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Endocrinology > Posterior Pituitary Disorders > Flashcards

Posterior Pituitary Disorders Flashcards

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1
Q

what hormones inhibit milk production until birth?

A

estrogen and progesterone

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2
Q

what hormones induces growth of milk secreting epithelial cells?

A

oxytocin - muscle cells contract
prolactin - milk production

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3
Q

what hormone is responsible for contraction and cervix dilation during childbirth?

A

oxytocin

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4
Q

actions of ADH

A
  1. Adjust water permeability of the collecting duct in kidneys
  2. Electrolyte handling
    - Mild increase in reabsorption of Na+ and secretion of K+
  3. Vascular resistance
    - High levels of ADH increase vascular resistance, increasing BP
  4. Association with cortisol
    - Cortisol has an inhibitory effect on the secretion of both CRH and ADH
    - Adrenal insufficiency leads to a persistent rise in ADH release
  5. Factor VIII and vWF release from vascular endothelium
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5
Q

The major stimuli to ADH secretion are ? and ?

A

hyperosmolality
effective circulating volume depletion

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6
Q

what receptors govern secretion of ADH? Where are they located?

A

Osmoreceptors - detect increased osmotic pressure
hypothalamus

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7
Q

what is the primary osmotic determinant of ADH release?

A

plasma sodium concentration
since Na+ salts are the major effective extracellular solutes

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8
Q

what other solute can act as an osmole and promote ADH secretion in uncontrolled diabetics

A

glucose

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9
Q

what are not as sensitive as a control as osmoreceptors but detect decreased blood pressure

A

Volume receptors (baroreceptors)

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10
Q

what can potentially lead to as much as a 500-fold rise in circulating ADH levels

A

nausea

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11
Q

who may have elevated levels of ADH for several days due to a stress response; therefore must be cautious with over hydration

A

surgical patients
may be elevated for a few days after operation

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12
Q

When ADH is present, what happens to the collecting duct?

A

becomes highly permeable to water, resulting with small volume of concentrated urine aka diluted blood

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13
Q

when ADH is absent, what happens to the collecting duct?

A

not permeable to water, resulting with large volume of dilute urine aka diluted urine

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14
Q

describe the feedback loop between hypothalamus and pituitary gland when water is consumed

A
  1. water is absorbed into the blood
  2. Plasma osmolality drops, diluting blood with the water.
  3. Hypothalamus senses drop and signals the pituitary gland to slow down the release of ADH
  4. Low ADH leads to large volume of diluted urine (urine with low osmolality), bring plasma osmolality back to normal.
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15
Q

condition that results from hyponatremia and hypo-osmolality from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume

A

Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)

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16
Q

Most common cause of euvolemic hyponatremia in hospitalized patients

A

SIADH

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17
Q

what would SIADH labs for euvolemic patients look like?

A

1. hyponatremia
2. elevated urine osmolality (>100 mOsm/kg)
3. serum hypo-osmolality
4. Urine Sodium > 30-40 mmol/L. (normal is 20 on random sample)

(diagnosed when these findings occur in the setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function; in the absence of diuretic therapy)

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18
Q

MC causes SIADH?

A
  1. inappropriate hypersecretion of ADH from the hypothalamus/pituitary
  2. ectopic production
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19
Q

3 categories that cause SIADH

A
  1. stimulate ADH release
  2. potentiate effects of ADH action
  3. have an uncertain mechanism:
    - Nervous system disorders
    - Neoplasms
    - Pulmonary diseases - hypercapnia can stimulate ADH release
    - Drug induced - can stimulate release of ADH or potentiate effects
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20
Q

presentation of SIADH

A
  1. 125-134 mEq/L - Anorexia, nausea, malaise, HA, disorientation/confusion, impaired memory
  2. <125 - HA, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, and coma
    - osmotic fluid shifts result in cerebral edema and increased intracranial pressure

s/s based on severity of hyponatremia and rate of progression

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21
Q

since most pts with SIADH are euvolemic and normotensive, what presentations should you not see?

A

Peripheral and pulmonary edema
dry mucous membranes
reduced skin turgor
orthostatic hypotension

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22
Q

If edema is seen in a hyponatremic pt, what should you consider?

A

consideration of another hyponatremic state
- CHF
- cirrhosis
- CKD

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23
Q

Prominent physical examination findings may be seen only in severe or rapid-onset hyponatremia and can include:

A

Confusion
disorientation
delirium
generalized muscle weakness
myoclonus, tremor
hyporeflexia
ataxia
dysarthria
pathologic reflexes
generalized seizures
coma

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24
Q

what is the diagnostic criteria for SIADH?

A
  1. Hyponatremia corresponds with serum hypoosmolality
  2. Continued renal excretion of Na+
  3. increased Urine osmolality and urine sodium concentration
  4. Absence of clinical evidence of volume depletion:
    - Normal skin turgor
    - normal BP
  5. Absence of other causes of hyponatremia:
    - Adrenal insufficiency (mineralocorticoid deficiency, glucocorticoid deficiency)
    - hypothyroidism
    - cardiac failure
    - pituitary insufficiency
    - renal disease with salt wastage
    - hepatic disease
    - drugs that impair renal water excretion
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25
how do you correct hyponatremia in SIADH?
Correction of hyponatremia by fluid restriction
26
you suspect SIADH, what labs are you ordering?
1. Serum Na+, potassium, chloride, and bicarbonate 2. Plasma osmolality 3. Serum creatinine 4. Blood urea nitrogen 5. Blood glucose 6. Urine osmolality 7. Serum cortisol 8. TSH
27
The treatment of SIADH and the rapidity of correction of hyponatremia depend on?
1. degree of hyponatremia 2. asx vs. symptomatic 3. acute (< 48 h) vs. chronic
28
what can happen if hyponatremia is treated too quickly for SIADH?
**central pontine myelinolysis (CPM)** 1. neurological disease caused by _damage of myelin sheath_ in the brainstem, specifically the _pons_ - acute paralysis - dysphagia - dysarthria - other neurological symptoms.
29
when correcting hyponatremia, what has more association with neurologic symptoms
magnitude of **daily plasma sodium rise** > hourly correction rate
30
hyponatremic pts with symptoms such as seizures, stupor, coma, and respiratory arrest, regardless of the degree of hyponatremia are warranted for what type of tx? how?
_aggressive_ 1. **3% hypertonic saline** - _Furosemide_ increases excretion of free water and has been used along in severe cases to limit tx-induced volume expansion
31
if a hyponatremic pt needs aggressive tx, what are the goals/objectives?
1. correct at a rate that does not cause neurologic complications 2. raise serum Na+ levels by _0.5-1 mEq/h, and not more than 10-12 mEq in the first 24 hrs, and aim at maximum serum sodium of 125-130 mEq/L 3. Neurological symptoms and serum Na+ monitored frequently
32
tx for acute SIADH (<48 hr since onset)
1. 3% hypertonic saline (513 mEq/L) 2. Loop diuretics (furosemide) with saline 3. Vasopressin-2 receptor antagonists - aquaretics - conivaptan 4. Water restriction - 500-1500 mL/d (or even lower in some cases)
33
what med is responsible for inhibition of the AVP V2 receptor reduces the number of aquaporin-2 water channels in the renal collecting duct and decreases the water permeability of the collecting duct
vasopressin receptor antagonists
34
agents that competitively block ADH action and increase water excretion are called ?
_aquaretics aka vaptan_ useful in the treatment of the hyponatremia in SIADH have a profound effect on serum Na - should be used by physicians experienced in the management of hyponatremia
35
a parenteral dual V1a- and V2-receptor antagonist, which is approved for use in hospitalized patients with euvolemic (dilutional) and hypervolemic hyponatremia.
Conivaptan (Vaprisol)
36
a selective oral V2 receptor antagonist approved for use in hospitalized patients for hypervolemic and euvolemic hyponatremia
Tolvaptan (Samsca)
37
what med should be avoided in hypovolemic hyponatremia
aquaretics
38
main risk with aquaretics
excessively rapid rate of correction of serum Na
39
tx for chronic asx SIADH
1. fluid restriction 2. V2 receptor antagonists
40
a disease characterized by an increase in thirst and the passage of large quantities of urine of low specific gravity, the urine is otherwise normal
Diabetes insipidus
41
causes of Diabetes insipidus
**deficiency of vasopressin or resistance to vasopressin** 1. _Primary central_: Without an identifiable lesion noted on MRI of the pituitary and hypothalamus 2. _Secondary central_: damage to the hypothalamus or pituitary stalk 3. _Nephrogenic_: a defect in the kidney tubules that interferes with water reabsorption 4. _Vasopressinase-induced_: enzyme destroys native vasopressin; however, synthetic desmopressin is unaffected
42
which type of DI - Accounts for about 1/3 of cases of DI - Many appear to be due to autoimmunity against hypothalamic argininevasopressin (AVP)-secreting cells - The cause may also be genetic
Primary central diabetes insipidus:
43
which type of DI - _have normal secretion of vasopressin, and the polyuria is unresponsive to it_ - X-linked trait if congenital
Nephrogenic diabetes insipidus - less severe if acquired and are seen in pyelonephritis, renal amyloidosis, myeloma, or Sjögren syndrome
44
which type of DI may be seen in the last trimester of pregnancy and in the puerperium
Vasopressinase-induced diabetes insipidus
45
pt with intense thirst - craving for ice water polyuria ingesting fluid from 2 L to 20 L daily with correspondingly large urine volumes what could they have?
Diabetes insipidus
46
diabetes insipidus may present with hypernatremia and dehydration how?
1. without free access to water 2. a damaged hypothalamic thirst center and altered thirst sensation Most of the time are able to maintain fluid balance bc they drink hella water
47
what can aggravate diabetes insipidus?
administration of high-dose corticosteroids = increases renal free water clearance
48
diagnostic evaluation for diabetes insipidus
1. **24-hour urine collection for volume and creatinine** - < 2 L/24 h = _R/O_ (absence of hypernatremia) 2. Serum glucose, urea nitrogen, calcium, potassium, sodium, and uric acid levels 3. Restrict water intake - _central DI_ = the urine with stay dilute 4. supervised “**vasopressin challenge test**” - Give Desmopressin acetate, then measure urine volume for 12 h before and 12 h after administration - _central_ = less thirst and polyuria 5. MRI of the pituitary/hypothalamus/skull to look for masses - nonfamilial central diabetes insipidus 6. measure serum vasopressin during modest fluid restriction - nephrogenic - usually vasopressin lvl is high
49
Central diabetes insipidus must be distinguished from polyuria caused by?
**psychogenic polydipsia**, DM, Cushing syndrome or corticosteroid treatment, lithium, hypercalcemia, hypokalemia, and the nocturnal polyuria of Parkinson disease
50
tx for diabetes insipidus
1. _mild_ - none, adequate fluid intake 2. _central and vasopressinase-induced_ - **Desmopressin acetate**
51
____ is a synthetic analogue of vasopressin with fast and longer onset more specific antidiuretic action ____increases water permeability in renal tubular cells, which in turn decreases urine volume and increases urine osmolality
Desmopressin acetate desmopressin
52
SE of Desmopressin acetate
hyponatremia, agitation, emotional changes, depression with an increased risk of suicide
53
s/s of pituitary adenomas
1. majority clinically unapparent 2. expanding intracranial mass - HA, vision changes 3. manifestations of excess/deficiency 1+ pituitary hormones
54
what type of adenomas are more likely to present with complaints related to hormone excess
Microadenomas (< 10 mm in diameter)
55
what type of adenomas can impinge on the optic chiasm or other structures, and may or may not affect hormones
Macroadenomas (> 10 mm in diameter)
56
etiology of pituitary adenomas
1. Any cell type in the pituitary gland can undergo hyperplasia or give rise to a tumor - adenoma: benign tumor of epithelial cell origin 2. Symptoms depend on the size, growth rate, and secretory characteristics of the tumor 3. Which hormones the tumor secretes is a reflection of the cell type from which the tumor originated
57
6 classifications of adenomas and correlating hormone and syndrome they cause
1. Lactotrope - PRL - Hypogonadism, galactorrhea 2. Gonadotrope - FSH, LH, subunits - Silent or hypogonadism 3. Somatotrope - GH - Acromegaly/gigantism 4. Corticotrope - ACTH - Cushing's disease 5. Mammosomatotrope - PRL, GH - Hypogonadism, galactorrhea, acromegaly 6. Thyrotrope - TSH - Thyrotoxicosis
58
4 familial pituitary tumor syndromes and their clinical features
1. Multiple endocrine neoplasia 1 (MEN 1) - Hyperparathyroidism - Pancreatic neuroendocrine tumors - Foregut carcinoids - Adrenal adenomas - Skin lesions - Pituitary adenomas (40%) 2. Multiple endocrine neoplasia 4 (MEN 4) - Hyperparathyroidsm - Pituitary adenomas - Other tumors 3. Carney complex - Pituitary hyperplasia and adenomas (10%) - Atrial myxomas - Schwannomas - Adrenal hyperplasia - Lentigines 4. Familial pituitary adenomas - Acromegaly/gigantism (15%)
59
the classic visual field defect in a patient with an expanding pituitary mass
Bitemporal hemianopia
60
Roughly 40% of tumors found in autopsies are ?
prolactinomas
61
work up for pituitary adenomas
1. MRI of the brain 2. Ophthalmologic exam 3. Lab: - presenting clinical features of functional pituitary adenomas (acromegaly, prolactinomas, or Cushing's syndrome) should guide the laboratory studies
62
The goals of pituitary tumor treatment include:
1. normalization of excess pituitary secretion 2. improve s/s of hormonal hypersecretion syndromes 3. shrinkage or ablation of large tumor masses with relief of adjacent structure compression
63
what is the desired approach to surgery for pituitary tumors
Transsphenoidal Surgery
64
3 factors that determine the incidence of surgical complications
1. Tumor size 2. the degree of invasiveness 3. experience of the surgeon
65
tx for pituitary tumor
1. **Transsphenoidal Surgery** 2. Radiation - primary therapy or adjunct to surgery or medical therapy 3. Medication - depends on tumor type
66
why is radiation therapy usually reserved for postsurgical management
slow onset of action Used to treat residual tumor and in an attempt to prevent regrowth.
67
tx that offers the only means for potentially ablating significant postoperative residual nonfunctioning tumor tissue
Radiation
68
dopamine agonists are the treatment of choice for what type of adenoma?
prolactinomas
69
somatostatin analogues and GH receptor antagonists are indicated for what type of adenoma?
acromegaly
70
_somatostatin analogues_ and occasionally dopamine agonists are indicated for what type of adenoma?
TSH-secreting tumors
71
what type of adenomas are generally not responsive to medications and require surgery and/or irradiation?
_ACTH-secreting tumors_ and non-functioning tumors

Endocrinology (15 decks)

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