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CM 1A: Heme/Onc/Endo > Lecture 20: Posterior Pituitary Disorders > Flashcards

Lecture 20: Posterior Pituitary Disorders Flashcards

1
Q

What two hormones does the posterior pituitary secrete?

A
  • ADH/Vasopressin
  • Oxytocin
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2
Q

What is the primary function of ADH?

A

Adjusting water permeability of the collecting duct in the kidneys.

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3
Q

What are the other functions of ADH?

A
  • Electrolyte handling (Increases Na+ resorption, secretion of K+)
  • Vascular resistance (high levels of ADH = high resistance = high BP)
  • Association with cortisol (Cortisol inhibits release of ADH, Adrenal insufficiency therefore leads to high levels of ADH)
  • F8 and vWF release from vascular endothelium (ADH can treat mild vWD.)
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4
Q

What are the major stimuli to ADH secretion?

A
  • Hyperosmolality
  • Effective circulating volume depletion
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5
Q

Where do I find the osmoreceptors that govern secretion of ADH?

A

Hypothalamus.

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6
Q

What specific osmolality/plasma concentration determines ADH release?

A

Serum sodium concentration

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7
Q

What can act as a secondary osmole to promote ADH release?

A

Glucose in uncontrolled DM.

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8
Q

What two physiological conditions/situations can lead to increased ADH levels?

A
  • Nausea (up to 500x rise)
  • Surgery (Post-op due to stress. AVOID OVERHYDRATION)
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9
Q

What are the two receptors that govern ADH release? Which is more sensitive?

A
  • Osmoreceptors in the hypothalamus (MOST sensitive)
  • Baroreceptors (volume)
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10
Q

When ADH is present in high levels in the collecting duct, what happens to our urine?

A

Urine concentrates. Our collecting duct becomes PERMEABLE to water, so we retain water.

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11
Q

What exactly does ADH work on in the collecting duct?

A

Aquaporins.

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12
Q

Clinical

Walter White, who likes to stay hydrated, suddenly drinks 3 glasses of water. Describe the effect this has on his plasma osmolality and the body’s process to restore it.

A
  1. Water is absorbed into the blood, lowering plasma osmolality (dilutes the blood)
  2. The hypothalamus uses its osmoreceptors to detect the change in osmolality, signaling the pituitary to SLOW DOWN the release of ADH.
  3. Low ADH = urine dilution, bc the collecting duct is IMpermeable to water.
  4. Our plasma osmolality returns to baseline as we get rid of the excess water.
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13
Q

Clinical

When extracellular fluid sodium concentration rises, plasma osmolality will…

A

Increase

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14
Q

Clinical

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

  • Thirst mechanism in hypothalamus is activated
  • Anterior pituitary decreases the release of ADH
  • ADH causes increased water absorption in collecting ducts
  • ADH causes vasoconstriction to increase BP
A

Anterior pituitary decreases the release of ADH.

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15
Q

Clinical

Based on what you know about ADH, high levels of ADH will do what to urine?

A

Decrease urine volume, increasing concentration. (high urine osmolality)

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16
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

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17
Q

What defines SIADH?

A
  • HYPOnatremia
  • HYPO-osmolality
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18
Q

What is SIADH the MCC of in hospitalized patients?

A

Euvolemic Hyponatremia

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19
Q

What 3 things characterize SIADH?

A
  1. Hyponatremia
  2. Elevated urine osmolality (>100)
  3. Decreased serum osmolality in a EUVOLEMIC pt
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20
Q

Is urine sodium elevated or decreased in a patient with SIADH?

A

Increased. They are retaining so much water from their ADH.

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21
Q

When do we diagnose SIADH?

A

If the 3 conditions occur with normal functioning of other organs and WITHOUT diuretic therapy.

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22
Q

What are the two MC of SIADH?

A
  • Inappropriate hypersecretion by hypothalamus/pituitary
  • Ectopic production
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23
Q

What are the 4 categories of SIADH causes and what are the 3 possible ways they cause SIADH?

A

4 categories:
* Nervous system disorders
* Neoplasms
* Pulmonary diseases (hypercapnia stimulates ADH release)
* Drug induced (stimulates release or potentiates)

3 mechanisms:
* Stimulate ADH release
* Potentiate effects of ADH
* Uncertain mechanism

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24
Q

What are the S/S of SIADH dependent on?

A
  • Severity of hyponatremia
  • Rate at which it progresses.
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25
Q

What are the early symptoms of hyponatremia? What serum level do they occur at?

A
  • Anorexia
  • Nausea
  • Malaise

Serum < 125mEq/L

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26
Q

As hyponatremia progresses, what symptoms does it typically present with?

A
  • HA
  • Muscle cramps
  • Irritability
  • Drowsiness
  • Confusion
  • Weakness
  • Seizures
  • Coma
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27
Q

What is the pathophysiological process behind the more severe symptoms of hyponatremia?

A

Osmotic fluid shifts lead to:
* Cerebral edema
* Increased ICP

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28
Q

What is mild hyponatremia? Advanced? Grave/severe?

A
  • Mild-moderate: 125-134
  • Advanced: < 125
  • Grave < 120

Slide contradicts previous just FYI LOL

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29
Q

If a patient with suspected SIADH presents with edema (not cerebral), what should we consider?

A

Edema is uncommon in SIADH, so consider CHF, cirrhosis, or CKD.

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30
Q

What is the diagnostic criteria for SIADH?

A
  • Hyponatremia with serum hypoosmolality
  • Continued renal excretion of Na+
  • Urine osmolality increased along with urine sodium.
  • Absence of any volume depletion (normal skin turgor/BP)
  • Absence of any other cause of hyponatremia
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31
Q

What is the primary treatment for SIADH?

A

Fluid restriction to correct hyponatremia.

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32
Q

What tests might we order to diagnose SIADH and r/o other etiologies?

A
  • Serum Na, L, Cl, Bicarb
  • Plasma osmolality
  • Serum creatinine
  • BUN
  • BG
  • Urine osmolality
  • Serum cortisol
  • TSH
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33
Q

What is treatment of SIADH dependent on?

A
  • Degree of hyponatremia
  • Symptomatic or not
  • Acute (< 48h) or chronic
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34
Q

Why can we not treat severe hyponatremia quickly?

A

Central pontine myelinolysis (CPM) can occur, causing PERMANENT neuro deficits.

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35
Q

When correcting sodium in a hyponatremic patient, what do we specifically monitor to prevent CPM?

A

Magnitude of the daily plasma sodium rise.

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36
Q

In what situations do we correct hyponatremia ASAP regardless of the degree of the condition?

A
  • Seizing
  • Coma
  • Stupor
  • Respiratory arrest

Emergency treatment protocol.

37
Q

What are the goals of aggressive sodium correction of a hyponatremic patient?

A

Primary goal: Correct hyponatremia without causing more neurological symptoms.

  • Raise serum Na by 0.5-1 mEq/h, no more than 10-12 mEq in 24 hours. MAX serum should only be 125-130.
38
Q

What kind of saline is used for aggressive treatment of hyponatremia?

A

3% hypertonic saline.

NS is 0.9%

39
Q

What two things do we monitor when correcting hyponatremia aggressively?

A
  • Neurological symptoms
  • Serum Na+
40
Q

Clinical

My patient begins developing edema and signs of hypervolemia, but is still hyponatremic. What can be given to help them without stopping their hypertonic saline?

A

Furosemide, which increases free water excretion.

41
Q

What are the treatment options for acute hyponatremia with moderate symptoms?

A
  • 3% hypertonic saline
  • Loop diuretics with saline
  • Vasopressin-2 receptor antagonists (vaptans/aquaretics)
  • Water restriction (500-1500 mL)
42
Q

What is the MOA of a vasopressin-2 receptor antagonist?

A

Inhibition of the AVP V2 receptor reduces the number of aquaporin-2 water channels in the collecting duct and decreases water permeability of collecting duct.

43
Q

What are the two approved aquaretics/vasopressin receptor antagonists? Differences?

A
  • Conivaptan (parenteral) dual V1a and V2 antagonist.
  • Tolvaptan (oral) V2 receptor antagonist.

Coni the combo

44
Q

What two hyponatremia types are vaptans indicated for?

A
  • Euvolemic hyponatremia
  • Hypervolemic hyponatremia

AVOID IN HYPOVOLEMIC HYPONATREMIA

45
Q

What is the primary risk of using a vaptan/aquaretic?

A

Excessively rapid correction of Serum Na.

46
Q

If I give my patient an aquaretic, what do they no longer need?

A

Fluid restriction.

47
Q

How do I treat chronic hyponatremia OP?

A
  • Fluid restriction
  • V2 receptor antagonist (tolvaptan)
48
Q

What is DI? Cause?

A
  • Increased thirst with urine of LOW specific gravity.
  • Deficiency of vasopressin OR resistance to vasopressin.
49
Q

What are the 4 types/causes of DI?

A
  • Primary central DI
  • Secondary central DI
  • Nephrogenic DI
  • Vasopressinase-induced DI
50
Q

What characterizes primary central DI?

A
  • No lesion of pituitary or hypothalamus
  • 1/3 of all cases.
  • Likely cause: autoimmunity vs hypothalamic AVP-secreting cells
  • Genetic component.
51
Q

What characterizes secondary central DI?

A

Damage to the hypothalamus or pituitary stalk.

52
Q

What characterizes nephrogenic DI?

A
  • Normal secretion of ADH, but they still have polyuria.
  • Congenital:defective expression of V2 receptors or water channels. (X-Linked)
  • Acquired: pyelo, amyloidosis, myeloma, Sjogren’s
53
Q

What characterizes vasopressinase-induced DI?

A
  • Generally last trimester or puerpium.
  • Circulating enzyme destroys vasopressin, but CANNOT destroy synthetic desmopressin :)
54
Q

How does a DI patient usually present?

A
  • Intense thirst
  • Loves ice water A LOT
  • Polyuria
  • Drinks 2-20L of water a day and pees a lot per pee.
55
Q

What drug aggravates DI if a patient takes it?

A

High-dose corticosteroids. They will pee even MORE water.

56
Q

How is DI diagnosed?

A

Clinically.
Ideally, you want a 24 hour urine for volume and creatinine.

57
Q

What result in a 24 urine collection rules OUT DI?

A

Urine volume of < 2L/24h.
They gotta pee a lot to have DI

58
Q

If a patient with central DI is put under fluid restriction, what will happen to their urine?

A

Stays very dilute.

59
Q

What is a vasopressin challenge test?

A
  1. Desmopressin acetate given.
  2. Urine volume measured after 12 hours and 24 hours.
  3. Central DI should have significant reduction in both thirst and polyuria.
60
Q

If we suspect acquired central DI, what should we order diagnostically?

A

MRI of the pituitary, hypothalamus, and skull to look for lesions.

61
Q

If nephrogenic DI is suspected, how should we modify the vasopressin challenge test?

A

Modest fluid restriction.
Result should ideally show high levels of vasopressin.

62
Q

What do we need to r/o to diagnose central DI?

A
  • Psychogenic polydipsia
  • DM
  • Cushing/corticosteroids
  • lithium
  • Hypercalcemia
  • Hypokalemia
  • Parkinson’s nocturnal polyuria
63
Q

How do we treat mild DI?

A

Adequate fluid intake.

64
Q

When is desmopressin acetate the treatment of choice?

A
  • Central DI
  • Vasopressinase-induced DI
65
Q

What should we monitor in someone being given desmopressin acetate?

A
  • Hyponatremia
  • Neurological changes due to hyponatremia.
66
Q

What is the MOA of desmopressin acetate?

A

Synthetic vasopressin analogue with a fast onset, high ADH activity, and longer duration.

67
Q

Clinical

A 26 year old female presents with S/S of DI. After a 24 hour fluid restriction, her urine osmolality normalizes. What form of DI does she most likely have?

  • Central
  • Psychogenic
  • Nephrogenic
A

Psychogenic.

68
Q

Clinical

A 51 year old male presents with S/S of DI. After 24 hour fluid restriction, urine osmolality remains low. After being given desmopressin acetate, it is still low. What form of DI does this represent?

  • Central
  • Psychogenic
  • Nephrogenic
A

Nephrogenic

69
Q

Clinical

A 33yo female presents with DI S/S. After 24hr fluid restriction, urine osmolality remains low. After desmopressin acetate, it normalizes. What form of DI is this?

  • Nephrogenic
  • Central
  • Psychogenic
A

Central

70
Q

Clinical

Which of the following stimulates the release of ADH?
* Nausea
* Hyponatremia
* Increased plasma volume
* Decreased plasma osmolality

A

Nausea

71
Q

Clinical

Which of the following lab findings would I expect in DI?
* Increased urine osmolality
* Hyponatremia
* Increased plasma osmolality

A

Increased plasma osmolality

72
Q

Clinical

In a pt with central DI, what happens during fluid restriction if vasopressin is given?

  • Treatment will concentrate urine
  • Treatment will have no effect
A

Concentrates urine.

73
Q

How does a pituitary adenoma typically present?

A
  • S/S of an expanding intracranial mass (HA, vision changes)
  • Excess or deficiency of a pituitary hormone.
74
Q

What qualifies as a microadenoma? Macro? How do they differ in terms of S/S?

A
  • Micro: < 10mm in diameter and typically hormone excess S/S.
  • Macro: > 10mm in diameter and typically optic chiasm symptoms. Does not always affect hormones.
75
Q

What exactly is a pituitary adenoma?

A

Benign tumor of epithelial cell origin in the pituitary.

76
Q

What would an adenoma of lactotrope origin cause?

A
  • Hypogonadism
  • Galactorrhea

PRL hypersecretion.

77
Q

What would an adenoma of gonadotrope origin cause?

A
  • Silent
  • Hypogonadism

The only one that does not cause hypersecretion.

78
Q

What would an adenoma of somatotrope origin cause?

A

Acromegaly/gigantism

79
Q

What would an adenoma of corticotrope origin cause?

A

Cushing’s Disease

80
Q

What would an adenoma of mammosomatotrope origin cause?

A
  • Hypogonadism
  • Galactorrhea
  • Acromegaly
81
Q

What would an adenoma of thyrotrope origin cause?

A

Thyrotoxicosis.

82
Q

A patient presents with a visual field defect. What is the most likely issue they are having with an expanding pituitary mass?

A

Bitemporal hemianopia, because the optic chiasm is being compressed.

83
Q

What is bitemporal hemianopia?

A

You only can see your nasal visual fields.

84
Q

What would I order if a pituitary adenoma is suspected?

A
  • MRI of the brain
  • Ophthalmologic exam
  • Lab studies corresponding to the syndrome if a functional pituitary adenoma.
85
Q

What are the 3 goals of pituitary tumor treatment?

A
  • Normalizing excess pituitary secretion
  • Ameriolation/improvement of S/S of hyperseretion syndrome
  • Shrinkage/ablation of larger masses to relieve structural compression.
86
Q

What is the desired surgery for pituitary tumors?

A

Transsphenoidal surgery (same as anterior)

87
Q

When is radiation used for pituitary tumor treatment?

A
  • Post surgical, due to slow onset.
  • Mainly to prevent regrowth of a tumor.
88
Q

If a patient has a prolactinoma, what is the DOC? Acromegaly? TSH tumors? ACTH-tumors?

A
  • Prolactinoma: Dopamine agonists
  • Acromegaly: Somatostatin analogues and GH receptor antagonists
  • TSH-tumors: Somatostatin analogues and sometimes dopamine agonists
  • ACTH-tumors: surgery/radiation :(

CM 1A: Heme/Onc/Endo (28 decks)

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