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Endocrine > Posterior Pituitary Disorder - Exam 3 > Flashcards

Posterior Pituitary Disorder - Exam 3 Flashcards

1
Q

Posterior pituitary hormones are synthesized in the _____ and travel to the posterior pituitary where they are released

A

hypothalamus

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2
Q

Hormones released from the posterior pituitary gland are controlled by ???

A

nerve impulses from hypothalamus that maintain homeostasis

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3
Q

_____ is peptide hormone that is released by posterior pituitary. What are the 2 main functions?

A

oxytocin

uterine muscle contraction

milk let-down reflex

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4
Q

______ produces milk and ____ releases milk

A

prolactin= produces milk

oxytocin= releases milk

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5
Q

In SIADH what are the 4 major players and are they increasing or decreasing?

A

increasing: ADH and urine osm

decreasing: serum Na and blood osm

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6
Q

In DI what are the 4 major players and are they increasing or decreasing?

A

increasing: serum Na and blood osm

decreasing: ADH and urine osm

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7
Q

What are 5 actions of ADH?

A

Adjust water permeability of the collecting duct in kidneys

Electrolyte handling

Vascular resistance

Inhibited by cortisol

Stimulates vactor VIII and vWF release from vascular endothelium

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8
Q

The major stimuli to ADH secretion are _____ and effective circulating _____

A

hyperosmolality

volume depletion

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9
Q

_____ governing secretion of ADH are located in the _____. Where are volume receptors (baroreceptors) found? name two additional causes of increase ADH?

A

Osmoreceptors

hypothalamus

kidneys, heart, brain

nausea and surgery

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10
Q

In general, the ______ is the primary osmotic determinant of ADH release. What about in uncontrolled diabetics?

A

plasma sodium concentration

Glucose can also act as an osmole and promote ADH secretion

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11
Q

______ has an inhibitory effect on vasopressin therefore adrenal insufficiency would cause a ____ in vasopressin

A

Cortisol

rise

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12
Q

ADH is synthesized in the ____ and released by the _____

A

hypothalamus

secreted by the posterior pituitary

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13
Q

In relation to ADH and water, when ADH is high, water is (excreted/reabsorbed). When ADH is low, water is (excreted/reabsorbed).

A

high ADH, water is reabsorbed (collecting duct is highly permeable to water)

low ADH, water is excreted (collecting duct is NOT permeable to water)

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14
Q

if you drink a glass of water, _____ drops. hypothalamus sees this drop and signals _____. _____ leads to a large volume of diluted urine

A

plasma osmolality drops

pituitary gland to slow down the release of ADH

low ADH

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15
Q

What is SIADH characterized by? What is the helpful way to remember it?

A

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

soaked inside

too much ADH, too much water

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16
Q

SIADH is defined by _____ and _____ resulting from inappropriate, continued secretion or action of the hormone despite normal or increased plasma volume

A

hyponatremia

hypo-osmolality

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17
Q

SIADH is the MC cause of _______ ______ in hospitalized patients

A

euvolemic hyponatremia

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18
Q

SIADH consists of ____, inappropriately ????, and decreased _____ in a euvolemic patient. Why?

A

hyponatremia

elevated urine osmolality (>100 mOsm/kg)

serum osmolality

due to RAAS

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19
Q

weight gain
anorexia
NO edema aka NO hypervolumic
N/V
low serum sodium (irritability, confusion, hallucinations, seizures)

What am I?

A

SIADH

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20
Q

What is SIADH caused by?

A

inappropriate hypersecretion of ADH from the hypothalamus/pituitary or by ectopic production

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21
Q

What are 4 broad categories of SIADH?

A

Nervous system disorders

Neoplasms (small cell lung tumor is most common - secretes ADH)

Pulmonary diseases - hypercapnia (too much CO2) can stimulate ADH release

Drug induced - can stimulate release of ADH or potentiate effects

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22
Q

**What is the MC cause of neoplasms that secrete ADH?

A

small cell lung tumor

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23
Q

** What is a common pulmonary cause of SIADH?

A

hypercapnia (too much CO2) can stimulate ADH release

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24
Q

What specific drug classes are known to induce SIADH? What state?

A

psych drugs

post op state secrete too much ADH

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25
How does the severity of SIADH depend on? 2 things
severity of hyponatremia and rate of progression aka the faster the drop in sodium the worse the s/s
26
**What are the early s/s of SIADH that can ve seen with the Na serum is less than 125. What are worse s/s? What are they due to?
anorexia, nausea, malaise headache, muscle cramps, irritability, drowsiness, confusion, weakness, seizures, and coma These occur as osmotic fluid shifts result in cerebral edema and increased intracranial pressure
27
HA, confusion, impaired memory are ____ clinical presentation confusion, disorientation, somnolence, hallucinations, acute psychosis are _____. Seizures, severe somnolence and coma are _____
mild/moderate advanced grave danger!!
28
PE finding: In SIADH, the patient is typically _____ and _____
euvolemic and normotensive
29
Edema in a hyponatremic patient makes you think of ???? NOT ____
CHF, cirrhosis or CKD NOT SIADH
30
What factors need to be present in order to dx SIADH?
Hyponatremia with corresponding serum hypo-osmolality Continued renal excretion of Na+ increased urine osm and increased urine sodium concentration NO volume depletion s/s: aka must have normal skin turgor and blood pressure NO other cause of hyponatremia aka it is a dx of exclusion
31
**How you do you treat the hyponatremia in mild SIADH?
fluid restriction: stop giving fluids and everything should even out
32
What lab tests would you want to order if you suspect SIADH?
BMP, serum cortisol and TSH
33
What is the treatment of SIADH based on?
degree of hyponatremia is the pt symptomatic? is it acute (less than 48 hours) or chronic?
34
**Correcting hyponatremia too rapidly may result in ______ with permanent neurologic deficits. The magnitude of ______ rise, rather than the _____ correction rate, has more association with neurologic symptoms.
central pontine myelinolysis (CPM) **daily plasma sodium hourly
35
CPM is a neurological disease caused by ?????, and is characterized by ?????
severe damage of the myelin sheath of nerve cells in the brainstem, specifically the pons acute paralysis, dysphagia, and dysarthria, and other neurological symptoms.
36
What is the tx of SIADH in am emergent setting? What is it important to monitor for?
raise serum Na+ levels by 0.5-1 mEq/h, and not more than 10-12 mEq in the first 24 hours (Goal serum sodim is 125-130) **3% hypertonic saline: Furosemide: increase excretion of free water monitor: Neurological symptoms and serum Na+
37
What is the tx in an acute setting with moderate s/s?
3% hypertonic saline (513 mEq/L) Loop diuretics (furosemide) with saline Vasopressin-2 receptor antagonists (aquaretics, such as conivaptan) Water restriction
38
_______ MOA 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
Vaptans: Conivaptan (Vaprisol) and Tolvaptan (Samsca)
39
Collectively, agents that competitively block ADH action and increase water excretion are called _____
aquaretics
40
_____ is a parenteral dual V1a- and V2-receptor antagonist, which is approved for use in hospitalized patients with euvolemic (dilutional) and hypervolemic hyponatremia
conivaptan (Vaprisol)
41
________ is a selective oral V2 receptor antagonist approved for use in hospitalized patients for hypervolemic and euvolemic hyponatremia
Tolvaptan (Samsca)
42
What types of pts should you NOT use vaptans with?
avoided in hypovolemic hyponatremia
43
What is the primary risk with using vaptans? What is a benefit?
excessively rapid rate of correction of serum Na which is why these should only be used by experienced providers producing water excretion without electrolyte excretion and eliminating the need for fluid restriction
44
What is the tx for chronic SIADH?
fluid restriction and V2 receptor antagonists refer to nephro!!!
45
What is DI characterized by? What are some s/s?
Dry Inside aka decrease in ADH and water is getting peed out frequent urination blurry vision increased hunger paresthesia in the feet excessive thirst extreme fatigue weight loss
46
Diabetes insipidus is an uncommon disease characterized by an ____ in thirst and the passage of ????
increase large quantities of urine of low specific gravity
47
What is DI caused by ?
deficiency or resistance to vasopressin/ADH
48
What is primary central DI?
without a lesion on the pituitary or hypothalamus Many appear to be due to autoimmunity against hypothalamic arginine vasopressin (AVP)-secreting cells: think GENETIC causes
49
What is secondary central DI?
due to damage of the hypothalamus or pituitary can be: tumor, hypophysitis, infarction, hemorrhage, anoxic encephalopathy, surgical or accidental trauma, infection (eg, encephalitis, tuberculosis, syphilis), or granulomas (sarcoidosis or multifocal Langerhans cell granulomatosis)
50
What is nephrogeneic DI causes by?
defect in the*** kidney tubules** that interferes with water reabsorption aka: do NOT respond to ADH but there is plenty floating around present at birth and is due to defective expression of renal vasopressin V2 receptors or vasopressin-sensitive water channels
51
What are acquired forms of vasopressin-resistant DI due to?
pyelonephritis, renal amyloidosis, myeloma, or Sjögren syndrome
52
What is gestational DI caused by? How do you tx it?
circulating enzyme destroys native vasopressin give synthetic desmopressin
53
intense thirst craving for ice water polyuria large urine volumes What am I? How do they maintain fluid balance? What happens if they cannot?
DI continuing to ingest large volumes of water hypernatremia and dehydration in patients without free access to water,
54
What is an aggravating factor of DI?
high-dose corticosteroids because it increases renal free water clearance
55
What are 3 main tests that we can use to check for DI?
24-hour urine collection for volume and creatinine Water restriction test Vasopressin challenge test (supervised)
56
What would you expect the results of the 24-hour urine collection for volume and creatinine to be in a pt with DI? What is the exception?
urine volume should be greater than 2 liters urine sodium and urine osm should be low (aka the urine is SUPER DILUTE) urine volume will be less than 2 Liters if the pt is hypernatremic
57
What is the expect result of water restriction test for a DI pt? For vasopressin challenge test? describe the test.
urine with stay dilute when given ADH -> Central DI: volume should go down and concentration should go up! aka urine osmolality should increase/go back to normal Nephogenic: no change Desmopressin acetate 0.05–0.1 mL (5–10 mcg) intranasally (or 1 mcg subcutaneously or intravenously) is given, with measurement of urine volume for 12 hours before and 12 hours after administration
58
During the vasopressin challenge test what will pts with central DI report?
notice a distinct reduction in thirst and polyuria
59
need to order _____ to look for a lesion in DI
MRI
60
What tests do you need to order to dx nephrogenic DI? What is the expected result?
Measurement of serum vasopressin is done during fluid restriction and desmopressin challenge; vasopressin level is high in nephrogenic DI and we don’t see a change in urine osmolality
61
What is a way to distinguish central DI from other non DI potential causes?
restrict fluids there will be no change in DI pts and in the other causes it will cause lab values to normalize
62
What is the tx for mild DI? Central and gestational DI?
mild: adequate fluid intake central and gestational: Desmopressin acetate
63
**What are the SE of Desmopressin acetate?
hyponatremia, agitation, emotional changes, depression, increased risk of suicide
64
**What is the difference between micro and macro adenoma? What s/s are common with each?
Microadenomas (< 1 cm in diameter): complaints related to hormone excess Macroadenomas (> 1 cm in diameter): impinge on the optic chiasm or other structures, and may or may not affect hormones
65
Somatotrope is an adenoma affecting what hormone?
Growth hormone
66
_____ is the classic visual field defect in a patient with an expanding pituitary mass
Bitemporal hemianopia: aka they lose vision on both temporal sides
67
What is the best way to eval a pituitary adenoma?
MRI of the brain Ophthalmologic exam Laboratory studies based on the clinical presentation aka what hormone is being affected
68
What is the tx for a pituitary adenoma?
Transsphenoidal Surgery radiation: usually reserved for post-surgical management due to its slow onset of action medication based on what hormone is affected
69
What are 4 possible complications of transsphenoidal surgical resection?
hypopituitarism Permanent diabetes insipidus cranial nerve damage nasal septal perforation visual disturbances CSF leak carotid artery injury hypothalamic damage meningitis
70
Name the treatment of choice for the following conditions: prolactinomas acromegaly TSH secreting tumors ACTH-secreting tumors
prolactinomas -> dopamine agonists acromegaly -> somatostatin analogues and GH receptor antagonists TSH-secreting tumors -> somatostatin analogues ACTH-secreting tumors -> surgery and/or radiation
71

Endocrine (14 decks)

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