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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
Q

How does the severity of SIADH depend on? 2 things

A

severity of hyponatremia and rate of progression

aka the faster the drop in sodium the worse the s/s

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26
Q

**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?

A

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

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27
Q

HA, confusion, impaired memory are ____ clinical presentation

confusion, disorientation, somnolence, hallucinations, acute psychosis are _____.

Seizures, severe somnolence and coma are _____

A

mild/moderate

advanced

grave danger!!

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28
Q

PE finding: In SIADH, the patient is typically _____ and _____

A

euvolemic and normotensive

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29
Q

Edema in a hyponatremic patient makes you think of ???? NOT ____

A

CHF, cirrhosis or CKD

NOT SIADH

30
Q

What factors need to be present in order to dx SIADH?

A

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
Q

**How you do you treat the hyponatremia in mild SIADH?

A

fluid restriction: stop giving fluids and everything should even out

32
Q

What lab tests would you want to order if you suspect SIADH?

A

BMP, serum cortisol and TSH

33
Q

What is the treatment of SIADH based on?

A

degree of hyponatremia

is the pt symptomatic?

is it acute (less than 48 hours) or chronic?

34
Q

**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.

A

central pontine myelinolysis (CPM)

**daily plasma sodium

hourly

35
Q

CPM is a neurological disease caused by ?????, and is characterized by ?????

A

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
Q

What is the tx of SIADH in am emergent setting? What is it important to monitor for?

A

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
Q

What is the tx in an acute setting with moderate s/s?

A

3% hypertonic saline (513 mEq/L)

Loop diuretics (furosemide) with saline

Vasopressin-2 receptor antagonists
(aquaretics, such as conivaptan)

Water restriction

38
Q

_______ 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

A

Vaptans: Conivaptan (Vaprisol) and Tolvaptan (Samsca)

39
Q

Collectively, agents that competitively block ADH action and increase water excretion are called _____

A

aquaretics

40
Q

_____ is a parenteral dual V1a- and V2-receptor antagonist, which is approved for use in hospitalized patients with euvolemic (dilutional) and hypervolemic hyponatremia

A

conivaptan (Vaprisol)

41
Q

________ is a selective oral V2 receptor antagonist approved for use in hospitalized patients for hypervolemic and euvolemic hyponatremia

A

Tolvaptan (Samsca)

42
Q

What types of pts should you NOT use vaptans with?

A

avoided in hypovolemic hyponatremia

43
Q

What is the primary risk with using vaptans? What is a benefit?

A

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
Q

What is the tx for chronic SIADH?

A

fluid restriction and V2 receptor antagonists

refer to nephro!!!

45
Q

What is DI characterized by? What are some s/s?

A

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
Q

Diabetes insipidus is an uncommon disease characterized by an ____ in thirst and the passage of ????

A

increase

large quantities of urine of low specific gravity

47
Q

What is DI caused by ?

A

deficiency or resistance to vasopressin/ADH

48
Q

What is primary central DI?

A

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
Q

What is secondary central DI?

A

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
Q

What is nephrogeneic DI causes by?

A

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
Q

What are acquired forms of vasopressin-resistant DI due to?

A

pyelonephritis, renal amyloidosis, myeloma, or Sjögren syndrome

52
Q

What is gestational DI caused by? How do you tx it?

A

circulating enzyme destroys native vasopressin

give synthetic desmopressin

53
Q

intense thirst
craving for ice water
polyuria
large urine volumes

What am I?
How do they maintain fluid balance? What happens if they cannot?

A

DI

continuing to ingest large volumes of water

hypernatremia and dehydration in patients without free access to water,

54
Q

What is an aggravating factor of DI?

A

high-dose corticosteroids because it increases renal free water clearance

55
Q

What are 3 main tests that we can use to check for DI?

A

24-hour urine collection for volume and creatinine

Water restriction test

Vasopressin challenge test (supervised)

56
Q

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?

A

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
Q

What is the expect result of water restriction test for a DI pt? For vasopressin challenge test? describe the test.

A

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
Q

During the vasopressin challenge test what will pts with central DI report?

A

notice a distinct reduction in thirst and polyuria

59
Q

need to order _____ to look for a lesion in DI

A

MRI

60
Q

What tests do you need to order to dx nephrogenic DI? What is the expected result?

A

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
Q

What is a way to distinguish central DI from other non DI potential causes?

A

restrict fluids

there will be no change in DI pts and in the other causes it will cause lab values to normalize

62
Q

What is the tx for mild DI? Central and gestational DI?

A

mild: adequate fluid intake

central and gestational: Desmopressin acetate

63
Q

**What are the SE of Desmopressin acetate?

A

hyponatremia, agitation, emotional changes, depression, increased risk of suicide

64
Q

**What is the difference between micro and macro adenoma? What s/s are common with each?

A

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
Q

Somatotrope is an adenoma affecting what hormone?

A

Growth hormone

66
Q

_____ is the classic visual field defect in a patient with an expanding pituitary mass

A

Bitemporal hemianopia: aka they lose vision on both temporal sides

67
Q

What is the best way to eval a pituitary adenoma?

A

MRI of the brain

Ophthalmologic exam

Laboratory studies based on the clinical presentation aka what hormone is being affected

68
Q

What is the tx for a pituitary adenoma?

A

Transsphenoidal Surgery

radiation: usually reserved for post-surgical management due to its slow onset of action

medication based on what hormone is affected

69
Q

What are 4 possible complications of transsphenoidal surgical resection?

A

hypopituitarism
Permanent diabetes insipidus
cranial nerve damage
nasal septal perforation
visual disturbances
CSF leak
carotid artery injury
hypothalamic damage
meningitis

70
Q

Name the treatment of choice for the following conditions:
prolactinomas
acromegaly
TSH secreting tumors
ACTH-secreting tumors

A

prolactinomas -> dopamine agonists

acromegaly -> somatostatin analogues and GH receptor antagonists

TSH-secreting tumors -> somatostatin analogues

ACTH-secreting tumors -> surgery and/or radiation

71
Q
A

Endocrine (14 decks)

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