Differential diagnosis of polyuria (physiological,psychological,pathological causes )

. 1. Physiological :

_ winter months.

_ excess coffee or tea.

_ Diuretics.

2. Psychological :

_ Hysterical polydepsia.

_ Differs from D.I. : → fluid deprivation → normal.

→ no improvement after ADH.
3. Pathological :

a. Endocrinal :

i. D.I.

ii. D.M.

iii. Adrenal : Conn’s , Cushing’s , Addison’s.

iv. Thyroid : thyrotoxicosis.

v. Parathyroid : hyperparathyroidism.

b. Renal :

i. Nephrogenic DI : end organ unresponsiveness.

ii. Acute renal failure → diuretic phase.

iii. Chronic renal failure.

iv. Fanconi syndrome

c. Miscellaneous :

_ After attacks of

migraine, epilepsy, bronchial asthma &
see the pictures

paroxysmal tachycardia.

Syndrome of inappropriate anti-diuretic hormone SIADH its causes and newest treatment

It means an excessive release of ADH

1. Physiology :

Refer to diabetes insipidus.

2. Etiology :

a. Tumor → oat cell carcinoma.

b. Pulmonary lesion :Legionella pneumonia , T.B.

c. CNS : meningitis, encephalitis & head injuries.

d. Drugs :

cholropropamide,carbamazepine,cyclophosphamide -
3. C / P :

· Increased ADH causes water retention→ water

intoxication → dilutional hyponatremia ( nausea,

vomiting, confusion, headache, convulsions &

coma.)

· No edema because of natriuresis.

4. Investigation :

1. ↓ Na (< 130m.Eq /L )

2. ↓ serum osmolarity(< 270m.osmol/L.) & ↑urine

osmolarity ( > 300 m.osmol/L.)

N.B. : Normal renal , adrenal & thyroid functions.

5. Treatment :

a. Fluid restriction → 800-1000 ml / day.

b. demeclocycline:

i. 600-1200 mg /day → inhibit i action of ADH.

ii. Given to patient unresponsive to fluid restriction.

c. For sever hyponatremia : hypertonic saline 1.8% slowly é

fursemide to treat hyponatremia

Diabetes insipidus its physiology,etiology,clinical picture,investigation and newest treatment

1. Physiology :

a. Hormone : ADH (antidiuretic hormone)[ vasopressin ].

b. Gland : Pituitary gland [ posterior lobe ].

c. Function of the hormone :

i. ↑↑ water reabsorption by renal tubules.

ii. Large dose → v.c. of bl. vessels.

N.B. :

ADH is synthesized in hypothalamus & then transported

along axons & stored in i post. Pituitary.

d. Regulation of this hormone :

i. ↑↑ ADH by :

1. ↑ osmolarity.

2. hypovolemia.

3. stress

4. drugs :

a. nicotine.

b. barbiturates.

ii. ↓↓ ADH by :

1. ↓ osmolarity.

2. hypertension.

3. cold weather.
2. Etiology :

a. Central DI → damage of hypothalmo-hypophyseal axis:

i. Idiopathic : starts in childhood.

ii. Tumor.

iii. Trauma : head injuries & after hypophysectomy.

iv. Granulomas : T.B. & sarcoidosis.

b. Familial DI ( Walfram syndrome) [ DIDMOAD ] hereditary

condition → defect in osmo-receptrs ass. é

i. DI diabetes insipidus.

ii. DM diabetes mellitus

iii. OA optic atrophy

iv. D deafness.

c. Nephrogenic DI ( Renal tubules not responding to ADH )

i. Hereditary .

ii. Acquired : 2ry to :

1. renal tubular acidosis.

2. kidney amyloidosis.

3. hypercalcemia.

4. hypokalemia.

5. drugs :

a. lithium.

b. cholchicine.

3. C / P :

a. C / p of i cause :

i. Surgery → hypophysectomy.

ii. Tumor → ↑ intracranial tension.

b. C / p of i hormone :

i. Polyuria & nocturia : 5 – 20 L/day.

ii. Dehydration , polydepsia,

weight loss & low grade fever.

iii. Hypovitamonosis : of water soluble vitamins.

iv. Complications : shock.

4. Differential diagnosis :

Other causes of polyuria. [discussed later].

_ especially ; psychogenic polydepsia.

N.B. :

_ DI :

- polyuria → polydepsia.

- so ; there is ↑↑ osmolarity.

_ Psychogenic polydepsia :

- polydepsia → polyuria .

- so ; there is ↓↓ osmolarity.

5. Investigation :

a. Inv. for i cause :

i. Imaging for i gland :

1. X-ray.

2. C.T. & M.R.I.

b. Assay of i hormone level :

i. In blood.

ii. In urine.

c. Inv. of i function of i hormone :

i. Urine analysis :

1. Polyuria é no pathological constitutes.

2. Specific gravity : low.

3. After fluid deprivation : - polyuria persists.

& - Sp.G. fails to rise.

ii. Plasma osmolarity

_ ↑↑ due to loss of free water é high plasma Na.

d. Tests for localization of i cause :

i. Test i hypothalamus :

_ material : nicotine.

smoking cigarette or inject 1-3 ml nicotine.

1. normal : oliguria.

2. in case of central DI : no change.

ii. Test osmo-receptrs :

_ material : I.V. hypertonic saline

( NaCl 2.5 % ) .

1. normal : oliguria.

2. if i lesion is in osmo-receptrs ( e.g. familial DI ) :

no change.

iii. Test kidney : [ to ( ) central DI & nephrogenic DI ]

_ material : vasopressin. [ test _

1. in central DI : oliguria.

2. in nephrogenic DI : no change.

6. Treatment :

a. TTT of i cause.

b. Diet : excess fluid, salts, fats, CHO & vitamins.

c. Replacement therapy :

_ Desmopressine ( synthetic ADH )

nasal spray ; twice daily.

d. Drugs :

_ Cholropropamide & Carbemazepine ( tegretol )

may be used in nephrogenic DI both sensitizerenal tubules to ADH.see the pictures

Hyperprolactinaemia its physiology ,etiology ,clinical picture,investigation and newest treatment

1. Physiology :

a. Hormone : Prolactin.

b. Gland : Pituitary gland [anterior lobe].

c. Function of the hormone :

i. Necessary for lactation.

ii. ↓↓ GnRH.

d. Regulation of this hormone :

i. ↑ prolactin :

_ PRH ( prolactin releasing hormone.)?

_ Recently it’s thought that TRH ( thyrotropin

releasing hormone ) is a prolactin releasing hor.

ii. ↓ prolactin :

_ PRIH ( prolactin release inhibiting hor.)

→ dopamine.

2. Etiology :

a. Physiological : pregnancy , lactation , stress,

sleep & nipple stimulation.

b. Drugs :

i. Dopamine antagonist : phenothiazines.

ii. Dopamine depletors : methyl-dopa & reserpine.

c. Diseases of many organs :

i. Pituitary :

1. tumors : prolactinoma.

2. diseases : grnuloma & sarcoidosis.

ii. Thyroid : 1ry hypothyroidism →↑ TRH→ ↑ prolactin.

iii. Renal : CRF → ↓ prolactin clearance.

iv. Liver cirrhosis : → ↓ metabolism.
3. C / P :

a. C / p of i cause :

i. Tumor.

ii. Dopamine antagonist.

iii. Liver cirrhosis or CRF.

b. C / p of i hormone :

i. ♀ :

1. glactorrhea.
2. amenorrhea.

3. osteoprosis (due to estrogen deficiency).

ii. ♂ :

1. impotence.

2. loss of libido.

3. infertility.

4. gynaecomastia.

5. never glactorrhea.

4. Investigation :

a. Inv. for i cause :

i. Imaging for i gland :

1. U/S.

2. C.T. & M.R.I.

ii. Liver & renal function tests.

b. Assay of i hormone level :

Prolactin > 300 n.gm/ml → suggestive of

[ n < 20 ng / ml ]. pituitary adenoma.

c. Inv. of i function of i hormone :

i. Glactorrhea.

ii. Infertility.

iii. Pressure manifestations.

5. Treatment :

a. Dopamine agonist :

i. Bromocriptine : dose 1.25 mg at bed time

↑ gradually to 15 mg/day.

ii. Cabergoline : drug of choice →less side effects.

b. Surgery: trans-sphenoidal or

trans-cranial → removal of i tumor.

c. Irradiation : proton or _ particles.
see the pictures

d. TTT of i cause : e.g. : myxoedema.

Differential diagnosis of short stature and its causes

Causes :

1. : familial & constitutional : the commonest

2. Endocrinal

a. ↓ GH : Levi-lorian, Frolich’s, Laurance Moon Biedle.

b. ↓ T4 : cretinism & juvenile myxoedema.

c. ↑ sex hormones : precocious puberty.

d. ↑ cortisol : Cushing or excess steroid ttt.

3. Chronic sever illness during childhood :

a. CVS : sever rheumatic fever,

congenital heart diseases.

b. Lung : polycystic lung disease.
c. GIT : mal-absorption & malnutrition

d. Kidney : chronic nephritis.

4. Skeletal causes :

a. Congenital :

i. Aconrdoplasia : short limbs é normal trunk.

ii. Osteochondrodystrophy :

both limbs & trunk are short & deformed.

b. Acquired :

i. Rickets.

ii. Pott’s disease of spine.

iii. Paget’s disease of bone.

5. Genetic causes :

a. Mongolism [Down’s syndrome] trisomy 21.

b. Turner’s syndrome [ 45+ XO ].c. Noonan’s syndrome
see the pictures

Hypopituitarism in adults (Pan hpypopituitarism) its causes and newest treatment

Etiology :

a. Destruction of pituitary gland by :

i. Surgery → in ttt of Hyperfunction.

ii. Irradiation → in ttt of Hyperfunction.

iii. Tuberculosis, sarcoidosis, heamochromatosis.

b. Sheehan’s syndrome :

pituitary infarction after sever post-partum hge ?

c. Neoplasm : acidophil adenoma.

d. Trauma : fracture base of i skull.

e. Idiopathic : auto-immune.

3. C / P :

a. C / p of i cause :

i. Surgery.

ii. Irradiation.

iii. Sever post-partum bleeding.

b. C / p of i hormone :

According to i frequency of appearance, i following occur :

Gondotrophines & GH (2g) are lost early

then → TSH then → ACTH deficiency.

i. Gonadal deficiency :

1. ♀ : amenorrhea, loss of libido, infertility, loss of

pubic & axillary hair.

2. ♂ : impotence, loss of libido, infertility, loss of

pubic & axillary hair.

ii. GH deficiency :

No clinical manifestations in adult

1. skin wrinkling & weakness.

2. ↑↑ sensitivity to insulin ( hypoglycemia ).

iii. TSH deficiency :

_ result in hypothyroidism.

iv. ACTH deficiency :

Results in 2ry adrenal insufficiency it

simulates Addison’s disease except :

1. no pigmentation → absent ACTH.

2. no marked hypotension due to presence of

aldosterone.

N.B. :

aldosterone production is mainly dependant on i

renin- angiotensin system not on ACTH.

v. Coma :

Causes of coma :

1. hypoglycemic coma due to GH & cortisone.

2. myxoedema coma.

3. pressure in cases of pituitary tumors.

N.B. :

If i patient has associated DI & hyperprolactinaemia

the problem is at i hypothalamus.
4. Differential diagnosis 

a. From 1ry hypognadism : → high FSH.

b. From 1ry Addison’s disease :

i. skin pigmentation.

ii. high ACTH.

iii. marked hypotension.

c. From anorexia nervosa :

i. normal hair & breast.

ii. aggressive attitude.

iii. normal cortisol.

iv. high G.H. due to hypoglycemia.

d. From thyroid myxoedema : see later

5. Investigation :

a. Inv. for i cause :

i. Imaging for i gland :

1. X-ray : shows i sella tursica.

2. C.T. & M.R.I. → i best.

b. Assay of i hormone level :

1. ↓ G.H. [ normal = 1 – 5 n.gm/ml.] & ↓ IGF-1.

2. ↓ FSH, ↓ LH & ↓ sex hormones.

3. ↓ TSH, ↓ T3 & ↓ T4.

4. ↓ ACTH & ↓ cortisol.
c. Inv. of i function of i hormone :

1. hypoglycemia.

2. hyponatremia.

d. Stimulatory test :

stimulatory test → for Hypofunction.

_ material : insulin.

_ I.V. insulin followed by TRH & GnRH.

1. normal → ↓ blood sugar → marked

elevation of GH, TSH, FSH, LH & cortisol.

2. in pan-hypopituitarism : no change.

6. Treatment :

a. TTT of i cause.

b. Replacement therapy :

i. Hydrocortisone : dose : 30 mg/ day.

20 mg a.m. & 10 mg p.m.

ii. Gonadal hor.s : ♂ → testosterone.

♀ → estrogen/progesterone.

iii. Thyroxin : dose 0.1 – 0.2 mg/day.

given after steroid replacement.

iv. Recently :

1. purified pituitary hor.s.

2. hypothalamic releasing factors.
see the pictures