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Endocrinology - Chapters > Chapter 65 - Hypothalmic-PItuitary Axis DISORDERS > Flashcards

Chapter 65 - Hypothalmic-PItuitary Axis DISORDERS Flashcards

0
Q

You are evaluating a patient and growth hormone deficiency (GHD) is in your differential diagnosis. Growth hormone levels are normally very low in even in normal individuals. How would you test for GHD?

A

ITT = Insulin Tolerance Test (GOLD STANDARD test for assessing GH RESERVE)

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1
Q
  1. WHat is GH stimulated by?
  2. What is GH inhibited by?
  3. What is the target organ of GH and what does it cause?
A
  1. GH is stimulated by growth hormone-releasing hormone (GHRH).
  2. GH is inhibited by somatostatin
  3. GH binds to receptors in the LIVER and induces secretion of INSULIN-LIKE-GROWTH-FACTOR (IGF-I)
    - IGF-I circulates in the blood bound to binding proteins (BP’s), the most important of which is IGF-BP3**
    - **    ***GH ALSO AFFECTS CARBOHYDRATE METABOLISM
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2
Q

The gold standard for assessing GH reserve is ITT. How would you educate your patient on the procedure?

A
  • You would explain to the patient that hypoglycemia is a potent stimulus for GH secretion. You are going to induce hypoglycemia in the patient using insulin.
    • ITT = Insulin (0.05 to 0.15 U/kg) is administered IV to reduce the patients blood glucose levels to 50% of initial blood glucose or to 40 mg/dL with serial sampling of serum GH and glucose.
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3
Q

You have just received the results of the insulin tolerance test (ITT) you just performed on the previous patient. Before checking for an abnormality you probably need to know the NORMAL VALUES of the ITT test!!! What is normal for adults? Children?

A

A normal response to the ITT is a peak GH level in excess of 5 ng/mL at 60 minutes in adults and 10 ng/mL in children

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4
Q

An elderly patient comes into your clinic and you suspect GH deficiency. What test is recommended for this patient to assess GH reserve?
What other patients is this test recommended for?

A
  • Combined infusion of GHRH (growth hormone-releasing hormone) and arginine
  • *this test is as sensitive and specific as insulin induced hypoglycemia in stimulating GH secretion in adulthood
  • it is recommended for elderly, and in patients with ischemic heart disease and seizures****
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5
Q

A single GH stimulation test is sufficient for the diagnosis of adult Growth Hormone Deficiency. (GHD) HOWEVER patients with LOW SERUM IGF LEVEL or 3 or MORE PITUITARY HORMONE DEFICIENCES have more than a 97% chance of having GHD. do you perform a GH stimulation test on these patients?

A

NO NO NO NO NO

:) just thought i would wake yah up

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6
Q

____ levels can be used as a screening test for GH deficiency.

A

IGF-I , because GH regulates IGF-I levels
-**remember GH binds to the receptors on the liver and induces secretion of IGF-I that then goes in the blood bound to binding proteins!!!! IGF-I mediates most of the growth promoting effects of GH.

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7
Q

Does a normal IGF-I level rule out the possibility of GHD?

A

NO!!!!!!!!

A low serum IGF-I level is suggestive of GHD; however a normal IGF-I level does not rule out GHD.

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8
Q

NO MORE DIFICIENCYYYY IN GH… WERE MOVING ON TO HYPERSECRETION OF GH :)

  1. Is growth hormone secreted in a pulsatile or continuously?
  2. Will you test a patient once to confirm hypersecretion of GH or multiple times before diagnosing?
  3. What would be a useful indicator of GH hypersecretion because this level does NOT fluctuate throughout the day?
A
  • GH is secreted in a pulsatile manner.
  • Continuous testing is a more valuable measurement than a single measurement when confirming Hypersecretion of GH.
  • IGF-I serum measurement is a useful indicator
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9
Q

What are 5 sicknesses associated with GH hypersecretion?

A
  1. Cirrhosis
  2. Starvation
  3. Anxiety
  4. Type 1 diabetes mellitus
  5. Acute Illness
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10
Q

What is a simple and dynamic test for GH hypersecretion?
What are the NORMAL findings of this test?
What would be the findings in a patient with Acromegaly??

A

administration of oral glucose

  • 100 g given orally
  • suppresses GH levels to less than 1ng/mL after 120 minutes in HEALTHY individuals
  • In a patient with ACROMEGALY, GH levels may increase, remain unchanged, or decrease (however not below 1ng/mL) after an oral glucose load
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11
Q

_______ during infancy and childhood is exhibited as growth retardation, short stature, and fasting hypoglycemia.

A

GH deficiency

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12
Q

Adult _____ manifests as increased abdominal adiposity, reduced muscle strength, and exercise capacity, decreased lean body mass and increased fat mass, reduced bone mineral density, glucose intolerance, and impaired psychosocial well being.
** is frequently accompanied by other symptoms of ________.

A

GH deficiency

**panhypopituitarism

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13
Q

What is the treatment of an adult with growth hormone deficiency?

A
  • **subcutaneous daily injection of Growth hormone.
  • growth hormone replacement therapy in adults decreases fat mass, increases lean body mass, and bone mineral density, and is associated with improved cardiovascular risk factors (e.g lipid profile, waist to hip ratio, central obesity)
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14
Q

In childhood, GH hypersecretion leads to _________

A

giantism

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15
Q

In adults whose long bone epiphyses are fused, GH hypersecretion causes ________ with local overgrowth of bone in the acral areas.

A

acromegaly

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16
Q

What is GH hypersecretion almost ALWAYS caused by?

A

GH secreting pituitary adenoma

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17
Q

About 70% of patients with acromegaly have _______.

A

macroadenomas

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18
Q

Patient complains of their ring, glove, and shoe size increasing.
Evaluating the patient you notice widening of the hands and feet and a coarsening of the facial features; frontal sinuses are enlarged, leading to prominent supraorbital ridges, and the mandible grows downward and forward, resulting in prognathism and wide spacing of the teeth. What is your diagnosis?

A

ACROMEGALY = GH hypersecretion in adults whose long bone epiphyses are fused. *acral enlargement (hint is in the name)

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19
Q

What is the initial treatment of choice for hypersecretion of GH?

A

Trans-sphenoidal microsurgery
(the pituitary is in the sphenoid bone remember :)*)

  • this surgery results in rapid reduction of GH levels with a low rate of surgical morbidity.
  • cure rates are proportional to preoperative tumor size with a 90% success rate for patients with microadenomas
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20
Q

Is radiotherapy an effective method of reducing GH hypersecretion? What makes it not as effective as trans-sphenoidal microsurgery?

A

it reduces hypersecretion; however it may take as long as 20 years for GH levels to fall after radiotherapy, and the incidence of hypopituitarism is HIGH.

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21
Q

What is the medical management for hypersecretion of GH?

A

Octerotide acetate, Bromocriptine, Pegvisomant

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22
Q

a long-acting somatostatin analogue, that is effective in reducing GH and IGF-I levels to normal and shrinks tumor masses in about 50% of its cases.
What is the recomended vehicle for this drug in treating a patient with GH hypersecretion?

A

Octerotide acetate
- a long acting, slow releasing depot preparation of octerotide adminstered once monthly is as effective as short acting subcutaneous octerotide prep

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23
Q

What are the side effects of Octerotide Acetate?

A

diarrhea, abdominal cramps, flatulence, and gallstone formation

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24
Q

a dopamine agonist, is effective in suppressing GH in only a monitory of patients with acromegaly.

A

Bromocriptine

***Very useful in treating PROLACTINOMAS :)

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25
Q

GH receptor antagonist that binds to the GH receptor on the hepatic surface and thus blocks the normal physiological action of GH.

A

Pegvisomant

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26
Q

What are two things that should be monitored on a long term basis in patients diagnosed with acromegaly?

A

liver function tests & pituitary adenoma size

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27
Q

What inhibits the secretion of prolactin?

What stimulates secretion of prolactin?

A
  • dopamine inhibits
  • TRH & vasoactive intestinal polypeptide are putative PRL-releasing factors; also ESTROGENS increase basal and stimulated PRL secretion; glucocorticoids and TSH blunt TRH-induced PRL secretion
  • PRL levels increase during pregnancy, after childbirth PRL stimulates secretion of milk
  • However, elevated PRL levels are not needed to maintain lactation, and basal PRL secretion falls as the infant’s suckling reflex maintains lactation
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28
Q

Microprolactinoma vs. Macroprolactinoma

  1. Which is more common in women?
  2. Which is more common in men?
A 
women = microprolactinomas
men = macroprolactinomas
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29
Q

in patients with a prolactinoma:

PRL inhibits pulsatile ______ secretion and suppresses the midcycle ____ surge with consequent menstrual irregulariies.

A

gonadotropin secretion ; LH surge

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30
Q

Hyperprolactinemia in women can cause hypogonadotropic hypogonadism, resulting in ________.

A

estrogen deficiency

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31
Q

In men who have hyperprolactinemia, _______ levels are usually suppressed.

A

testosterone

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32
Q
  1. What are two symptoms that occur in women that allow for early recognition of a prolactinoma?
  2. What are the two symptoms associated with men with a prolactinoma? (not recognized as early as women)
A
  1. Women who have menstrual irregularities and infertility

2. Men who have decreased libido and erectile dysfunction

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33
Q

About 90% of women who have hyperprolactinoma have ____, _____, or _____. If the prolactinoma occurs in adolescents before the onset of menarche, they may have _______.

A

amenorrhea, galactorrhea, or infertility

* in adolescents = primary amenorrhea

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34
Q

A patient with a hyperprolactinoma presents with osteopenia, vaginal dryness, hot flashes, and irritability. What is the underlying problem causing these symptoms?

A

estrogen deficiency

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35
Q

A patient is diagnosed with a Prolactinoma, while educating the patient of the associated risks of this disease you start with telling him that PRL stimulates adrenal androgen product, and that androgen excess can cause _________?

A

weight gain and hirsutism

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36
Q

T/F Hyperprolactinemia can be associated with anxiety and depression.

A

true

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37
Q

Men usually exhibit a loss of ____ and _____ as a result of hypogonadism. These symptoms are often attributed to causes other than prolactinoma, which results in frequent delay in diagnosis until visual impairment, headache, and hypopituitaryism develops to confirm prolactinma.

A

loss of libido and erectile dysfunction

38
Q

what medications cause an increase in PRL secretion?

A

phenothiazine, methyldopa, cimetidine, metoclopramide

39
Q

what physiologic conditions cause an increase in PRL secretion?

A

pregnancy, stress, nipple stimulation

40
Q

What pathological stressors cause an increase in PRL secretion?

A

hypothyroidism, chronic renal failure, chest wall lesions

41
Q

PRL levels in excess of _____ usually imply PROLACTINOMA!!!

what confirms the diagnosis?

A

> 200 ng/mL in EXCESS

MRI confirms diagnosis

42
Q

What drug would you prescribe to a patient with a prolactinoma who is wanting to restore gonadal function and fertility?

A

Bromocriptine or Cabergoline

*both are dopamine agonists

43
Q

Dopamine agonists like Bromocriptine and Cabergoline cause a decrease in tumor size in a number of patients with macroadenomas. What are the side effects of Bromocriptine that are not seen when using cabergoline?

A

Dizziness, nausea, vomiting, nasal stuffiness, and orthostatic hypotension

44
Q

What are the side effects associated with cabergoline when used to treat a patient with a prolactinoma?

A

cabergoline-related cardiac valvulopathy was recently reported in patients with Parkinsons disesae receiving doses of cabergoline far greater than whats used for the treatment of prolactinoma. However valvulopathy is a concern in young patients requiring long term dopamine agonists therapy, and bromocriptine, if tolerable, is the drug of choice.

45
Q

In patients with a prolactinoma, medical management with drugs is the first line of care. What is the recommended therapy for a patient who is resistant or intolerant of the medical treatment?

A

Trans-sphenoidal therapy

46
Q
  1. What stimulates TSH?
  2. What inhibits TSH?
  3. What is the target of TSH?
  4. What is its function?
A
  1. TSH is stimulated by TRH.
  2. TSH is inhibited by somatostatin augmenting the negative feedback inhibition of TSH secretion by peripheral thyroid hormones
  3. TSH attaches to receptors on the thyroid gland and activates adenylyl cyclase, stimulating iodine uptake and the synthesis and release of T3 and T4
    - T3 and T4 exert negative feedback inhibition on pituitary TSH and hypothalamic TRH secretion
47
Q

What is the test used to measure the amount of TSH?

A

ultrasensitive assays - immunoradiometric assays, which can accurately distinguish low, normal, and high TSH levels.

48
Q

Using the ultrasensitive assays to evaluate the amount of TSH in a patient, your findings indicate the presence of low circulating TSH levels in the presence of low thyroid hormone levels. What is your diagnosis?

A

Secondary (Central) Hypothyroidism as a result of hypothalamic-pituitary dysfunction

49
Q

Using the ultrasensitive assay, your findings indicate low thyroid hormone levels, with concomitant high TSH levels. What is your diagnosis?

A

Primary hypothyroidism

50
Q

TSH deficiency causes thyroid gland involution, hypofunction, and clinical hypothyroidism. What are the clinical features of hypothyroidism?

A

lethargy, constipation, cold intollerance, bradycardia, weight gain, poor appetite, dry skin, and delayed relaxation time of peripheral refelxes.

51
Q
  1. What are patients with central hypothyroidism treated with?
    * *Central hypothyroidism = low thyroid hormone & low TSH
  2. What do you use to monitor thyroid replacement dosage in secondary (central) hypothyroidism?
A
  1. thyroxine
  2. Measuring the serum FT4 levels assesses the adequacy of thyroid replacement
    * *TSH levels cannot be used to monitor thyroid hormone replacement dosage in secondary hypothyroidism
52
Q

_________ = tumor that is very rare exhibiting hyperthyroidism, goiter, and inappropriately elevated (or normal) TSH levels in the presence of elevated serum thyroid hormone levels.
**HIGH THYROID HORMONE LEVEL w/ normal or high TSH LEVEL.
These tumors are usually plurihormonal, secreting GH, PRL, and the glycoprotein hormone alpha subunit, as well as TSH.

A

Thyrotropin-secreting pituitary hormone

53
Q

What is the treatment for Thyrotropin secreting pituitary hormone?
What would u need to control thyrotoxicosis?

A
  • these tumors are often resistant to removal, which necessitates several surgical procedures or radiotherapy.
  • octreotide acetate, a somatostain analog, has been found useful in decreasing TSH secretion in patients with tumors and has been shown to shrink tumors in some cases.
  • Iodine-131 thyroid ablation or thyroid surgery may be needed to control thyrotoxicosis.
54
Q
  1. What stimulates the release of ACTH?
  2. What is the function of ACTH?
  3. What inhibits the release of ACTH?
A
  1. Hypothalmic corticotropin-releasing hormone (CRH) and to a lesser extent ADH stimulate ACTH
  2. ACTH stimulates cortisol synthesis and secretion from the adrenal gland ; also stress increases ACTH secretion and release
    * *Cortisol exhibits a negative feedback on ACTH and CRH secretion.
  3. Glucocorticoids inhibit ACTH secretion as well as CRH and ADH synthesis and release
    * *ACTH ALSO maintains ADRENAL SIZE by increasing protein synthesis
55
Q

Excess secretion of ACTH results in hypercortisolemia, which may be caused by _________ or _______.

A
  1. an ACTH-secreting pituitary adenoma (CUSHINGS DISEASE)

2. ectopic ACTH secretion

56
Q

ACTH deficiency results in _________, with decreased secretion of cortisol.

A

adrenocortical insufficiency
**aldosterone secretion is largely regulated by the renin-angiotensin axis, therefore aldosterone secretion remains intact

57
Q

How can you test the Basal ACTH levels, using ACTH levels or cortisol levels? why?

A
  • ACTH measurements are unreliable because of short plasma half life and pulsatile secretion of hormone.
  • Because ACTH regulates Cortisol secretion, plasma cortisol levels better reflect hypothalamic-pituitary-adrenal function
58
Q

At what time would u want to measure cortisol levels in the body when trying to measure the basal ACTH levels? What are the normal values at this time?

A

ACTH is secreted in pulses and is under circadian control, reaching maximal levels in the last hours before awakening, followed by a steady decline to a nadir in the evening.
**8:00 A.M. cortisol less than 3 mcg/dL suggests adrenal insufficiency

59
Q

Even though you cannot use ACTH to measure the basal level of ACTH, what CAN YOU USE ACTH FOR when evaluating basal ACTH levels?

A

ACTH levels can be used to differentiate primary from secondary adrenal insufficiency

  • Plasma ACTH levels are normal to high in adrenal insufficiency b/c of PRIMARY ADRENAL DISORDER
  • Plasma ACTH levels are low to absent in adrenal insufficiency SECONDARY to hypothalmic pituitary hypofunction
60
Q

Now forget the basal ACTH level… How do you test for ACTH reserve?

A

The insulin - induced hypoglycemia test
**same that was used for pituitary GH release, this test also stimulates the hypothalmic pituitary adrenal axis :) U KNOW THIS ONE ALREADY!! WHOOP WHOOP

61
Q

When administering an insulin induced hypoglycemia test to test for the amount of ACTH reserve in a patient, what are the normal ACTH values?

A

A peak cortisol level of atleast 18 mcg/dL confirms normal ACTH reserve
*** THIS IS THE MOST RELIABLE TEST OF THE ACTH SECRETORY RESPONSE TO STRESS

62
Q

Who is the insulin induced hypoglycemia test contraindicated in when testing for ACTH reserve? What test would you use in these patients?

A

elderly and in patients with cerebrovascular disorders, siezure disorders, or cardiovascular disease
- in these patients Metyrapone (30mg/kg orally at midnight) is the test to use

63
Q

Evaluation of ACTH Reserve using Metyrapone is recommended in elderly patients. What is the mechanism behind the use of Metyrapone? How do you know if the patient has normal ACTH levels?

A

Metyrapone inhibits the 11-beta-hydroxylase enzyme in the adrenal gland, which coverts 11-deoxycortisol to cortisol.

  • Low cortisol stimulates ACTH and CRH secretion.
  • An 11-deoxycortisol level greater than 7 mg/dL, with a simultaneous serum cortisol level less than 5 mg/dL, the morning after metyrapone administration, indicates an adequate response = [ACTH was secreted when cortisol levels got low :))]
64
Q

When can ACTH be measured indirectly by measuring adrenal cortisol reserve?

A

when the patient has Adrenal atropy (which is caused prolonged ACTH deficiency)

65
Q

__________ correlates well with the ITT. About 250 mcg administered IV or intramuscularly results in a peak cortisol level of more than 20 mcg/dL within 60 minutes in normal individuals. An adequate response implies either impaired pituitary ACTH secretion or primary adrenal failure.

A

Cortosyn-stimulation testing

66
Q

A patient comes into your clinic with features suggesting a moon face, plethora, hirsutism, and enlarged supraclavicular fat pads. Initially, a diagnosis of hypercortisolemia (Cushions syndrome) must FIRST be confirmed HOW????

A

CHOOSE ONE OF THESE :)

  1. measuring 24 hour urinary free cortisol levels
  2. midnight plasma or salivary cortisol levels
  3. or lack of suppression of an 8 am serum cortisol after 1 mg of dexamethasone administration at 11:00 pm on the evening before (1 mg overnight dexamethasone suppression)
67
Q

After confirming cushing syndrome and hypercortisolemia, what do you do next to differentiate between ACTH-dependent Cushing syndrome (pituitary or ectopic ACTH secretion) and ACTH independent Cushing Syndrome (adrenal adenoma or hyperplasia)?

A

measure plasma ACTH levels

68
Q

ACTH deficiency results in ________, causing lethargy, weakness, nausea, vomiting, dehydration, orthostatic hypotension, coma, and if untreated, death.

A

adrenal failure

69
Q

How do you treat patients with adrenal insufficiency aka adrenal failure?

A

hydrocortisone
cortisone acetate
prednisone
-dose increased with stress

70
Q

Gonadotroph secretion of LH and FSH is regulated by hypothalmic -______.

A

GnRH - gonadotrophin-releasing hormone

71
Q

What regulates the negative feedback inhibition of LH and FSH?

A

gonadal steroids = Estrogen and Testosterone

peptids = Inhibin and Activin

72
Q

_______ release determines the onset of puberty and generates the midcycle gonadotropin surges necessary for ovulation.

A

GnRH

73
Q

T/F Gonadal steroids, Estrogen & Testosterone, exert both positive and negative feedback effects on gonadotroph secretion.

A

true

74
Q

_______ negatively inhibits FSH secretion.

Where is this polypeptide produced?

A

Inhibin- produced by ovarian granulosa cells and testicular Sertoli cells.

75
Q

_____ stimulates FSH secretion (which peptide)

A

Activin

76
Q

What is the MOA of LH and FSH?

A

LH and FSH bind to receptors in the ovaries and testes
and
1. stimulate sex steroid secretion( predominantly LH)
2. stimulate gametogenesis (predominately FSH)
***LH stimulates gonadal steroid secretion by testicular Leydig cells and by the ovarian follicles. In women, the ovulatory LH surge results in rupture of the follicle and then luteinizaiton. FSH stimulates Sertoli cell spermatogenesis in men and follicular dev. in women.

77
Q

________ occurs when a patient has a posterior pituitary dysfunction and leads to diabetes insipidus with polyuria, polydipsia, and nocturia.

A

vasopressin deficiency

78
Q

______ = origin where the posterior lobe of the pituitary fails to secrete adequate amounts of ADH.

A

Neurogenic - CENTRAL Diabetes Insipidus

79
Q

failure of the kidney to to respond to adequate amounts of circulating ADH

A

nephrogenic origin of Diabetes Insipidus

80
Q

definition: _____ - secreting large volumes of dilute urine

A

polyuric

81
Q

Regardless of the cause of Diabetes Insipidus, all patients with this dianosis are secreting ______ urine.

A

secreting large volumes of dilute urine

82
Q

What are going to be a patients main complaint when coming in with Diabetes Insipidus? (hint: cellular and extracellular response to this disease)

A

Cellular and Extracellular dehydration = THIRSTY!!!!!!

which results in POLYDIPSIA

83
Q

Diabetes insipidus (central or nephrogenic) must be distinguished from ___________ = a compulsive disorder of thirst in which patients drink in excess of 5 to 10 L per day of water, resulting in decreased ADH secretion and subsequent diuresis.

A

primary polydipsia

84
Q

What is one possible distinguishing clinical feature between patients with Diabetes Insipidus and patients with primary polydipsia?

A

patients with diabetes insipidus want COLD BEVERAGES

85
Q

TO confirm the diagnosis of Diabetes Insipidus and differentiate between the syndrome from primary polydipsia: random simultaneous samples of plasma and urine for evaluation of sodium and osmolarity are obtained.
What are the results to confirm Diabetes Insipidus?

A

In diabetes insipidus (central or nephrogenic) inappropriate diuresis results in a urine osmolarity LESS than that of plasma osmolarity. *Plasma osmolarity could be elevated due to patients state of hydration at the time of test :)
-In Primary Polydipsia, both plasma and urine are dilute

86
Q

What is the name of the primary test used to differentiate the cause of polyuria?

A

water deprivation test

87
Q

What are the steps in performing the water deprivation test? NOT RESULTS! just how do you do it?

A
  1. The patient is denied fluids for 12-18 hours.
  2. Body weight, blood pressure, urine volume, urine specific gravity, and plasma and urine osmolarity are measured every 2 hours.
  3. Water deprivation is continued until the urine osmolarity plateaus (an hourly increase of <30 mOsm/kg for 3 successive hours)
  4. at this point 5 units of aqueous vasopressin are administered subcutaneously and the urine osmolarity is measured after 1 hour.
88
Q

What is a NORMAL response to the water deprivation test?

*the patient does not have diabetes insipidus nor primary polydipsia.

A

a decrease in urine output up to 0.5 mL per minute, as well as an increase in urine concentration to greater than that of plasma.

89
Q

What would be the result of the water deprivation test in a patient with Diabetes Insipidus?

A
  1. in either central or nephrogenic Diabetes Insipidus a high urine output is maintained and is still dilute despite water deprivation
  2. In patients with COMPLETE CENTRAL diabetes insipidus urine osmolarity increases above plasma osmolarity
  3. In patients with NEPHROGENIC diabetes insipidus urine osmolarity increases less than 50% in response to ADH
  4. Patients with nephrogenic diabetes Insipidus have normal or increased levels of ADH during water deprivation, whereas patients with central DI have suppressed levels of ADH
90
Q

What are the results of the Water Deprivation test for patients with primary polydipsia?

A
  1. urine osmolarity increases to values greater than plasma osmolarity
  2. increases of less than 10% ADH levels
91
Q

Patients should be cautioned not to drink large amounts of fluid until the effects of the aqueous vasopressin have worn off (4 to 8 hours) to avoid _________

A

Hyponatremia

92
Q

What is the treatment for CENTRAL Diabetes Insipidus

A 
Desmopressin acetate (DDAVP)
- it is a synthetic analog of ADH, is usually administered intranasally or orally in treatment of CENTRAL Diabetes Insipidus
93
Q

What is the treatment for Nephrogenic diabetes Insipidus?

A

as far as possible, the underlying disease process should be reversed.
Specific treatment of nephrogenic diabetes insipidus is designed to
1. maintain a state of mild sodium depletion with reduction in the solute load on the kidneys
2. Susequent increased proximal tubular reabsorption
**DIURETICS COUPLED WITH DIETARY SALT RESTRICTION CAN BE USED TO ACHIEVE THIS GOAL

Endocrinology - Chapters (20 decks)

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