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Endocrine > Posterior PItuitary > Flashcards

Posterior PItuitary Flashcards

1
Q

The primary determinant of free water excretion in humans is the regulation of urinary water excretion by circulating levels of

A

arginine vasopressin (AVP) [antidiuretic hormone {ADH}] in plasma.

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2
Q

where is ADH stored?

A

In the posterior pituitary in large amounts

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3
Q

The supraoptic and paraventricular nuclei of the anterior hypothalamus synthesize AVP, package it into granules, and transport the granules along their axons to nerve terminals in the

A

posterior lobe of the pituitary (the magnocellular neurons).

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4
Q

Levels of circulating AVP depend on both the

A

rate of AVP release from the posterior pituitary and the rate of AVP degradation.

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5
Q

The major factor controlling AVP release is _____The half-life of AVP in the circulation is 18 minutes. Diseases of the liver and kidney may impair AVP degradation and may thereby contribute to water retention.

A

plasma osmolality.

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6
Q

ADH binds to the V 2 receptor (a G-protein-linked receptor) on the basolateral membrane of the _______, and activates adenylyl cyclase increasing the intracellular concentration of cyclic adenosine monophosphate (cAMP).

A

renal collecting tubule

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7
Q

cAMP binds to the regulatory subunits of protein kinase and induces a conformational change, causing these subunits to dissociate from the catalytic subunits. These activated subunits (C) as shown here are anchored to an ______containing endocytic vesicle via an A-kinase anchoring protein (AKAP).

A

aquaporin-2 (AQP2)

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8
Q

When AVP is not available, what happens to AQP2?

A

AQP2 water channels are retrieved by an endocytic process, and water permeability returns to its original low rate. AQP3 and AQP4 water channels are expressed constitutivelyat the basolateral membrane

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9
Q

What is the end result of ADH release?

A

increase AQP2 translocation to the renal tubulels to REABSORB water into the body thus you should get hypertonic urine in normal perso

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10
Q

The release of ADH in response to changes in volume or pressure is less sensitive than the release in response to osmoreceptors, and generally a ______ reduction in blood volume or pressure is needed to stimulate the release of ADH

. However, once arterial pressure falls below this threshold, the stimulated response is exponential, and plasma levels of ADH are markedly greater than those from osmotic stimulation.

A

10 to 15%

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11
Q

The collecting duct is the primary site of ADH response, which leads to

A

urine concentration

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12
Q

Increases in plasma osmolality above approximately 290 to 295 mOsm/kg result in increases in plasmaADH but no further concentration of the urine, which is limited by

A

the maximal osmolality in the inner medulla.

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13
Q

• Urine volume does not change substantially until there is nearly absent ADH secretion, after which urine volume

A

increases dramatically.

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14
Q

defined by continuous inappropriate secretion of ADH, despite normal or increased plasma volume, causing impaired water excretion and resulting in hyponatremia and hypo-osmolality

A

SIADH

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15
Q

Symptoms associated with SIADH

A

depend upon the rate of onset and degree of hyponatremia.

Rapid or severe hyponatremia/hypo-osmolality leads to acute edema of the brain cells. :neurological symptoms that range from headache, apathy, agitation, muscle cramps, weakness, and may develop into confusion, seizures, and coma

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16
Q

Etiologies of SIADH

A

Cerebral, Drugs, lung disease, miscellaneous

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17
Q

The cardinal feature of SIADH is______, and often this is an incidental lab finding without any obvious clues in the history or physical examination.

A

hyponatremia

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18
Q

You order labs for a pt and notice they are HYPOnatremic, you know this can be caused by SIADH, What lab would you order next?

A

Measure pts serum osmolality:

are they isotonic, hypertonic or hypotonic

*PT with SIADH will have HYPOtonic serum osmolality

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19
Q

YOu are doing a work up on a pt while rotating through endocrinology. They are hyponatrermic and has a HYPOtonic serum osmolality. What would you do next if you suspect SIADH?

A

Assess pts volume status

for SIADH, most are Euvolemic

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20
Q

Pt is:

HYPOnatremic

HYPOtonic (<275) serum osmolality

Euvolemic

what is the next step of your work up for SIADH?

A

Get urine osmolality:

>100 = SIADH/hypothryoidism or adrenal insuffuciency

If <100 they have water intoxication

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21
Q

What do we expect for pt with SIADH

Hypo/hypernatremic

serum osmolality:

volume status:

urine osmolality:

A

HYPOnatremic

Hypotonic (<275) for serum

Euvolemic

>100 for urine osmolality

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22
Q

SIADH is a diagnosis of:

A

Exclusion:

• Hypothyroidism and adrenal insufficiency have both been ruled out

23
Q

What do we see for urine osomolality and urine sodium in SIADH

A

A urine osmolality >100 mM (ie urine is not maximally dilute despite low serum Osm!!) • A urine sodium >20 mEq/L

24
Q

What do we do for tx in pt with SIADH

A

Try to find out cause and correct it: may need a CT or MRI but get very specific pt history

25
Q

What is the focus of tx pt’s with SIADH

A

correct hyponatremia and hypo-osmolality

26
Q

Tx recommendation for SIADH (not including drugs)

A
  • Fluid Restriction o Usually the first step in management of mild or chronic SIADH o Oral fluid intake is limited to < 1 L per day
  • IV salt solution o Typically reserved for us in symptomatic patients o Solution given must be of greater osmolality than the urine, or will exacerbate hyponatremia
  • Oral salt tablets
27
Q

MOA of Conivaptan and Talvaptan

A

Vasopressin Receptor Antagonists

Block V2 receptors thereby limiting AQ2 channels and reducing water permeability.

28
Q

What are some concerns with Conivaptan and Talvaptan to tx SIADH

A

o Typically limit the overall use < 30 days

o Expensive to use

o Rarely associated with liver failure

29
Q

MOA of furosemide and bumetanide

A

Loop diuretics

o Directly diminish the renal medullary gradient

o Furosemide 20 mg twice daily o Must be careful to monitor other serum electrolytes (eg potassium)

30
Q

How do we correct hyponatremia in SIADH

A

• The rate of sodium correction should reflect the acuity or severity of disease. • Overly rapid resolution can cause water to leave brain cells too quickly, leading to osmotic shrinkage that results in severe damage to the myelin sheath of the axons (“osmotic demyelination syndrome”). This can cause various symptoms that include confusion, paralysis, and altered speech/swallow.

31
Q

heterogeneous disorder that is due to either deficient production/release of AVP from the posterior pituitary, or due to renal resistance to AVP activity. This results in high volumes (> 3 L/day) of dilute urine.

A

Diabetes Insipidus (DI)

32
Q

Deficient production/release of AVP is called _____ Diabetes Insipidus.

A

Central (or neurogenic)

33
Q

Renal resistance to AVP is called____ Diabetes Insipidus

A

Nephrogenic

34
Q

causes of central Diabetes insipidus

A
  • Autoimmune injury to the hypothalamus/pituitary
  • Head Trauma or Surgery
  • Cerebral hypoperfusion
  • Tumors (pituitary adenoma, craniopharyngioma, meningioma)
  • Infiltrative disorders (sarcoidosis, histiocytosis)
35
Q

Causes of Nephrogenic Diabetes inspipidus

A

• X-linked recessive disorders • Hypokalemia • Hypercalcemia • Renal Diseases • Drugs (eg Lithium)

36
Q

persistent consumption of oral fluids results in an appropriate diuresis that resembles the high urine volumes seen above.

A

Primary polydipsia

37
Q

The individual with diabetes insipidus can often consume sufficient (large) volumes of fluids to replace free water loss and maintain the

A

measured sodium in the normal/high normal range.

38
Q

if there is any limit to the availability of water, or if there is any impairment of the thirst mechanism, hypernatremia may rapidly develop in these pts.

A
39
Q

In diabetes insipidus, Rapid or severe hypernatremia/hyper-osmolality leads to loss of water from brain cells. This may cause a similar spectrum of neurological symptoms that range from

A

headache, apathy, agitation, muscle cramps, weakness, and may develop into confusion, seizures, and coma

40
Q

Your pt comes in with HYPERnatremia and your attending want you to do a workup, what do you do next?

A

Asses volume status!

These pts are Euvolemic (but decreased total body water)

41
Q

Pt is HYPERnatremic, euvolemic and is peeing like crazy, what do you need to assess next?

A

Urine osmolality

for DI: see <300mOsm

42
Q

A urine osmolality test shows up with <300 mOsm, what is your next step to find out why this pt is HYPERnatremic and is experiencig polyuria

A

Do water deprevation test

43
Q

Results form water depreveation test:

urine osmolality <300

plasma osmollality >300

A

Diabetes insipidus

44
Q

You perfrom a water deprivation test and results are: serum osmolality and sodium do NOT rise above normal ranges and the urine osmolality concentrates (>500 mM), this is consistent with

A

primary polydipsia

45
Q

You perform the water deprivation test, If the serum osmolality reaches 295 mM and the urine osmolality does not increase _____has been established

A

Diabetes insipidus

46
Q

If the serum osmolality reaches 295 mM and the urine osmolality does not increase Diabetes insipidus has been established

Measure the AVP level at this time and give the patient

A

(Give synthetic AVP (DDAVP) subcutaneously to assess response:

47
Q

urine osmolality increases by >50% if complete, and by 15-50% in partial. In both cases, the urine osmolality will rise>300 mM

A

central DI

48
Q

Nephrogenic DI: urine osmolality increases by ____, but remains_____

A

< 10%

< 300 mM

49
Q

Central DI: urine osmolality increases by >50% if complete CDI, and by 15-50% in partial DI. In both cases, the urine osmolality will _____

A

rise>300 mM after DDVAP

50
Q

Pt comes in with diabetes insipidus and is very dehyrdrated, what do you do?

A

restore volume. We may provide initial isotonic saline until the effective circulating volume is corrected. Then, IV or enteral free water is given to lower the serum sodium.

51
Q

What are teh guidelines for correction rate of pt with hypernatremia?

A

o The correction rate must reflect the acuity and severity of illness.

o Correct >1-2 mEq/hr if symptomatic or if severe hypernatremia (>160 mEq/L)

o Otherwise, correct 0.5 mEq/L/hr and aim for no more than 10-12 mEeq/L/day

52
Q

In central diabetes insipidus, we can tx the patient by replace the missing hormone with a synthetic form of ADH called

A

DDAVP (desmopressin,1-deamino-8-D-arginine vasopressin). (DDAVP is the preferred drug for the treatment of central diabetes insipidus)

53
Q

DDVAP has a long half-life of:

o Start with DDAVP 1 mcg IV/SC and repeat the dose when polyuria returns

o Can transition to DDAVP 0.1 mg PO by mouth, typically twice daily

A

(8 to 12 hours)

54
Q

Tx for neprhogentic DI

A

low salt, low protein diet

start a thiazide

use NSAIDS to inhibit renal prostaglandins

Endocrine (20 decks)

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