insipidus. After a 24 hour fluid restriction period, his urine osmolality remains low. After administration of desmopressin, urine osmolality is still low. Which form of DI does this likely represent?
Nephrogenic
53
A 33 year old female presents with signs and symptoms of diabetes insipidus. After a 24 hour fluid restriction periods, her urine osmolality remains low. After administration of desmopressin, urine osmolality normalizes. Which form of DI does this likely represent?
Central
54
Which of the following stimulates the release of ADH? increased plasma volume, decreased plasma osmolarity, hyponatremia, nausea
Nausea
55
Which of the following lab findings would you expect to find with diabetes insipidus? Increased plasma osmolarity, increased urine osmolarity, hyponatremia
Increased plasma osmolarity
56
In a patient with central DI, what happens during water deprivation when ADH is given?
Treatment with ADH with concentrate urine
57
How common are pituitary adenomas?
One in 6 autopsies
58
What are symptoms and signs of pituitary adenomas?
Related to expanding intracranial mass (headaches, vision changes) and/or manifestations of excess or deficiency of one or more pituitary hormones
59
Which type of pituitary adenoma is more likely to present with complaints related to hormone excess?
Micro adenomas
60
Which type of pituitary adenoma can impinge on the optic chiasm or other structures and may or may not affect hormones?
Macro adenomas
61
What is the etiology of pituitary adenomas?
Benign tumor of epithelial cell origin Any cells type undergoes hyperplasia
62
What are clinical syndromes of lactotrope adenomas?
Hypogonadism, galactorrhea
63
What are clinical syndromes of gonadotropin adenoma cell origin?
Silent or hypogonadism
64
What is the clinical syndrome associated with somatotrope adenoma cell origin?
Acromegaly/gigantism
65
What is the clinical syndrome associated with corticotrope adenoma cell origin?
Cushing’s disease
66
What is the clinical syndrome associated with mammosomatotrope adenoma cell origin?
Hypogonadism, galactorrhea, acromegaly (PRL, GH product)
67
What is the clinical syndrome associated with thyrotrope adenoma cell origin?
Thyrotoxicosis
68
What are clinical features of MEN 1?
Hyperparathyroidism Pancreatic Neuro endocrine tumors Foregut carcinoids Adrenal adenomas Skin lesions Pituitary adenomas
69
What are the clinical features of MEN 4?
Hyperparathyroidism Pituitary adenomas Other tumors
70
What are the clinical features of carney complex?
Pituitary hyperplasia and adenomas Atrial myxomas Schwannomas Adrenal hyperplasia Lentigines
71
What is the classic visual field defect in a patient with an expanding pituitary mass?
Bitemporal hemianopia
72
How is pituitary adenoma diagnosed?
MRI of the brain Opthalmologic exam Laboratory studies: presenting clinical features of functional pituitary adenomas should guide studies
73
What is treatment of pituitary adenoma?
Goals: normalize excess pituitary secretion, amelioration of symptoms and signs, shrinkage or ablation of large tumor masses Transphenoidal surgery is desired surgical approach Radiation Medication, depending on tumor type
74
What are complications of transphenoidal surgery?
(Mortality rate 1%), transient DI, hypopituitarism, permanent DI, nasal septal perforation, visual disturbances Less common: carotid artery injury, loss of vision, hypothalamic damage, meningitis
75
Why would radiation be used for pituitary adenoma treatment?
Primary therapy or adjunct to surgery, usually for post surgical management
76
What medication is the treatment of choice for prolactinomas?
Dopamine agonists
77
What is the treatment with medication for acromegaly?
Somatostatin analogues, GH receptor antagonists
78
What are the treatments for TSH secreting tumors?
Somatostatin analogues and dopamine agonists
79
What are the medication treatments for ACTH secreting tumors?
Generally not responsive to medications and require surgery and/or irradiation

Endocrinology (6 decks)

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