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NM-7317 Endocrine > Posterior Pituitary: 
Function and Disease > Flashcards

Posterior Pituitary: 
Function and Disease Flashcards

1
Q

thyroid
pituitary
hypothalamus

A

primary
secondary
tertiary

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2
Q

Diabetes insipidus-

1. Hypothalamus

A

Central “Neurogenic”

  • Lithium patients (#cause)
  • Renal insufficiency
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3
Q

Diabetes insipitus

2. kidney

A

“Nephrogenic” /Hypothalamic

  • deficiency in secretion of ADH from the posterior pituitary.
  • Nephrogenic diabetes insipidus occurs when the kidney is unable to respond to ADH

*Transient (Bad for a month, then better)

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4
Q

Diabetes Insipidus - Neurogenic:
Risk factors:
Associated conditions:

A

Lesion is central: root cause problem

Risk factors
Majority idiopathic (autoimmune?)
Trauma, infectious (TB, Sarcoidosis), vascular, TBI
Cancer - Craniopharyngioma

Associated conditions
Dehydration

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5
Q

Diabetes Insipidus - Neurogenic:
Six (presentation):
Diagnosis ( PE/labs/imaging):

A

Lesion is central: root cause problem

SSx (presentation)
3 Ps, nocturia, neurological disruption, attraction to cold drinks

Diagnosis ( PE/labs/imaging)
#1-> Water Deprivation Test
#2-> Copeptin levels – fragment of AVP precursor (Copeptin/ADH released together)

Antibodies against arginine vasopressin-secreting cells (AVPc-Abs)

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6
Q

Neurogenic Diabetes Insipidus - Labs

A 
*Polyuria and polydipsia due to diminished ability of the patient to concentrate urine
Urine osmolality < 200mmol/L 
Urine Na < 20 mEq/L
Plasma osmolality: > 290mOsmol/kg 
Plasma Na 150-160  mEq/L

*Water deprivation test 
Urine abnormally dilute
Urine osmolality < plasma osmolality

*Exogenous AVP (aqueous vasopressin) 
Urine osmolality increases by > 50%

*Copeptin – part of the AVP prohormone

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7
Q

Neurogenic Diabetes Insipidus most concerns in plasma & urine test.

A
  1. Osmolality
  2. Sodium

Def. in ADH->urine dilute low osmolality, low sodium (peeing water)
Plasma->High osmolality, high sodium (Dehydrated in plasma)

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8
Q

Neurogenic Diabetes Insipidus Diagnose with these numbers:

A

Urine: Urine osmolality < 200mmol/L
Urine Na < 20 mEq/L

Plasma osmolality: > 290mOsmol/kg
Plasma Na 150-160 mEq/L

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9
Q

Neurogenic Diabetes Insipidus next step after diagnosis..

A

Water deprivation test: (make sure he is not dehydrated)

Osmolality (with water deprivation)
(Norm pp: osmolality->up/neuro & nephrogenic-> low.
***give Desmopressin= neuro->50%/nephrogenic 10-15%

Sodium (Norm Pp->up/neuro & nephrogenic-> low.
***give Desmopressin= central.->norm/nephrogenic norm

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10
Q

Diabetes Insipidus: Neurogenic

Naturopathic Treatment Plan:

A

Lesion is central: root cause problem

Problem with water regulation (dehydration)
Match water intake to diuresis
Fiber to decrease constipation
Omega-3 FA for skin dryness

Counsel on adequate electrolyte intake

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11
Q

Nephrogenic Diabetes Insipidus, what is happening?

A

Kidney can’t respond to ADH, can’t concentrate urine

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12
Q

Nephrogenic Diabetes Insipidus:
Urine osmolality?
Serum electrolytes?
Due to?

A

Urine osmolality can be <200mmol/L
After water deprivation, urine remains dilute
After exogenous AVP, minimal rise in urine osmolality
High levels of vasopressin in plasma at end of dehydration

Serum electrolytes
Normal or even elevated Na

Due to: chronic renal insufficiency, Li toxicity, hypercalcemia, and sometimes genetic

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13
Q 
Diabetes Insipidus - Nephrogenic:
Risk factors?
Associated conditions?
SSx (presentation)
Diagnosis ( PE/labs/imaging):?
A

Risk factors
Occurs in >50% of patients on chronic lithium therapy
Congenital defects
Chronic disease: sickle cell anemia, renal sarcoidosis, renal amyloidosis

Associated conditions
Dehydration and hypernatremia
Bladder dysfunction
Insomnia

SSx (presentation)
Polyuria
Nocturia
Obtundation (less responsive) - hypernatremia

Diagnosis ( PE/labs/imaging):
24 hour urine
Water Deprivation Test

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14
Q

Diabetes Insipidus: Nephrogenic
Management Strategies:
Pharmaceutical:
Follow up/ Referrals:

A

Management Strategies:
Monitor patient symptoms
Low sodium diet < 500mg daily
http://www.ndif.org/pages/5-Low_Sodium_Diet_Basics (Great Resource)
Lower protein diet, switch to plant based proteins
Adequate hydration

Pharmaceutical
Thiazide-like diuretics to excrete sodium (HCTZ 12.5-50mg oral daily)
Potassium sparing diuretic Amiloride if lithium etiology

Follow up/ Referrals
Urology consult
Endocrinology consult
Serum electrolytes and visit every 6 months

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15
Q

Diabetes Insipidus: Nephrogenic

Sample Naturopathic Treatment Protocol:

A

Role for nephroprotective herbal therapies?
Do not combine with lithium

Possible anti-inflammatory diet and supplements
May have elevated Prostaglandin E2
Curcumin inhibits cyclooxygenases 1 and 2 thereby reducing PGE2 production
PMID: 21372035
Fish oil shows greater reduction in PGE2 compared to olive oil or safflower oil
PMID: 8694022
If dietary restrictions for sodium and protein
Diet counseling
Multivitamin prescription

Remove offending agents
In patients with bipolar consider alternatives to lithium therapy
Screen supplements for “lithium”
Colchicine, amphotericin B, loop diuretics can all contribute to acquired NDI

Support for other diseases leading to NDI
Chronic kidney failure
Abnormal high Ca++ or low K+
Protein restriction (excessive)

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16
Q

SIADH, what is it?

A

*ADH Excess - SIADH
Syndrome of inappropriate excessive ADH secretion (SIADH)

*This is a diagnosis of exclusion: must rule out other conditions – see differential diagnosis.

17
Q

SIADH consists of serum hyponatremia & vasopressin

A

SIADH consists of serum hyponatremia (< 135 mmol/L), decreased serum osmolality, elevated urine osmolality (>200 mOsm/kg), excessive urine sodium

Elevated vasopressin enhances the reabsorption of water, causing hyponatremia, and decreased serum osmolality. Not due to sodium deficiency

18
Q

SIADH Cancer to look out for?

A

Small cell cancer of the lung

19
Q 
SIADH:
Risk factors:
Associated conditions:
Six (presentation)
Diagnosis ( PE/labs/imaging): Diagnosis of Exclusion
A 
Risk factors:
Cancer
Pulmonary Disease
CNS infection or pressure
Drug induced (SSRIs, Tricyclic antidepressants, narcotics, NSAIDs, ACE-I
Idiopathic

Associated conditions:
Hypo-electrolytes (magnesium, calcium, potassium,

SSx (presentation)
Anorexia, nausea, and malaise are the earliest findings, followed by headache, irritability, confusion, muscle cramps, weakness, seizures, and coma. Edema less likely caused by SIADH

Diagnosis ( PE/labs/imaging): Diagnosis of Exclusion
Hyponatremia: Serum sodium < 135 mmol/L
Urine osmolarity > 100 mOsm/kg
Urine sodium > 40 mEq/L

20
Q

Uncontrolled diabetes mellitus:

A

Sodium decreased as well

21
Q

SIADH:

Management Strategies:

A
  • Depends on severity
  • Do not correct hyponatermia with IV (high level intervention with known potential for harm – can result in central pontine myelinolysis)
  • Rule out diabetes – extreme hyperglycemia can decrease serum Na
  • Correct Na level in hyperglycemia:
  • http://reference.medscape.com/calculator/sodium-correction-hyperglycemia
  • Hypo-osmolar hyponatremia is more common and dangerous
22
Q

SIADH:

Example Naturopathic Treatment Plan

A

High salt intake from healthy food sources
High protein diet via increase in urea production may diuresis free fluid
Support around fluid restriction < 1.5 L/day
Urea?? Maybe – case study: PMID: 8459886

23
Q

SIADH Labs

A 
Serum Na < 135 mEq/L; K and HCO3 normal
Serum osmolality < 280 mOsm/kg
BUN and serum uric acid low 
Elevated urinary sodium level >20 mEq/L
Urine osmolality high, 300-1400 mOsm/L
Normal plasma cortisol level will exclude adrenal insufficiency
24
Q

SIADH:
Emergencies
Bad Ideas:

A

Emergencies
Na <105 mEq/L = life-threatening complications

Bad Ideas:
Sodium restriction
IV sodium correction > 1 mEq/hour –may cause central pontine myelinolysis

NM-7317 Endocrine (7 decks)

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