preparation for USMLE STEP 2 ENdocrinology (source from MTB2,Kaplan internal disease step 2 ck,medbullets,step up ck and google).

2. 
 Surrounded by sphenoid bone,cover by sellar
diaphragm.
 2 lobes: Adenohypophysis ( anterior)
Neurohypophysis (posterior)
 Hypothalamus-pituitary axis
Pituitary gland- general

3. 
Pituitary gland

4. 
Summary of action

5. 

6. 
Microadenoma<1cm in diameter
Macroadenoma >1cm
Large tumor can compress the optic
chiasm and can cause visual
deficits(Bitemporal hemianopsia).
Microadenoma are more common than
macroadenoma
Disease of Anterior
Pituitary

7. 
Prolactin - 50-60%
Growth hormone - 15-20%
ACTH - 10-15%
Gonadotroph - 10-15%
Pituitary adenoma by
function

8. 
A 30 year old women comes to your office because of
milk-like discharge for over 4 weeks. She also states
that she has not menstruated in 2 months. Her
examination reveals galactorrhea but is otherwise
normal.
 What is the next most appropriate test?
 What is the nxt most appropriate management?
Hyperprolactinemia

9. 
Physiology cause: Pregnancy, intense
exercise , renal insufficiency, and increase
chest wall stimulation
Tumors: Functional pituitary adenoma
Drugs : antipsychotic drug, methyldopa,
metochlopromide, opioids, TCA, verapamil.
Primary hypothyroidism (increase TRH and
increase prolactin release)>>check TSH
Hyperprolactinemia -
Etiology

10. 
 Women
Galactorrhea, amenorrhea and infertility.
 Men
Erectile dysfunction and decrease libido,
gynecomastia(rare).
Hyperprolactinemia-
Presentation

11. 

12. After prolactin level is found to be high ,perform:
 Thyroid function test (check TSH)
 Pregnancy test
 Bun/creatinine (kidney disease elevates prolactin)
 Liver function tests ( cirrhosis elevates prolactin)
 Exclude drugs
MRI is done after :
1. High prolactin level>100ng/ml
2. Secondary cause like medication are excluded
3. Pt is not pregnant
Hyperprolactinemia-
diagnostic test

13. 
1. Dopamine agonist:
Carbegoline is better tolerated than bromocriptine
2. Transphenoidal surgery is appropriate for those not
responding to medication.
3. Radiation is rarely needed.
Hyperprolactinemia -
treatment

14. 
ACROMEGALY

15. A 52 year-old man complains of increased hat
size and headaches when he wakes up in the
morning. He is a famous wrestler. Physical
exam reveals mild diastolic HTN, prominant
jaw with spaces between the teeth, large hands
and feet, and generalized muscle weakness.
Acromegaly

16. 
-overproduction of growth hormone leading to soft tissue
overgrowth throughout the body
ACROMEGALY -
Definition :

17. 
 MCC pituitary adenoma.
 Association with one of the multiple endocrine
neoplasias when it is combined with parathyroid
and pancreatic disorders like gastrinoma or
insulinoma.
 Rarely, acromegaly is caused by ectopic GH or
GHRH production from a lymphoma or bronchial
carcinoid.
Acromegaly - etiology

18. 
Acromegaly enlarges soft tissue like cartilage
and bone, resulting in:
• Increased hat, ring, and shoe size
• Carpal tunnel syndrome(bilateral) and
obstructive sleep apnea from soft tissues
enlarging
• Body odor from sweat gland hypertrophy
• Coarsening facial features and teeth widening
from jaw growth
• Deep voice and macroglossia (big tongue)
Acromegaly - Clinical
finding:

19. 
• Colonic polyps and skin tags
• Arthralgias from joints growing out of
alignment
• Hypertension for unclear reasons in 50%
• Cardiomegaly and CHF(MCC of death)
Erectile dysfunction from increased prolactin
co-secreted with the pituitary adenoma
Diabetes/impair glucose tolerance
Acromegaly - Clinical
finding:

20. 

21. 
1. Insulin growth factor-1 (IGF-1)
Confirmatory testing involves measurement of GF after
100g of glucose is given orally,this test is positive if GH
remains high(>5ng/ml) and suggests acromegaly.
Normally,a glucose load should completely supress
level of GH.
2. MRI should be done only after the laboratory
identification of acromegaly.
Acromegaly - Diagnostic

22. 1. Surgery: Acromegaly responds to transphenoidal
resection of the pituitary in 70% of cases. Larger adenomas
are harder to cure.
2. Medications:
• Cabergoline: Dopamine will inhibit GH release.
• Octreotide or lanreotide: Somatostatin inhibits GH
release.
• Pegvisomant: A GH receptor antagonist, it inhibits IGF
release fromthe liver.
3. Radiotherapy: Radiation is used only in those who do
not respond to surgeryor medications.
Acromegaly-treatment

23. 
Pressure of tumor surrounding
structures ,invasion of tumor into brain,
sinuses
Cardiac failure (most common cause of
death)
Diabetes mellitus
Cord compression
Visual field defect
Acromegaly -
Complication

24. 
A 42-year-old man presents to a new family physician to establish care.
According to the patient, he has been healthy his entire life and rarely
visits doctors, although he recently got married and his wife insisted that
he see a doctor at least once. He reports no past medical or surgical
history. His physical exam is notable for an elevated blood pressure
(150/90), and the findings seen in Figures A and B. What will be the most
likely cause of death for this patient?
 1. Respiratory disease
 2. Cardiovascular disease
 3. Malignancy
 4. Chronic kidney disease
 5. Liver failure

25. 
 Correct answer =2
 this patient has acromegaly, the most common cause of death from which is
cardiovascular disease.
 Acromegaly is defined by an excess of growth hormone. This most commonly occurs in
the setting of a pituitary adenoma, but may also occur due to other factors (see
illustration A). The excess growth hormone in acromegaly results in significant
organomegaly. In the case of the cardiovascular system, patients can develop
hypertension, left ventricular hypertrophy, asymmetric septal hypertrophy, diastolic
heart failure, and even cardiomyopathy. Treatment of acromegaly involves resection of
the pituitary adenoma when possible and medical management of growth hormone
excess with somatostatin analogues.
 Lake et al. review pituitary adenomas. They note that the most common types of
pituitary adenomas are prolactinomas and non-functioning adenomas. Acromegaly,
hyperprolactinemia and Cushing's syndrome can result from pituitary adenomas.
 Ciresi et al. examine the metabolic characteristics of newly acromegalic patients. In an
examination of 307 newly diagnosed patients, they noted that women have a higher
rate of metabolic syndrome, insulin resistance and visceral adiposity dysfunction in this
disease.
 Figure A shows the typical facial changes that accompany acromegaly: prominent
cheekbones, bulging forehead, and an enlarged jaw.
 Figure B shows a close up of the prominent brow ridge that may be seen in patients
with acromegaly.

26. 

27. 

28. 

29. 

30. 
 Panhypopituitarism is caused by any condition that
compresses or damages the pituitary gland.
 Tumors of many types can compress the gland, such as
metastatic cancer, adenomas, Rathke cleft cysts,
meningiomas, craniopharyngiomas,or lymphoma.
 Trauma and radiation are damaging to the pituitary.
 Inflammatory disease: granulomatous ds(sarcoidosis,
tb,syphilis), autoimmune and lymphocytic infiltration
 Vascular ds: sheehan postpartum necrosis and infiltrative ds
include hemochromatosis and amyloidosis
 Stroke.
Hypopituitarism-
etiology

31. 

32. 

33. 
SHEEHAN SYNDROME
Postpartum hemmorhage-induced infarction of the pituitary gland
result of hypovolemic shock pituitary normally very enlarged during
pregancy due increased lactotrophs there is no corresponding increase
in blood supply to the pituitary gland and can infarct when systemic
blood pressure drop hypopituitarism results in reduced prolactin
secretion
Symptoms
 sudden cessation of lactation or failure to commence lactation
 loss of prolactin
 fatigue
 loss of TSH
 loss of pubic and axillary hair
 loss of LH/FSH
 anorexia
Evaluation
 Only clinically significant cause of lower than normal serum
prolactin levels
 Imaging MRI shows infarction of the pituitary gland

34. 
 5 days post-vaginal delivery, a 26-year-old woman
presents to her pediatrician with the inability to
breast feed her child. History reveals that her vaginal
delivery was complicated by a postpartum
hemomorhage.
Sheehan syndrome

35. 
 A 28-year-old G2P1 female with a history of hypertension presents to
the emergency room at 33 weeks with headache and blurry vision.
On exam, her vitals include BP 186/102 mmHg, HR 102 beats per
minute, RR 15 breaths per minute, and T 98.9 degrees Fahrenheit. She
undergoes an immediate Caesarian section, and although she is
noted to have large-volume blood loss during the procedure, the
remainder of her hospital course is without complications. Four
weeks later, the patient returns to her physician and notes that she
has had blurry vision and has not been able to lactate. A prolactin
level is found to be 10 ng/mL (normal: 100 ng/mL). Which of the
following is the most appropriate next step? Topic Review Topic
 1. Galactogram
 2. Observation of materal-child interactions
 3. Brain MRI
 4. Head CT
 5. Breast ultrasound

36. 
 PREFERRED RESPONSE ▼ 3
 This patient's clinical condition is consistent with Sheehan's syndrome,
which is best diagnosed with a brain MRI.
 Sheehan's syndrome is characterized by peripartum pituitary necrosis due
to hypotension during or immediately after childbirth. During pregnancy,
increased lactotrophs cause enlargement of the pituitary gland without a
corresponding increase in blood supply. This makes the pituitary gland
particularly vulnerable to infarction due to hypotension. The major
characteristics of Sheehan's syndrome are explained by the loss of pituitary
hormone products, including thyroid stimulating hormone (symptoms of
hypothyroidism), prolactin (inability to lactate), and gonadotrophs (loss of
pubic hair). Treatment of the condition includes life-long hormone
replacement.
 Samra discusses the ocular complications of Sheehan's syndrome. She notes
that pituitary hemorrhage and swelling from infarction can impact the
neighboring ocular structures. Overall, 78% of patients with Sheehan's
syndrome have opthalmoplegia and 64% have decreased visual acuity.
 Soares et al. performed a case-control study to evaluate the effects of long-
term growth hormone replacement in patients with Sheehan's syndrome.
They find that hormone treatment is associated with a decreased high-
density lipoprotein and visceral fat and increased rates of glucose
intolerance.

37. 
 Incorrect Answers:
 Answer 1: Galactogram should be considered if the cause
of this patient's inability to lactate is thought to be
structural.
 Answer 2: There is no indication that this patient has poor
maternal-child interactions.
 Answer 4: Although pituitary infarct is visible on head
CT, the more sensitive imaging test is a head MRI.
 Answer 5: Breast ultrasound is useful for diagnosing a
breast abscess, which can cause a plugged duct. Abscesses
are usually unilateral, and may be associated with breast
tenderness and fever.

38. 
Illustration A shows a T1-weighted head MRI with
gadolinium showing an enlarged, rim-enhancing pituitary
gland, suggesting Sheehan's syndrome with non-
hemorrhagic pituitary ischemia.

39. 
 Prolactin deficiency: There are never any symptoms
of prolactin deficiency in men. In women, prolactin
deficiency inhibits lactation after childbirth.
 (LH) and follicle-stimulating hormone (FSH):
 Women will not be able to ovulate or menstruate
normally and will become amenorrheic.
 Men will not make testosterone or sperm. Both will
have decreased libido and decreased axillary, pubic,
and body hair. Men will have erectile dysfunction
and decreased muscle mass
Hypopituitarism –
clinical findings

40. 
 Growth hormone (GH) deficiency:
 Children present with short stature and dwarfism.
 Adults have few symptoms of GH deficiency
because several other hormones, such as
catecholamines, glucagon, and cortisol, act as stress
hormones.
 Adults deficient in GH have subtle findings such as:
• Central obesity
• Increased LDL and cholesterol levels
• Reduced lean muscle mass
Hypopituitarism –
clinical findings

41. 

42. 
Hyponatremia is common secondary to
hypothyroidism and isolated glucocorticoid
underproduction.
 Potassium levels remain normal because aldosterone
is not affected and aldosterone excretes potassium.
 MRI detects compressing mass lesions on the
pituitary.
Diagnostic Tests

43. 
 Older, Less Useful Tests
• Metyrapone: Metyrapone inhibits 11-beta
hydroxylase. This decreases the output of the adrenal
gland. Metyrapone should normally cause ACTH levels
to rise because cortisol goes down. Cortisol is the
feedback inhibition on the pituitary.
• Insulin stimulation: When insulin decreases glucose
levels, GH should usually rise. Failure of GH to rise in
response to insulin indicates pituitary insufficiency.
Diagnostic Tests

44. 
 Low (TSH) and low thyroxine levelsDecreased
TSH response to (TRH)
 Decreased ACTH and decreased cortisol
levelNormal response to cosyntropin stimulation
of the adrenal.Cortisol will rise (adrenal is normal) in
recent disease, but a bnormal in chronic disease
because of adrenal atrophy.No response (rise) in
ACTH level with CRH.An elevated baseline cortisol
level excludes pituitary insufficiency.
Specific diagnostic test
for each hormone

45. 
 Replace deficient hormones with:
• Cortisone
• Thyroxine
• Testosterone and estrogen
• Recombinant human growth hormone
Replace cortisone before starting thyroxine.
Treatment

46. 
Empty sella syndrome
(ESS)

47. 
 Caused by herniation of the suprasellar
subarachnoid space through an incomplete
diaphragm sella.
 No pituitary gland is visible on CT/MRI.
 Most patient are obese, multiparous womens with
headache,30% will have hypertension; endocrine
symptoms are less.
ESS

48. 

49. 

50. 
Posterior pituitary gland

51. 
Definition:
Diabetes insipidus (DI) is a decrease in either the
amount of ADH from the pituitary (central DI) or its
effect on the kidney (nephrogenic DI).
Diabetes insipidus (DI)

52. 
 25 year old male complains of a unabated thirst that
began three weeks ago. He is constantly drinking
and goes to the bathroom around five times a night.
He has lost five pounds over the last few weeks, and
is on lithium for a bipolar disorder. His BP is 115/70.
Diabetes insipidus (DI)

53. 

54.  Central DI (CDI): Any destruction of the brain from
stroke, tumor, trauma,hypoxia, or infiltration of the gland
from sarcoidosis or infection can cause CD I.
 Nephrogenic DI (NDI):
 kidney diseases such as chronic pyelonephritis,
amyloidosis, myeloma,
 sickle cell disease
 Hypercalcemia(severe dehydrate)
 Hypokalemia
 Drugs:lithium,demeclocycline,colchicine
DI-Etiology

55. 
 Polyuria,polydipsia
 Excessive dilute urine
 Hypernatremia(losing free water) if severe develop
neurological symptoms such as confusion,
disorientation, lethargy,and eventually seizures and
coma. Neurological symptoms occur only when
volume losses are not matched with drinking
enough fluid
 Low urine osmolality
 Increase serum osmolality
Clinical finding

56. 

57. 
Water restriction test

58. 

59. 
 Central DI is treated with long-term vasopressin
(desmopressin) use.
 Nephrogenic DI is managed by trying to correct the
underlying cause (e.g.,hypokalemia or
hypercalcemia). Also responds to
hydrochlorothiazide,amiloride, and prostaglandin
inhibitors such as NSAIDs (e.g.,indomethacin).
Treatment

60. 
 A 45-year-old female undergoes a transphenoidal
approach for a pituitary prolactinoma. Surgery proceeded
without complications and the entire mass was removed.
The patient’s urine output is 4 L on post-operative day 1,
and labs are significant for serum Na of 145 mEq/L
(normal: 135-145). Urine osmolality is 185 mOsm/kg, and
urine specific gravity is 1.004 (normal: 1.012 to 1.030).
Which of the following choices is the next best step?
 1. Water restriction
 2. Loop diuretic
 3. CT scan of the brain
 4. 0.45% NaCl administered intravenously
 5. Desmopressin

61. 
 PREFERRED RESPONSE ▼ 5
 The patient’s history and lab results are consistent with post-surgical central diabetes
insipidus. The most reasonable next step is administration of desmopressin or
chlorpropamide.
 Diabetes insipidus (DI) can be classified as central or nephrogenic. Central DI is caused
by a deficiency in antidiuretic hormone (ADH) secretion, while nephrogenic DI is caused
by resistance to ADH. In this situation, the patient has recently undergone transphenoidal
resection of a pituitary adenoma and central DI is a known complication. Symptoms of
central DI include polyuria, nocturia, and polydipsia. Lab work typically shows elevated
serum sodium, low urine osmolality (50-200 mOsm/kg), and elevated serum osmolality.
First line treatment for central DI is administration of desmopression, an ADH analog.
Alternatively, chlorpropamide, carbamazepine, and thiazide diuretics have also been
used to treat central DI.
 Kugler and Hustead discuss the approach to serum sodium imbalance in the elderly.
They discuss common causes of hyponatremia, such as medications, glucocorticoid
deficiency, hypothyroidism, polydipsia, and SIADH, which is the opposite of DI. They
also discuss common causes of hypernatremia, including primary hypodipsia and DI,
and present an algorithm for the workup of hypernatremia.
 Schreckinger et al. discuss the development of DI following pituitary tumor resection,
commenting that the course of DI has three patterns - transient, permanent, and triphasic.
Transient DI tends to resolve after 3-5 days, permanent DI occurs when the hypothalamus
or infundibulum are damaged, while triphasic is a combination of the two and results
from hypothalamic neuronal shock.

62. 
 Incorrect answers:
 Answer 1: Water restriction can be used to distinguish
central DI from primary polydipsia - however, in this
situation, the clinical picture points toward central DI.
 Answer 2: Loop diuretics are not used in the treatment of
DI.
 Answer 3: CT scan of the brain would likely reveal post-
operative changes, but not help diagnose DI.
 Answer 4: Administration of fluids would not be
sufficient for treatment of D

63. 

64. 
SIADH
 Mrs. Jones, a type II diabetic, presents with mental
status changes. She is taking 250 mg of
chlorpropamide daily. Physical exam is
unremarkable. Lab studies show Na 120, K of 3.2, Cl
of 90, bicarb of 21, glucose of 14, and BUN of 5.
Random urine sodium is 80 with a urine osmolarity
of 306.

65. 
 Free water retention
 ECF volume expansion
 Euvolumic hyponatremia
 No EDEMA or hypertension(escape mechanism)
 Natriuresis
 Symptoms when hyponatremia is severe:
1.Irritability
2.Confusion
3. Seizure
SIADH

66. 

67. 

68. Pulmonary disorders:
1. Malignancy(oat cells,small cell carcinoma)
2. TB,sarcoidosis
3. Lung abscess
CNS Disorder
1. Head injury
2. Cerebral vascular accident(stroke)
3. Encephalitis
Drugs
 Chlorpropamide
 Vincristine,vinblastine,cyclophosphamide
 SSRI(sertraline)
 Carbamazepine
 clofibrate
SIADH-Etiology

69. 
1. Hyponatremia<130meq/L
2. Plasma osmolality<270osm/kg
3. Urine sodium concentration > 20meq/L
(inappropriate natriuresis)
4. Hypervolemia
5. Low BUN, creatinine, uric acid, albumin
Diagnosis

70. Treat underlying cause
Fluid restriction 800-1000mL/day
Drug treatment :
1. Demeclocycline(inhibit ADH action at collecting
duct)
2. Conivaptan and tolvaptan (v2 receptor blocker)- for
moderate to severe SIADH.
-For very symptomatic (severe confusion,convulsion
coma)hypertonic saline(3%)200-300mL IV in 3-4h.
SIADH-Management

71. 
A 67-year-old female presents with complaints of fatigue,
nausea, and headache that have developed over the past
several weeks. Her past medical history is significant for
hypertension, diabetes mellitus, CHF, and small cell lung
cancer diagnosed and treated 3 years previously. Vital signs
are as follows: T 37.3 C, HR 82, BP 142/86, RR 16, O2Sat 97%
on RA. On physical exam, peripheral edema is absent, and she
is alert and oriented to person, place, and time. Abnormalities
noted on initial labwork include glucose 138 mg/dL and
sodium 122 mEq/L. Follow-up testing reveals a urine
osmolality of 310 mmol/kg and a serum osmolality of 268
mmol/kg; BUN and creatinine levels are within normal limits.
Which of the following is the best next step in the
management of this patient

72. 
A.Demeclocycline administration
B. Initiate demospressin nasal spray
C. Fluid restriction
D. Hypertonic saline infusion
E. Lithium carbonate administrati
Question

73.  This patient's presentation of hyponatremia, history of small cell
lung cancer, and urine/serum osmolality values is consistent with a
diagnosis of syndrome of inappropriate secretion of antidiuretic
hormone (SIADH). Initial treatment of SIADH is with water
restriction.
 There are numerous potential etiologies of SIADH; however, a
commonly tested cause is the aberrant production of ADH by a
primary or recurrent small cell lung cancer. Edema is typically absent
in the clinical presentation of SIADH because, although volume
expansion occurs due to water retention, edema is prevented from
forming due to salt-wasting in the urine. Clinical manifestations of
severe or overtly symptomatic SIADH, often neurologic due to
swelling of brain cells, include altered mental status, seizures, coma,
and even death. In the treatment of hyponatremia, there is always
concern for precipitating central pontine myelinolysis by increasing
serum Na levels too quickly; generally, the rise should not exceed 0.5
mEq/L per hour.
Correct answer =C

74. 
 A 34-year-old man with a history of major depressive
disorder presents to the emergency room with altered
mental status. Vital signs are stable, and he appears
euvolemic on exam. Serum sodium is 120. The patient's
hyponatremia is attributed to newly prescribed
fluoxetine. Which of the following is another cause of
euvolemic hyponatremia?
A.Congestive heart failure
B. Nephrosis
C.. Prerenal acute kidney injury
D.Mineralocorticoid deficiency
E. Lung malignancy

75. 
 : A cause of euvolemic hyponatremia is SIADH as a result of a paraneoplastic
production of ADH from a small cell lung cancer. Plasma osmolality will be
low, and urine osmolality will be inappropriately high.
 Euvolemic hyponatremia may be caused by SIADH, psychogenic polydipsia,
postoperative hyponatremia, hypothyroidism, or iatrogenic administration
of excess free water. The inappropriate release of ADH may be caused by
factors that either stimulate the release of ADH from the hypothalamus or
decrease the sensitivity to ADH of the collecting duct in the kidneys.
Neoplastic conditions, such as those encountered with small cell carcinoma
of the lung, result in ectopic ADH production. Other common causes of
SIADH are drugs, including: NSAIDS, antidepressants (such as fluoxetine),
chemotherapy, clofibrate, morphine, and carbamazepine. Other causes of
SIADH, less commonly tested by the USMLE, are CNS disturbances,
pulmonary disease, hypothyroidism, and Conn's syndrome. Important
causes of hypovolemic hyponatremia to remember are diarrhea, vomiting,
burns, and pancreatitis. In contrast, important causes of hypervolemic
hyponatremia to remember are heart failure, nephrotic syndrome, and liver
disease.
Correct answer=E

76. 
 Answers A and B: Congestive heart failure and
nephrosis cause hypervolemic hyponatremia, which
would result in Urine Na < 10, Fractional Excretion
Na < 1%.
 Answer C: Prerenal acute kidney injury is a cause of
hypovolemic hyponatremia. One would expect
Urine Na < 20, Fractional Excretion Na < 1%.
 Answer D: Mineralocorticoid deficiency causes
hypovolemic hyponatremia. One would expect
Urine Na > 20 and Fractional Excretion Na > 1%.

77. 
 A 39-year-old female presents with confusion. Her husband reports
that she doesn't know where she is and cannot remember the date.
She was recently diagnosed with small cell lung cancer. Vital signs
are T 37C, HR 80, BP 120/80 mmHg, RR 14, and O2 sat 99% on
room air. She is not orthostatic. Physical examination reveals moist
mucous membranes and normal capillary refill. A basic metabolic
profile reveals that serum sodium is 129. Regarding this patient's
illness, which of the following is true?
 1. Urinary osmolarity will be > 100, and this illness will not correct
with saline infusion
 2. Urinary osmolarity will be < 100, and another potential cause of
this disorder is excessive water drinking
 3. Urinary sodium will be > 20 and fractional excretion of sodium
will be >1%
 4. Urinary sodium will be < 10, and fractional excretion of sodium
will be <1%
 5. Urinary sodium will be > 20 and another potential cause of this
disorder is renal failure

78. 
 Correct answer =1
 DISCUSSION: The patient has a lung cancer causing ectopic release
of ADH. In syndrome of inappropriate ADH (SIADH), patients have
euvolemic hyponatremia, decreased serum osmolarity, elevated
urine osmolarity, increased urine sodium concentration, and failure
to correct with saline infusion.
 Hyponatremia occurs when the body maintains excess water relative
to sodium. It is almost always due to increased ADH, either
appropriately secreted as in hypovolemia or hypervolemia with
decreased effective arterial volume, or inappropriately as in SIADH.
Hyponatremia should first be divided into hypovolemic causes (such
as renal losses, mineralocorticoid deficiency, or extra renal losses),
euvolemic (such as SIADH and primary polydipsia), and
hypervolemic hyponatremia (secondary to CHF, cirrhosis, nephrosis,
or renal failure). The differential is narrowed by assessing the
volume status of the patient and then measuring urine and serum
electrolytes.

79. 
 Answer 2: These factors describe euvolemic
hyponatremia secondary to primary polydipsia.
 Answer 3: These factors describe hypovolemic
hyponatremia secondary to renal losses or
mineralocorticoid deficiency.
 Answer 4: These factors describe hypervolemic
hyponatremia secondary to CHF, cirrhosis, or nephrosis.
 Answer 5: These factors describe hypervolemic
hyponatremia secondary to renal failure. Fractional
excretion of sodium would be >1%.

80. 

81. 

82. 

83. 
1. Define diabetes insipidus (DI). What are the two
types?
2. What causes central DI?
3. What causes nephrogenic DI?
4. What diagnostic test can reveal whether DI is
central or nephrogenic? How are these conditions
treated?
5. Define the syndrome of inappropriate
antidiuretic hormone secretion (SIADH).How is it
diagnosed?
6. What causes SIADH?
7. How is SIADH treated?

84. 
1. Define diabetes insipidus (DI). What are the two
types?
 DI is a lack of antidiuretic hormone (ADH), or
vasopressin, effect in the body. Patients with DI
secrete inappropriately dilute urine because of the
lack of ADH effect and may urinate up to 25 L of
urine per day, resulting in dehydration and
hypernatremia. Such patients die rapidly if they are
unable to drink water. Normally, when the body is
dehydrated, ADH causes urine to become highly
concentrated through retention of free water. In DI,
the urine remains dilute even though the serum
osmolarity is quite high as a result of dehydration.
The two types are central and nephrogenic.

85. 
2. What causes central DI?
 Central DI is caused by a lack of ADH production by
the posterior pituitary. Although it is often
idiopathic,look for trauma, neoplasm, or
sarcoid/granulomatous disease as the cause. Order a
CT or MRI scan of the head, if indicated.
3. What causes nephrogenic DI?
 Nephrogenic DI is caused by kidney
unresponsiveness to ADH. Look for medications
(e.g., lithium,demeclocycline) as the cause

86. 
4. What diagnostic test can reveal whether DI is central or
nephrogenic? How are these conditions treated?
 Give the patient a dose of ADH, and measure urine osmolarity. If
central DI is the cause, urine osmolarity increases with ADH
challenge. In nephrogenic DI, the urine remains inappropriately
dilute after the patient is given ADH. Treatment for central DI is
ADH replacement (given orally or as a nasal spray). Treatment for
nephrogenic DI involves stopping any offending drug and giving
a thiazide diuretic; ADH does not help. Although giving a diuretic
to a patient with DI seems counterintuitive, it has the paradoxical
effect of decreasing urine output.
5. Define the syndrome of inappropriate antidiuretic hormone
secretion (SIADH).How is it diagnosed?
 The name says it all: ADH is released inappropriately. SIADH is a
consideration in patients with hyponatremia and normal volume
status (euvolemic). In SIADH, serum osmolarity is low, but urine
osmolarity is high (inappropriate urine concentration). Look for the
values of all electrolytes and lab tests to be low (the classic example is
uric acid) because of dilution of the serum with free water secondary
to inappropriate ADH.

87. 
6. What causes SIADH?
 Central nervous system causes: Stroke, hemorrhage, infection,
trauma.
 Medications: Narcotics, oxytocin (in pregnant patients),
chlorpropamide, antiepileptic agents.
 Trauma: Pain is a powerful stimulus for ADH. Watch for the
postoperative patient who is receiving fluids (and often narcotics)
and has pain.
 Lung problems: Simple pneumonia or ADH-secreting small cell
cancer of the lung.
7. How is SIADH treated?
 Treat with water restriction. Stop intravenous fluids and restrict
oral fluid intake. For Step 2 purposes, do not give hypertonic
saline unless the patient has active seizures. You may cause
brainstem damage or central pontine myelinolysis from too rapid
correction of sodium level. Demeclocycline is sometimes used to
treat SIADH if water restriction fails because it induces
nephrogenic DI, which allows the patient to eliminate free water.

88. 
THANK YOU