In Capsule Series

Internal Medicine

Endocrinology

Third edition

By :
Dr. Ahmed M.Mowafy
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 Preface
- First and foremost, thanks are due to ALLAH, to whom I relate
any success in achieving any work in my life.

- My words stand short of my supreme gratitude and thanks to

Prof. Dr. Hossam Mowafy ; Head of critical care unit, Kasr El Ainy.

- My thanks are extended to all my medical students whom I produce this

series:“In Capsule Series” to obtain a higher degree in internal medicine

by a simple effort.

- Finally, I wish to thank all members of My Family, my colleagues , my

Friends and even all my patients for their continuous help,

encouragement and support.

Ahmed Mowafy
In Capsule Series Endocrine www.incapsuleseries.com

Index
Subject Page
Endocrinology scheme 1
Pituitary gland
 Pituitary gland 3
 Acromegaly 5
 Hyperprolactinaemia 9
 Hypopituitarism in adults 11
 Diabetes insipidus 15
 SIADH 19
Thyroid gland
 Thyroid gland 20
 Thyroid diseases 21
 1ry thyrotoxicosis 22
 Mxyedema 31
 Cretinism 37
Parathyroid gland
 Ca metabolism 38
 Hyperparathyroidism 39
 Hypoparathyroidism 44
Suprarenal gland
 Conn`s syndrome 47
 Cushing`s syndrome 50
 Adrenogenital syndrome 54
 Addison`s disease 55
 Pheochromocytoma 60
 Steroid preparations 61
Diabetes mellitus 63
Hypoglycemia 91
Hirsutism & Gynaecomastia 92
Obesity 93
Loss of weight 95
Endocrinology MCQ 96
MCQ answers 104
Collections of endocrine 109
In Capsule Series Endocrine www.incapsuleseries.com

Endocrine scheme
These points should be discussed in any endocrinal disease:
1. Physiology.
2. Etiology.
3. Clinical picture.
4. Differential diagnosis.
5. Investigation.
6. Treatment.
1. Physiology : 4 items

a. Hormone.
b. Gland.
c. Function of the hormone.
d. Regulation of this hormone.
2. Etiology :
a. Hyper : 
i. Tumor : adenoma. ( benign > malignant )
ii. Hyperplasia.
iii. Paramalignant syndrome.

b. Hypo : 
i. Surgery.
ii. Irradiation.
iii. Tuberculosis, sarcoidosis, hemochromatosis. 

3. C / P :
a. C / p of the cause : e.g. pressure manifestations , tumor ….
b. C / p of the hormone :
i. Hyperfunction = function of the hormone.
ii. Hypofunction = opposite the function of the hormone.
N. B. Neurological manifestations : depression & polyneuropathy → may
occur in any endocrinal disease.

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4. Differential diagnosis : Differs according to each hormone.

5. Investigation :
a. Inv. for the cause : e.g. Imaging for the gland : U/S , CT , MRI .
b. Assay of the hormone level :
i. In blood : ↑in hyper , ↓in hypo
 2 - 3 times to avoid the diurnal variation.
 It's not an ideal method because the plasma level of all hormones
varies through the day ( because of pulsatile secretions ).

ii. In urine :
1. hormone.
2. metabolite of the hormone.

c. Investigations of the function of hormone : see function .

d. Dynamic test : The principle is :

 If a hormone level is high → suppress it.

 If a hormone level is low → stimulate it.

o Suppression test → for Hyperfunction.

- normal : +ve ( suppression of the hormone )
- in this case (……) : - ve (no suppression ).

o Stimulatory test → for Hypofunction.

- normal : +ve ( stimulation of the hormone )
- in this case (……) : - ve ( no stimulation ).

6. Treatment :
a. Hyper : 
i. Surgery.
ii. Irradiation.
iii. Medical antagonist.
b. Hypo :
i. Replacement therapy.
ii. Treatment of the cause.

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In Capsule Series Endocrine www.incapsuleseries.com

Pituitary gland
Present in Sella turcica at the base of the skull.
Weight 0.5 gm.
It is divided into 2 lobes :
i. Anterior lobe.
ii. Posterior lobe.
Connected to the hypothalamus by the pituitary stalk.
- Anterior lobe → connected to the hypothalamus by vascular connection
- Posterior lobe → connected to the hypothalamus by neural connection.

anterior lobe :
- Chromophobe : non functioning ( non secreting ).
- Chromophil :
 acidophil : GH & prolactin.
 basophile : ACTH, TSH, FSH, LH & MSH.

Posterior lobe : secretes ADH & Oxytocin .

In fact, ADH & oxytocin are synthesized in the hypothalamus & stored in the
posterior pituitary .

Regulation of pituitary hormones :

i. hypothalamus secretes :
 Releasing factors : GHRH , TRH , CRH , GnRH
- GHRH ( GH releasing hormone ) → ↑the secretion of GH.
- TRH (thyrotropin-releasing hormone ) → ↑the secretion of TSH & Prolactin ?
- CRH ( corticotropin releasing hormone ) → ↑the secretion of ACTH
- GnRH ( gonadotropin releasing hormone ) → ↑the secretion of LH , FSH

 Release inhibiting factors : ↓secretion of pituitary hormones.

ii. Secretion of hormones is also regulated by -ve feedback mechanism :

e.g. ↑T 3 → ↓TSH , ↑cortisol → ↓ACTH.

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Function of the pituitary hormones :

- GH :
 CHO : hyperglycemia.
 fat : lipolysis.
 protein : anabolic (bone, muscle & viscera)
 minerals : ↑all i minerals ( Na, K, Ca & PO4).

- Prolactin : milk secretion.

- FSH :

♀ → maturation of graffian follicle.

♂ → spermatogenesis.

- LH :

♀ → ovulation.
♂ → testosterone formation by the testis.

- ACTH :
 secretion of suprarenal hormones :
o cortisone +++
o androgen ++
o aldosterone + ( under stress only )

- TSH : secretion of thyroxin by thyroid gland.

- MSH : skin pigmentation.

Studying medicine without teacher is like sailing without a boat, and studying
Internal medicine without Dr/Ahmed M.Mowafy is like not going to the sea at all.

Alsayed Dawoud
KasAlainy School of medicine

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Acromegaly
Excessive secretion of GH in adults ( after fusion of the epiphysis )

Physiology :
a. Hormone : Growth hormone ( GH )
b. Gland : Pituitary gland ( anterior lobe )
c. Function of the hormone :
i. CHO : hyperglycemia.
ii. fat : lipolysis.
iii. protein : anabolic (bone, muscle & viscera).

iv. minerals : ↑all minerals ( Na, K, Ca & PO4).

d. Regulation of this hormone :

i. ↑GH :

1. GHRF. ( growth hormone releasing factor )

2. hypoglycemia.
3. sleep.
ii. ↓GH :
1. GHRIF( growth hormone release inhibiting factor )
2. hyperglycemia.
3. stress & exercise.

2. Etiology :
a. Adenoma.
b. Hyperplasia.
c. Paraneoplastic syndrome.
3. C / P :
a. C / p of the cause :
pressure manifestations of pituitary adenoma : visual field defect.

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b. C / p of the hormone :
i. CHO : DM in 25 % of cases.

ii. Fat : excess lipolysis → loss of sc fat , wrinkling of the skin.

iii. Protein : excess growth of bone, muscles, viscera.

1. bone :
a. face : Ape like
i. big skull , enlarged nose, ears, lips & tongue.
ii. prominent supra-orbital ridges & mastoid processes.
iii. prognathism : prominent lower jaw with separated teeth.
iv. hypertrophy of larynx : hollow deep voice.
b. hands & feet :
i. spade hands & enlargement of feet.
ii. frequent change in rings & shoes.
iii. Osteoarthritis.
2. visceromegaly :
a. hepatosplenomegaly.
b. Cardiomegaly → congestive heart failure.
c. Endothelial hyperplasia → hypertension.
3. muscle power :
a. ↑
↑early. b. ↓
↓late.
iv. Minerals :
a. ↑Na → hypertension.
b. ↑K → muscle weakness , arrhythmias.
v. Neurological manifestations :

a. depression.
b. Peripheral neuropathy & carpal tunnel syndrome.
vi. Associated endocrinal manifestation :

hyperprolactinaemia & DM in 25 % of cases.

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4. Investigation :
a. Investigations for the cause : Imaging for the gland : Skull X-ray , CT & MRI
b. Assay of the hormone level :
1. ↑G.H. [ normal < 5 n.gm/ml ]
2. ↑insulin growth factor ( IGF-1 , somatomedin )
3. ↑prolactin in 1/3 of cases.
GH is difficult to measure because of its pulsatile secretions So , insulin growth
factor ( IGF-1 ) produced by the liver in response to GH is measured instead.

c. Investigations of the function of the hormone :

i. Blood :
1. ↑glucose.
2. ↑free fatty acids.
3. ↑Ca & ↑P.
ii. X-ray :
1. skull : thick cortex , prognathism.
2. hand : tufting of the terminal phalanges ( mushroom shape)

d. Suppression test : glucose IV

1. normally → +ve ( ↓GH level )
2. in acromegaly → -ve ( no suppression ).

5. Treatment :
a. Surgery : hypophysectomy.
b. Irradiation.
c. Antagonist : Somatostatine analogue [GHRIF] : octereotide.
d. Symptomatic treatment : DM , Hypertension.

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Gigantism
Definition : ↑↑GH secretion before fusion of epiphysis.
C/P :
1. Generalized overgrowth of skeleton & soft tissue.
2. Disproportionate gigantism.
3. Later on features of acromegaly develops.
4. Lastly decline stage usually occurs ( pituitary hypofunction)

Differential diagnosis of tall stature

1. Familial & racial : [ the commonest ]
2. Gigantism.
3. Excess androgen → tall children , short adult
4. 1ry hypogonadism : Disproportionate gigantism with feminine character.
5. Cerebral gigantism.
6. Marfan’s syndrome.
7. Klinefelter syndrome (xxy)

First they ignore you, then they laugh at you, then they fight you, then you win.
Mahatma Gandhi

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In Capsule Series Endocrine www.incapsuleseries.com

Hyperprolactinaemia
1. Physiology :
a. Hormone : Prolactin.
b. Gland : Pituitary gland [ anterior lobe ].
c. Function of the hormone : milk secretion.
d. Regulation of this hormone :
i. ↑prolactin : PRH ( prolactin releasing hormone) ?
Recently it’s thought that TRH ( thyrotropin releasing hormone ) is a
prolactin releasing hormone.
ii. ↓prolactin : prolactin release inhibiting hormone ( PRIH , dopamine )

2. Etiology :
a. Physiological : pregnancy , lactation , stress & nipple stimulation.
b. Drugs : Antidopaminergic drugs MCQ
i. phenothiazines. ii. methyl-dopa. iii. reserpine.
c. Pathological :
i. Pituitary : prolactinoma ( prolactin secreting pituitary adenoma )
ii. Thyroid : 1ry hypothyroidism →↑TRH→ ↑prolactin.
iii. Renal : CRF → ↓prolactin clearance.
iv. Liver cirrhosis : → ↓metabolism.

3. Clinical picture :
a. C / p of the cause : visual disturbance due to pituitary adenoma.
b. C / p of the hormone :
i. In female :
1. glactorrhea : persistent milk production in a ♀who is not postpartum.
2. amenorrhea.
3. osteoprosis ( due to estrogen deficiency ).

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ii. In male :
1. impotence & ↓libido.
2. infertility.
3. gynaecomastia , never glactorrhea.

4. Investigation :
a. Investigations for the cause : Pituitary imaging : X ray , CT , MRI.
b. Assay of prolactin level :
Prolactin > 300 ng/ml suggest probable pituitary adenoma. [ n < 20 ng/ml ]

5. Treatment :
a. Dopamine agonist :
i. Bromocriptine : 1.25 mg at bed time↑gradually to 15 mg/d.
ii. Cabergoline : drug of choice : less side effects.
b. Surgery: for macroadenoma not responsive to medical treatment.
c. Irradiation : proton or particles.
d. treatment of the cause : e.g. myxoedema.

Pituitary tumors

Tumor Type Secretory Product(s) Relative Frequency (%)

Prolactinoma (Lactotroph Adenoma) Prolactin 50
Somatotroph Adenoma Growth Hormone 10
Corticotroph Adenoma ACTH 5
Thyrotroph Adenoma TSH 1
Non secreting Adenoma ----- 34

Nelson's syndrome : big pituitary adenoma with very high ACTH & hyperpigmentation
after bilateral adrnalectomy in a case of pituitary Cushing.
Pituitary apoplexy : sudden enlargement of the pituitary by hemorrhage into the tumor ,
causing combination of pressure manifestations ( e.g.visual defect ) &
panhypopituitarism.

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Panhypopituitarism in adults
( Loss of anterior pituitary function )
1. Physiology : see before .
2. Etiology :
a. Destruction of pituitary gland by :
i. Surgery .
ii. Irradiation.
iii. Tuberculosis, sarcoidosis, heamochromatosis.
b. Sheehan syndrome : pituitary infarction after sever postpartum hemorrhage ?
c. Neoplasm : acidophil adenoma.
d. Autoimmune.
3. C / P :
a. C / p of the cause : Surgery , Sever post-partum hemorrhage.
b. C / p of the hormones :
According to the frequency of appearance : 2 G → GH & Gondotrophins ( FSH , LH )
are lost early then TSH then ACTH deficiency.
i. Gonadal deficiency :
1. ♀: amenorrhea, ↓libido, infertility, loss of pubic & axillary hair.
2. ♂: impotence, ↓libido, infertility, loss of pubic & axillary hair.
ii. GH deficiency : Not clinically detectable in adults , just :
1. fine wrinkles & weakness.
2. ↑
↑sensitivity to insulin ( hypoglycemia ).
iii. TSH deficiency : result in 2ry hypothyroidism.
iv. ACTH deficiency : Results in 2ry adrenal insufficiency it simulates
Addison’s disease but :
1. no pigmentation ( absent ACTH )
2. no marked hypotension , due to normal aldosterone.

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v. Coma : due to
1. hypoglycemic coma due to ↓GH & cortisone.
2. myxoedema coma.
3. pressure in cases of pituitary tumors.
NB : If the patient has associated DI : the problem is at the hypothalamus.

4. Differential diagnosis :
a. From 1ry hypognadism → high FSH.
b. From 1ry Addison’s disease :
c. From1ry hypothyroidism : see later
d. From anorexia nervosa :
i. normal hair & breast.
ii. aggressive attitude.
iii. normal cortisol.
iv. high GH due to hypoglycemia.

5. Investigation :
a. Investigations for the cause : Pituitary imaging : X-ray , CT & MRI
b. Assay of the hormones level :
1. ↓GH [ n : 1 – 5 n.gm/ml ] & ↓IGF-1.
2. ↓FSH, ↓LH & ↓sex hormones.
3. ↓TSH, ↓T3 & ↓T4.
4. ↓ACTH & ↓cortisol.
c. Investigations of the function of the hormone : e.g.
1. hypoglycemia.
2. hyponatremia.
d. Stimulatory test : insulin test
1. In normal : +ve ( ↑GH, TSH, FSH , LH & cortisol )
2. in pan-hypopituitarism : -ve ( no stimulation ).
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6. Treatment :
a. Treatment of the cause.
b. Replacement therapy : Multiple hormones must be replaced.
i. Hydrocortisone : 30 mg/ d. ( 20 mg a.m. & 10 mg p.m. )
ii. Gonadal hormones : ♂→ testosterone.
♀→ estrogen / progesterone.
iii. Thyroxin : 0.1 – 0.2 mg/d , given after steroid replacement.
iv. Recently :
1. purified pituitary hormones.
2. hypothalamic releasing factors.

Addiction-Free Nation Program should consider in capsule series its 1 st priority, as it has
been proved that almost all internal medicine seekers are addicted to it.
Dr. Alsayed Dawoud
Kasr-Alainy School of Medicine

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Differential diagnosis of short stature

1. familial & constitutional : the commonest.

2. Endocrinal :
a. ↓GH : Levi-lorain , Frolich’s, Laurance Moon Biedle *
b. ↓T4 : cretinism & juvenile myxoedema.
c. ↑sex hormones : precocious puberty.
d. ↑cortisol : Cushing or excess cortisone therapy.
e. Type 1 DM.

* Levi-Lorain syndrome : proportionate dwarfism , hypogonadism , normal mentality.

* Frolich's syndrome : trunk obesity , hypogonadism , polyphagia.

* Laurance moon biedle : like Frolich's + MR , Skull deformity & retinitis pigmentosa.

3. Chronic sever illness during childhood :

a. CVS : sever rheumatic fever, congenital heart diseases.
b. Chest : polycystic lung disease , TB.
c. GIT : malabsorption syndrome & malnutrition.
d. Kidney : chronic nephritis.

4. Skeletal causes :
a. Congenital :
i. Achonrdoplasia : short limbs with 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.

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Diabetes insipidus
Deficiency of ADH

1. Physiology :
a. Hormone : ADH ( antidiuretic hormone , vasopressin ).
b. Gland : Pituitary gland ( posterior lobe ).
ADH is synthesized in hypothalamus & then transported along axons & stored in
the posterior Pituitary.

c. Function of the hormone :

i. ↑
↑water reabsorption by collecting tubules.
ii. Large dose → vasoconstriction of blood vessels.

d. Regulation of this hormone :

i. ↑↑ ADH by :
1. ↑osmolality.
2. Hypovolemia & hypotension.
3. drugs : nicotine , barbiturates.
ii. ↓↓ADH by :
1. ↓osmolality.
2. hypertension.
3. cold weather.

2. Etiology :
a. Central DI : ( damage of hypothalmo-hypophyseal axis )
i. Idiopathic : most common cause
ii. Injury : after hypophysectomy.
iii. Infection : T.B.
iv. Infiltration : sarcoidosis
v. Infarction : Sheehan syndrome.
vi. pituitary tumor.

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b. Familial DI ( Walfram syndrome , DIDMOAD )

hereditary condition in which there is a defect in osmo-receptrs
i. Diabetes Insipidus.

ii. Diabetes Mellitus

iii. O ptic atrophy

iv. Deafness.

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

i. Hereditary .
ii. Acquired : MCQ
1. renal tubular acidosis.
2. kidney amyloidosis.
3. hypercalcemia.
4. hypokalemia.
5. drugs : lithium , cholchicine.

3. C / P :
a. C / p of the cause : e.g. history of hypophysectomy.
b. C / p of the hormone :
i. Polyuria ( up to 20 L/day ) & polydepsia.
ii. Severe dehydration → weakness , weight loss & fever.
iii. Hypovitamonosis : of water soluble vitamins.
iv. Complications : shock & death.

4. Differential diagnosis : DD of polyuria. [ discussed later ]

5. Investigation :
a. Investigations for the cause : Pituitary Imaging : X-ray , CT & MRI
b. Assay of the hormone level : 

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c. Investigations for the function of ADH :

i. Urine analysis :
1. Polyuria with low Specific gravity.
2. No pathological constitutes.
3. After fluid deprivation : polyuria persists.
ii. Plasma osmolality : ↑due to loss of free water.

d. Stimulation tests :
i. Test the hypothalamus : nicotine test ( 1-3 mg nicotine )
1. normal : oliguria due to stimulation of ADH.
2. central DI : -ve ( no stimulation )
ii. Test osmo-receptrs : IV hypertonic saline ( NaCl 2.5 % ) .
1. normal : oliguria.
2. osmo-receptrs defects : -ve ( no olguria )
iii. Test kidney ( vasopressin test ) :
to differentiate between central DI & nephrogenic DI
1. in Central DI : oliguria ( Concentrated urine )

2. in Nephrogenic DI : No change.

6. Treatment :
a. Replacement therapy : synthetic ADH (Desmopressine) 20 μg/d intra nasal

b. Diet : ↓Na , ↑vitamins.

c. Drugs : MCQ
 Cholropropamide.
 Carbemazepine.
 Thiazide may be used in nephrogenic DI.

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Differential diagnosis of polyuria

1. Physiological :
 Winter months.
 Excess coffee or tea.
 Diuretics.
2. Psychological : Hysterical polydepsia.

DI Hysterical polydepsia
C/P : Polyuria then polydepsia Polydepsia then polyuria
Fluid deprivation test : polyuria persists No polyuria
Osmolality ↑
↑ ↓↓

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 .
ii. Chronic renal failure
iii. Diuretic phase of acute renal failure.

c. After any attack :

i. Migraine
ii. Epilepsy
iii. Bronchial asthma
iv. PSVT.
v. Also after the internal medicine exam. ☺

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Syndrome of inappropriate ADH secretion

( SIADH )
It means an excessive release of ADH

1. Physiology : Refer to diabetes insipidus.

2. Etiology :
a. Tumors release ADH : oat cell carcinoma & lymphoma.
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 → dilutional hyponatremia
(weight gain , weakness , confusion, convulsions & coma )
 No edema because of natriuresis.

4. Investigation :
1. ↓Na (< 130 mEq /L )
2. ↓serum osmolality (< 270 mosmol/kg) .
3. ↑urine Na concentration ( > 20 mEq/L ).

5. Treatment :
a. Fluid restriction → 0.8 -1 L / day.
b. demeclocycline:
i. 600 -1200 mg /day → inhibit the action of ADH.
ii. Given to patient unresponsive to fluid restriction.
c. For sever hyponatremia : hypertonic saline ( 5% ) IV slowly.

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Thyroid gland
Anatomy :
 The thyroid gland is located in the front of the neck below the larynx on

either side of the trachea, and is formed of 2 lobes connected to each other

by an isthmus. Its normal weight is about 20 – 40 gm.

 It’s attached to the thyroid cartilage & to the upper end of trachea so , it

moves with swallowing.

Physiology : ( hormone synthesis )

1. Iodine trapping : Iodine uptake by the thyroid gland .

2. Binding : Tyrosine bind to iodine to form mono & di-iodotyrosine.

3. Coupling :

 2 molecules of di-iodotyrosine → T4 ( Thyroxin ) : 80 mcg per day

 Mono + di-iodotyrosine → T3 ( Tri iodothyronine ) : 4 mcg per day

 T3 is 3-5 more potent than T4 and acts more rapidly.

 T4 is converted to T3 in the peripheral tissue.

4. Release :

 T3 & T4 release under the control of TSH.

 Thyroid hormones circulate in 2 forms :

 Protein bound, mainly thyroxin binding globulin ( TBG ): > 99 %

 Free part ( active part ) : less than 1 %

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Thyroid diseases

Causes of thyrotoxicosis :
1. Toxic diffuse goiter : The commonest cause

( Grave's disease in USA, Basedow's disease in Europe).

2. Toxic nodular goiter.

3. Toxic solitary adenoma.
4. Excess production of TSH by pituitary tumor ( very rare ).
5. Extrathyroid source of hormone :
a. Thyrotoxicosis factiscia : exogenous intake of thyroxin.
b. Ectopic thyroid tissue e.g. strauma ovarii .
6. Iatrogenic : amiodarone.

--------------------------------------------------------------------------------------------------------------------------

Classification of hypothyroidism :
 According to the age of onset :
1. Cretinism : during infancy.
2. Juvenile myxoedema : before puberty.
3. Myxoedema : after puberty.
 According to the site of the cause :
1. 1ry hypothyroidism : cause in the thyroid gland.
2. 2ry hypothyroidism : cause in the pituitary gland.
3. 3ry hypothyroidism : cause in the hypothalamus.

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1ry thyrotoxicosis
(Grave’s disease)
Autoimmune disorder consists of :

Hyperthyrodism plus one or more of the following triad

Painless diffuse goiter ( 90 % )

Ophthalmopathy ( 60 % )

Dermopathy. ( 2 % )

1. Physiology :
a. Hormone : T3 & T 4 .
b. Gland : Thyroid gland.
c. Function of the hormone : Hormone of metabolism
i. stimulate physical , mental & sexual growth.
ii. ↑energy production & O2 consumption.
iii. ↑glucose absorption & uptake by cells.
iv. ↓cholesterol level.
v. ↑the respiratory & heart rate.
vi. stimulation of erythropoiesis ( ↑RBCs ).
vii. ↑the tissue responsiveness to catecholamine.
viii. Hepatic conversion of carotene to vitamin A .
d. Regulation of this hormone :
i. TSH. ii. TRH.

2. Etiology :
Autoimmune disorder in which there is Formation of auto antibodies( Thyroid
stimulating immunoglobulin - TSI ) that bind to and activate the thyroid TSH

receptors .

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3. Clinical picture : ( ♀ 30 – 40 years ).

a. C / p of the cause :
Association of autoimmune diseases as myasthenia & DM.
b. C / p of the hormone :
General :

o polyphagia with loss of weight.

o intolerance to hot whether.
o progressive muscle weakness.
GIT :

o ↑
↑appetite ( with loss of weight ).
o diarrhea.
o Just palpable spleen.

Genital :

o ♀: amenorrhea.
o ♂: Impotence & gynaecomastia.
Cutaneous :

o skin is thin ,warm & flushed with generalized sweating.

o hair : fine & thin.
o nails : clubbing of fingers. ( Thyroid acropachy )
o preitibial myxoedema : ( dermopathy )
irregular, itchy, tender& hairy swelling over the chin of the

tibia & usually symmetrical, due to deposition of mucin-like

substance in the S.C. tissue.

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CVS : (more common in older patients)

1- pulse :
o rate : ↑ , the sleeping pulse rate is usually > 100 b/m .
o rhythm : may be irregular due to AF or extrasystole.
o character : water hummer pulse due to big pulse volume.
o equality : unequal on both sides → retro-sternal goiter.
Thyroid function tests are mandatory in any patient with atrial fibrillation

2- heart : Hyperdynamic circulation  volume overload  cardiac

enlargement then heart failure.

3- Blood Pressure :
o systolic : ↑ ( isolated systolic hypertension )
o diastolic : ↓( thyroxin → VD )
So, there is big pulse volume

CNS : ( more common in younger patients).

- psychic : 4 mnemonic : naim

o nervousness.
o anxiety & agitation.
o insomnia.
o mental disturbance.
- organic : 4
o fine tremors in tongue & hands.
o polyneuropathy.
o myopathy.
o myasthenia.
It's important to note that elderly patients with hyperthyroidism may be lethargic rather
than agitated ( apathetic thyrotoxicosis ).

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Eye :

1. Exophthalmos :
o bilateral , but may start unilateral.
o May occur even before the appearance of thyrotoxicosis.
o AE: oversecretion of autoantibody called exophthalmos producing
substance (EPS)  lymphocytic infiltration of retrobulbar tissue
& extrinsic muscles.
o Blindness may occur secondary to corneal ulcers or optic nerve compression .
2. certain eye signs : ( DR must be very simple )
a. Dalrymple’s sign ( Lid retraction ) : rim of sclera is seen between the
cornea & upper lid.
b. Rosenbach’s sign : fine tremors of eyelids on slight closure of eye.
c. Moebius’ sign : lack of convergence due to weak medial recti muscles.
d. Von-Grave’s sign : lid lag on looking down.
e. Stellwag’s sign : infrequent blinking.

N.B: ocular manifestations can be divided into 2 types:

 Infiltrative ophthalmopathy (mechanical , due to accumulation of
autoantibodies ) e.g. exophthalmos & mobius sign → so both are specific
to Grave’s disease.
 Non- Infiltrative ophthalmopathy ( due to ↑thyroxin ) e.g. lid lag, lid
retraction , stellwag & Rosenbach’s sign → occur with any thyrotoxicosis
(not specific to Grave’s disease).

Gland :

a. Inspection : mild to moderate enlargement of the gland.

b. Palpation : - consistency : fleshy or firm. – surface : smooth.
c. Percussion : dullness over manubirum-sterni in retro-sternal extension.
d. Auscultation : systolic bruit may be heard due to high vascularity.

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Thyrotoxic crisis ( thyroid storm):

o an extreme form of thyrotoxicosis with a mortality of 10 %.

o it's precipitated by stress ( acute illness , surgery ) or infection.
o it's considered one of the medical emergencies.
o C/P : sever manifestations of thyrotoxicosis that include :
a. general : fever > 41C̊.
b. C.V.S. : sever tachycardia, acute HF & AF.
c. C.N.S. : marked irritability, mental disorientation & coma.
Differential diagnosis :
a. Neurosis : → cold hand & normal sleeping pulse.
b. ↑
appetite with loss of weight: DM , parasitic infection.
c. Hyperdynamic circulation.
d. Muscle diseases : myopathies, myasthenia gravis.
e. Difference between 1ry & 2ry thyrotoxicosis :
1ry thyrotoxicosis 2ry thyrotoxicosis
- Other name : Grave’s disease. toxic multi nodular goiter.

- Cause : Auto-immune. On top of nodular goiter.

- Age of onset : 30 – 50 year. 50 year.

- Thyroid gland : Diffusely enlarged. Nodular.

- CVS : Mild. Sever.

- CNS : Sever. Mild.

- Exophthalmos : Present. Absent.

- Monosymptomatic cases: Un-common. Common.

- TTT : Usually medical. Usually surgical.

monosymptomatic cases : when one of the manifestations of thyrotoxicosis predominates

e.g. thyrocardia : cardiac symptoms only ( AF ) .

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Investigation : ( Thyroid function tests )

I. Investigations for the cause : 

1. TSH level : [ n = 0.5 – 5 µu/L ]

a) It's the most sensitive test of thyroid function.

b) ↓
↓in most cases of thyrotoxicosis by –ve feed back mechanism.
c) ↑
↑only in TSH producing pituitary tumor : very rare.
2. Imaging for the gland :
a) thyroid scan :
o hot nodules : benign.
o cold → do U/S.
b) U/S : indicated in cold solitary thyroid nodule :
o cystic → benign.
o solid : malignant → do needle aspiration biopsy.
3. Thyroid receptor antibodies : thyroid stimulating immunoglobulin
(TSI) can be detected in Grave's disease.
T
Thhe teerm LAT
TSS ( llonng aaccting thhyroid sttimuulattor )) reffeerring too thhis anttiboddy is noo longerr ussedd.

II. Assay of the hormone level : 6

a) Total T3 ↑
↑: [ n : 70 – 170 ngm% ] → not accurate.

b) Total T4 ↑↑: [ n : 5 – 12 µgm% ] → not accurate.

T3 & T4 are over 95% protein bound to TBG (thyroxin binding globulin) so,….
o Increased TBG as in pregnancy → ↑↑total T3 & T4 but free T3 & T4 are normal.

o Decreased TBG as in liver cirrhosis & nephrotic syndrome → ↓total T3 , T4 but free T3 , T4 are normal.

c) free T 3 ( n : 0.4 ng % )
d) free T 4 ( n : 1.6 ng % ) difficult to measure , we use free T4 index.
e) T3 resin uptake : ↑
Radioactive T3 is added to the patient's serum it's fixed to the unoccupied binding sites
of TBG → the remaining radioactive is then absorbed into a resin ( n = 25% - 35% ).

f) free thyroxin index : ↑( > 11.5 ) = T3 resin uptake хtotal T4.

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III. Investigations for the function of the hormone :

o Blood :
 ↓cholesterol , ↑Ca , ↑Calcitonin in medullary carcinoma.
 Lag sugar curve.
o Urine : Polyuria , ↑glucose.
IV. Suppression test : material : T3 .
 Normally → ↓RAIU ( radio active iodine uptake ).
 in thyrotoxicosis → no effect.
Treatment :

I. Medical :
Indication :
o 1ry thyrotoxicosis ( Grave's disease ).
o 2ry cases : pre-medication before operation.
o Treatment of complications e.g. HF.
o pregnancy.
Contraindications :
o huge goiter. o retro-sternal goiter.
o suspicion of malignancy.

Lines of medical treatment :

 β-blockers e.g. propranolol to provide rapid symptomatic control.
They also decrease peripheral conversion of T4 to T3.
 Anti-thyroid drugs :
- methyl thiouracil : 200mg t.d.s. then reduce after 4-6 w to 100 mg t.d.s.
- propyl thiouracil : 100mg t.d.s. then reduce after 4-6 w to 50 mg t.d.s.
- Carbimazol (Neomercazol): 20 mg t.d.s. then reduce after 4-6 w to 10 mg t.d.s

Duration : 1 - 2 years. ( until thyroid hormone stores become depleted)

Mechanism : These drugs inhibit the formation of thyroid hormones.
Propylthiouracil : also inhibits conversion of T4 to T3.

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 Side effects :
 Allergy .  Agranulocytosis .
 Hypothyroidism.  Goiter : due to ↑TSH.
 Relapse : on sudden stoppage.
 Others : GIT upset, cholestatic jaundice .

II. Radio-active iodine :

Indication :
 failure of medical treatment.  patient is unfit for surgery.
 recurrence after thyroidectomy.  toxic adenoma.
Contraindications :
 during pregnancy, lactation & childhood.
 huge goiter & retro-sternal goiter.
Side effects :
 hypothyroidism.  bone marrow depression.
 fetal anomalies, if taken in pregnancy.
 ↑incidence of malignancy, so → not given in childhood.
Precautions :
It's important to stop anti-thyroid drugs 4 days before & 4 days after radioactive iodine
therapy as it prevents radioactive iodine uptake by the gland.

III. Surgical : ( sub-total thyroidectomy )

Indication :
 2ry thyrotoxicosis.
 failure of medical treatment in 1ry case of young age.
 huge or retro-sternal goiter.
 suspicion of malignancy.
Pre-operative preparations :
Lugol's iodine ( 5% iodine in 10% K iodide ) : ↓size & vascularity of the gland.
Complications :
Laryngeal nerve palsy , transient hypocalcaemia , hypothyroidism.

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IV. Treatment of complications :

 Ocular complications :
 protect eye by ointment, sun glasses.
 prednisone → ↓
↓lymphocytic infiltration.
 radiotherapy of the orbit.  orbital decompression.
 Heart failure :
 bed rest, salt restriction, digitalis & diuretics.
 persistence of AF → Digitalis or DC shock
 Preitibial myxoedema : local Betamethasone cream ( local steroid )

 Thyrotoxic crisis : 6
1. propranolol in full dose is started immediately for tachyarrhythmias
( 1 mg every 5 min IV until the desired effect is achieved then 20 - 120 mg/6h orally)

2. propylthiouracil : 100 mg/8h. ( orally, rectally or nasogastric tube ).

3. Na iodide: 1 gm over 24h IV → ↓
↓thyroxin release from thyroid gland.
4. hydrocortisone : 100 mg/8h IV , to correct the hypotension.

 Thyrotoxic crisis → ↑↑cortisol metabolism → relative adrenal

insufficiency → refractory hypotension
 Hydrocortisone correct this hypotension. Also, steroids prevent
peripheral conversion of T4 → T3

5. Treatment of precipitating factor : antibiotics for infections.

6. symptomatic treatment :
 hyperthermia : ice bags.  dehydration : IV fluid.

Thyrotoxicosis in pregnancy :
 Medical treatment : propyle thio-uracil.
 Radioactive iodine : absolutely contraindicated as it is teratogenic & carcinogenic
 Surgery indicated in : appearance of side effects.
 Follow up: should be done to diagnose neonatal thyrotoxicosis because TSI can cross
the placenta & stimulate fetal thyroid gland.

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Myxedema
(Hypothyroidism in adult)
1. Physiology :
Refer to hyperthyroidism.

2. Etiology & types :

a. 1ry mxyedema : (5 I +H)

i. Idiopathic atrophy of the gland.
ii. Iatrogenic :
1. post thyroidectomy.
2. radioactive iodine.
3. anti-thyroid drugs.
4. lithium.
5. amiodarone.
iii. Infections : viral infection ( De Quervain's thyroiditis )
iv. Iodine deficiency.
v. Infiltration : tumor.
vi. Hashimoto’s thyroditis :
1. auto-immune disease. ( thyroid antibodies : +ve ).
2. gland is replaced by lymphocytic infiltration.
3. gland is firm, symmetrically enlarged & not tender.
4. transient thyrotoxicosis may occur followed by hypothyroidism.

b. 2ry Myxedema : 2ry to pituitary failure e.g. tumor ( ↓TSH ).

c. 3ry myxedema: deficiency of TRH secreted from hypothalamus.

d. Peripheral resistance to thyroid hormone : very rare .

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3. Clinical picture : ♀> ♂ 30 – 50 years. ☺

a. C / p of i cause : Surgery , Anti-thyroid drugs.
b. C / p of i hormone :
In hypothyroidism every thing slows down except the period !!

i. General :
1. intolerance to cold.
2. lethargy & fatigue.
3. weight gain.
4. serous effusions (pleural , pericardial & ascites).
5. face :
a. expressionless .
b. puffy eye lids.
c. loss of outer 1/3 of eye brows.
d. large tongue.

ii. GIT :
1. slow motility → constipation
2. slow absorption → malabsorption syndrome.

iii. Genital :
1. ♀ → menorrhagia.

2. ♂ → impotence & gynaecomastia.

iv. Cutaneous :
1. dry, cold, pale & non sweaty skin.
2. non pitting edema : due to intradermal accumulation
of proteins, not interstitial edema fluid.
3. yellowish discoloration due to carotinemia.
4. hair loss.

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v. CVS :
1. hypercholesterolemia → ischemic heart disease.
2. diastolic HTN due to  thyroxin ( thyroxin  VD )
3. sinus bradycardia.
4. Pericardial effusion.
vi. CNS :
1. slow intellectual & motor activity.
2. deposition of mucopolysaccharide in :
a. tongue : slow speech.
b. vocal cords : hoarseness of voice.
c. flexor retinaculum : carpal tunnel syndrome.
d. peripheral nerves : peripheral neuropathy.
e. joints & muscles : slow relaxed reflexes.

vii. Heamatological :
1. normocytic normochromic anemia : BM inhibition.
2. microcytic hypo-chromic anemia : menorrhagia.
3. macrocytic :associated pernicious anemia ( 12% )

viii. Hypothyroid coma ( Myxedema coma ) :

1. untreated long standing hypothyroidism.
2. precipitated by cold exposure or infections.
3. manifested by : 5 H
a. Hypothyroidism with loss of consciousness.

b. Hypothermia. c. Hypoglycemia.

d. Hypoventilation ( respiratory depression ).

e. Heart failure.
Although this condition is called Myxedema coma , frank coma is uncommon !!

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ix. Gland :
1. ↑size as → Hashimoto’
s thyroditis.
2. atrophy → 1ry idiopathic forms.
3. scars of previous operations.

4. Differential diagnosis :
a. Nephrotic syndrome.
b. Depression.
c. Other causes of hypothermia : cold weather , shock ,
Addison's disease , hypoglycemia.
d. Difference between thyroid & pituitary myxedema :

Pituitary myxedema thyroid myxedema

1. Clinical picture :
a- Of thyroid :
Dry skin puffy lid : - Not marked - Marked
Body weight : - ↓↓ - ↑↑
b- Of hypogonadism - Marked - Absent
2. Investigation :
a- TSH : - Low - High
b- FSH/LH : - Low - Normal
c- ACTH, Cortisol : - Low - Normal

5. Investigation :
a. Investigations for the cause :
i. TSH : [ test of choice ]
↑
↑in thyroid myxedema , ↓
↓in pituitary myxedema.
ii. Thyroid antibodies.

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b. Assay of the hormones level :

1. serum hormones :
a. TSH : ↑
↑in 1ry type. [test of choice]
b. T4 & T3 : ↓
↓
It is important to note that normal T4 not exclude hypothyroidism
2. radio-active iodine uptake :↓
c. Investigations of the hypofunction of thyroid hormone :
i. Blood :
1. CBC : anemia
2. blood glucose → flat sugar curve.
3. ↑cholesterol.
4. ↑CPK ( creatinin phospho-kinase).
5. ↑LDH ( lactate dehydrogenase).
ii. ECG findings : sinus bradycardia , low voltage.
iii. BMR : low.

DD of low voltage ECG :

 Hypothyroidism.
 Pericardial effusion.
 Obesity.

6. Treatment :
a. Replacement therapy : life long
 L-thyroxin : start small dose 0.05 mg/d & gradually up to
maintenance dose ( 0.2 – 0.3 mg/day ).
 The dose is increased very gradually to avoid
precipitation of angina & HF .

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b. Treatment of myxedema coma : 6

a. Hypothyroidism : T3 : 5 μg/8h IV.
b. Hypothermia : gradual rewarming.

c. Hypoglycemia : glucose IV.

d. Hypoventilation (respiratory depression) : O2 & ventilation.
e. Heart failure : cardiac support.
f. Treatment of precipitating factors e.g. antibiotics for infections.

Goitre

Definition : Enlargement of the thyroid gland.

classification:

i. Simple goitre : ( non toxic , non inflammatory , non neoplastic )

Persistent low level of thyroid hormones → ↑TSH → thyroid enlargement.
○Physiological : Puberty , Pregnancy. ( due to increased the demond
of iodine, so there is relative iodine deficiency )
○Iodine deficiency.
○Drugs : Anti-thyroid drugs , lithium.
ii. Toxic goitre : ( goitre with hyperthyroidism )
○Diffuse : Grave's disease ( 1ry thyrotoxicosis )
○Toxic nodular goitre ( 2ry thyrotoxicosis , Plummer's disease )
iii. Inflammatory goitre : e.g. Hashimoto's thyroiditis .
iv. Neoplastic goitre .

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Cretinism
Hypothyroidism during infancy
1. Physiology : Refer to hyperthyroidism.

2. Etiology :
a. Congenital.
b. Endemic cretinism → iodide deficiency.
c. Excess anti-thyroid drugs during pregnancy.

3. Clinical picture :
a. Persistent physiological jaundice.
b. Hoarse cry & feeding problems.
c. Disproportionate dwarfism.
d. Big lips & protruding tongue & Delayed dentation.
e. Delayed walking.
f. Muscle weakness( pot belly with umbilical hernia).
g. Dry & cold skin.
h. Mental detoriation if not treated within 6 months.

4. Investigation :
a. T4 & T3 : ↓↓
b. TSH :↑
↑
c. X-ray of carpal bone : delayed appearance of ossification centers

5. Treatment : Replacement therapy

 L-thyroxin 0.025 mg/day & ↑↑dose up to 0.2 mg/day
 It should be started before the 1 st 6 months to avoid mental
retardation.

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Parathyroid gland

Ca metabolism
- Normal Ca level : 8.5 – 10.5 mg%.

A. Ionized ( active ) : 50%

B. Non-ionized ( reserve ) : 50%
- 40% bound to albumin. - 10% any other bond ( Ca carbonate, phosphate ….)

Liver cirrhosis & nephrotic syndrome → ↓albumin → hypocalcaemia ,

but no tetany because ionized Ca is still normal.

- Regulation of Ca :
 Ca level is closely affected & related to P [ n. 3 - 4.5 mg% ]
 Notice that Ca X P = constant [ 40 ].
 Serum Ca & P levels are controlled by certain hormones :
a. Parathormone.
b. Calcitonin.
c. Active vitamin D.
 Ca regulation involves 3 sites : bone, intestine & kidney.

Parathormone* vitamin D Calcitonin

Absorption ↑Ca ↓P ↑Ca ↑P ↓Ca

( intestine )
Reabsorption ↑Ca ↓P ↑Ca ↑P ↓Ca ↓P
( kidney )
Resorption ↑Ca ↓P ↑Ca ↑P ↓Ca ↓P
( bone )
Blood ↑Ca ↓P ↑Ca ↑P ↓Ca ↓P
( net result )

*PTH acts directly on bone & kidney & indirectly on intestine (through activation of vit.D ).

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Hyperparathyroidism
1. Physiology :
a. Hormone : Parathormone ( PTH )
b. Gland : Parathyroid gland.
c. Function of the hormone : ↑Ca , ↓P
i. GIT : ↑↑ absorption of Ca.
ii. Kidney : ↑↑ reabsorption of Ca.
iii. Bone : ↑↑ resorption of Ca.
iv. ↑Renal Phosphate excretion.

d. Regulation of this hormone :

hypo Ca or hyper P → ↑PTH .

2. Etiology :
a. 1ry :
i. Adenoma of the parathyroid gland. ( most common )

ii. Hyperplasia of the parathyroid gland.

iii. As a part of Multiple Endocrine Neoplasia ( MEN -1 ) : 3 p

1. hyper-parathyrodisim.

2. pituitary tumor.

3. pancreatic tumor.

b. 2ry :
Due to prolonged ↑P & ↓Ca as in Chronic renal failure
which leads to hyperplasia of the parathyroid gland.

c. 3ry : usually in end stage CRF

- Longstanding 2ry hyperparathyroidism → irreversible

parathyroid hyperplasia . ( start 2ry → end 1ry )

- Parathyroidectomy is the only appropriate treatment.

d. Paramalignant syndrome ( oat cell carcinoma ).
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3. C / P : 50% → asymptomatic.

a. C / p of the cause : parathyroid adenoma , CRF.

b. C / p of the hormone : disease of bone & renal stone ♫♫

i. Bone : (2)

1. pain.
2. pathological fracture.

ii. Renal : ( 3 )

1. repeated stones.
2. polyuria ( Ca diabetes ) & polydepsia.
3. nephrocalcinosis with renal failure may occur.

iii. Others : (4) X2

1. CNS :
a. drowsiness.
b. depression.

2. GIT :
a. peptic ulcer.
b. pancreatitis ( abdominal pain ).

3. CVS :
a. ECG : short Q-T interval & arrhythmia.
b. Hypertension.

4. Skin :
a. dry.
b. itching.

Ca > 11mg%. → Clinical manifestations of Ca

Ca > 13mg%. → Renal impairment
Ca > 14 mg% → Coma & cardiac arrest ( endocrinal emergency )

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4. D. D. of hypercalcemia : (4 Х3 )

a. Endocrine :
i. Hyperparathyroidism ( 1ry & 3ry ). The most common cause

ii. Hyperthyroidism.

iii. Addison’s disease (Cortisone → -- vit.D).

b. Malignancy :
i. Bronchogenic carcinoma .

ii. Multiple myeloma.

iii. Lymphoma → activation of vitamin D .

c. Bone :
i. T.B.

ii. Sarcoidosis.

iii. Immobilization.
d. Others :
i. Hypervitaminosis ( vitamin D ).

ii. Drug induced : thiazide , lithium.

iii. Familial hypocalciuric hypercalcemia.

5. Investigation :
a. Investigations for the cause : Parathyroid imaging: CT, MRI , radioisotope scan
b. Assay of the hormone level : parathormone : ↑↑[ n: 0.5 – 1 ngm/ml ]

c. Investigations of the function of the hormone :

i. Blood :

1ry 2ry 3ry

1. Ca ↑ ↓ ↑
2. P ↓ ↑ ↑
3. Alkaline phosphatase ↑ ↑↑ ↑↑↑

NB : Persistent hypercalcemia , hypo P & an elevated PTH confirm

the diagnosis of 1ry hyperparathyroidism.
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ii. Urine :

1. ↑Ca [ n : 150 mg / day ]

2. ↑P [ n : 1 gm / day ]

3. ↑hydroxyproline & c-AMP due to ↑bone resorption.

iii. X- ray :

1. bone : 
a. loss of lamina dura of the teeth. ( the earliest sign)
b. sub-periosteal erosions in the middle phalanges.
c. ground glass appearance of the bones.
d. skull → mottling of the skull. ( salt & pepper skull ).
e. spine → cod fish spine ( indentation of vertebrae by discs)
2. renal : urinary stones , nephrocalcinosis.

iv. Bone biopsy : osteomalacia with excess osteoclasts.

d. Suppression test : ( steroid test )

i. +ve ( ↓Ca level ) → normal.
ii. –ve ( no suppression ) → Hyperparathyroidism.

6. Treatment :
a. Surgery :
i. Removal of the parathyroid glands.

ii. Ca & vitamin D supply to avoid tetany.

b. Medical treatment of hypercalcemia :

i. ↓intake & ↑↑fluid intake.

ii. ↓absorption : by oral phosphate.

iii. ↑loss of Ca : saline then fursemide or dialysis in sever cases.

iv. Calcitonin .
v. β-blocker : ↓the adverse effect of hypercalcemia on the heart

vi. Cortisone is effective in some cases (vit.D excess & sarcoidosis)

vii. Alendronate (Osteomax) : ↓

↓osteoclastic activity.

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Hypercalcemic crisis ( serum Ca level > 14 mg % )

a. Manifestations ( non secific ) :

i. GIT : Nausea , vomiting ,constipation & abdominal pain.
ii. Renal : Polyuria & dehydration.
iii. CNS : Confusion & coma.
iv. CVS : Arrythmia , shortened QT interval.
b. Treatment :
i. IV normal sline : 4-6 L/day may be nessary. (the first goal)
ii. Lasix ( 40 – 80 mg IV every 2 hours ) , but be sure that the

patient is adequatly hydrated.

iii. IV pamidronate ( Aredia ) : drug of choice.

iv. Calcitonin : it inhibits bone resorption.

v. Cortisone.

vi. Dialysis is effective in removing Ca in patients with renal

failure.

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Hypoparathyroidism
(Tetany)
Definition of tetany :
state of ↑
↑neuro-muscular irritability due to: ↓ionized Ca , ↓Mg or alkalosis.

Etiology of tetany : ( ↓ionized Ca , ↓Mg or alkalosis )

a. Hypocalcaemia :
i. Hypoparathyroidism :

1. surgery removal.
2. irradiation.
3. Di- george syndrome : absent parathyroid & thymus glands.
ii. ↓Ca intake : starvation.
iii. ↓Ca absorption :

1. malabsorption syndrome.
2. ↓active vitamin D.
iv. Precipitation of Ca in tissue e.g. acute pancreatitis.
v. ↑Ca excretion : CRF ( most common cause of hypocalcemia).

N.B. tetany rarely occurs in RF because of acidosis which convert non

ionized Ca into ionized Ca.

b. Hypomagnesaemia : Excess diuretic , Malabsorption syndrome.

c. Alkalosis : ( Ionized Ca → non ionized Ca ).

i. Respiratory alkalosis : any case of hyperventilation :

ii. Metabolic alkalosis :

1. loss of HCl : vomiting , gastritis , gasterectomy.

2. milk alkali syndrome.
3. hypokalemia e.g. Conn’s syndrome.

hypokalemia ( K loss )  Al-K-Lossis ☺

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C / P of Tetany :
iii. Latent tetany : ( serum Ca = 7 – 9 mg% )
1. manifestations of tetany are not present.
2. manifestations appear by provocative tests :
a. Chvostek’s test :
tapping over the facial nerve → contraction of the facial muscles.
b. Trousseau’s test :
Inflation of a BP cuff above SBP for 3 minutes → carpal spasm.
c. Erb’s test : ( normally : 8 mili-ampers at least are needed for stimulations )
electric current < 4mili-ampers → muscle contraction.

iv. Manifest tetany : ( serum Ca < 7 mg% )

1. irritability & parasthesia around mouth & fingers.
2. muscle twitches & may be convulsion in severe cases.
3. spasm :
a. eye lids : blepharospasm.
b. mouth : trismus of jaw.
c. larynx : laryngospasm.
d. carpo-pedal spasm.
e. diaphragm : Hiccough.
f. GIT : abdominal colic.
4. Cardiovascular : QT prolongation , refractory HF , hypotension.
5. on ectodermal structures : ( only in hypocalcemia )
brittle nail , hypoplastic teeth , cataract.

Investigation : ( for the cause )

 In hypoparathyrodism : ↓PTH , ↓serum Ca , ↑P.
 In hypomagnesaemia : Refractory hypokalemia. MCQ
 In alkaosis : ↑PH , ↓ionized Ca.

Treatment :
a. Acute attack : IV Ca gluconate 10 ml 10% very slowly.
b. Treatment of the cause :
 Hypocalemia : oral Ca , vitamin D
 Hypomagnesemia : oral Mg.
 Alkalosis : Treatment of the cause , acidifying drugs.
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Suprarenal gland
( Adrenal gland )

- There are 2 adrenal glands at the superior pole of each kidney.

- They are composed of outer cortex & inner medulla :

i. Adrenal cortex ( the outer part ) which is formed of 3 separate layers :

○ Zona Glomerulosa : secretes aldosterone ( mineralocorticoids ).

○ Zona Fasciculata : secretes cortisol ( glucocorticoids )

○ Zona Reticularis : secretes androgen.

ii. Adrenal medulla ( the inner part ) : secrets catecholamines.

Disorders of suprarenal gland :

 Hyperfunction of adrenal cortex :

○ Conn's syndrome : ↑aldosterone.

○ Cushing syndrome : ↑Cortisol.

○ Adrenogenital hyperplasia : ↑androgen.

 Hyperfunction of adrenal medulla : Pheochromocytoma.

 Adrenal cortical hypofunction : Addison's disease ( 1ry adrenal failure )

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Conn’s syndrome
( 1ry hyperaldosteronism )

1. Physiology :
a. Hormone : Aldosterone.

b. Gland : Suprarenal gland ( Zona glomerulosa ).

c. Function :
i. ↑Na , ↑H 2O.
ii. ↓K , ↓H+.
d. Regulation : Aldosterone secretion is stimulated by :
i. Hypovolemia → ↑Renin → ↑aldosterone
ii. ↑K ( hyperkalemia )& ↓Na ( hyponatremia )
iii. A.C.T.H. → during stress only.

2. Etiology :
a. Adenoma of zona glomerulosa.
b. Hyperplasia of zona glomerulosa.
c. Paraneoplastic syndrome.
3. Clinical picture :
a. C/p of the cause : Adenoma , Paraneoplastic syndrome ….

b. C/p of the hormone : ( ↑Na , ↑H2 O , ↓H + , ↓K )

i. hypernatremia & hypervolemia :

1. Mild HTN. ( never sever )

2. No edema inspite of hypervolemia, it is due to :
a. renal escape phenomenon.
b. hypokalemic nephropathy → polyuria.
ii. ↓↓H. ( alkalosis ) : leading to tetany.

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iii. ↓↓K. ( hypokalemia ) : muscles

1. skeletal muscles : weakness, flaccidity up to paralysis.

2. Smooth muscles (GIT) : atony, constipation.
3. Cardiac muscle : arrhythmia , ECG changes ( prominent U wave)
4. others : nephropathy , glucose intolerance.

4. Differential diagnosis : form 2ry hyperaldosteronism (stimulus is extra-adrenal )

1ry hyperaldosteronism 2ry hyperaldosteronism

Source - Adrenal Gland. - Renal artery stenosis.
- Heart failure.
- Nephrotic syndrome.
- Liver cirrhosis.
Aldosterone +++ +
Renin ↓↓ ↑
↑
HTN mild. No HTN except in renal
artery stenosis → sever.

↑Blood volume

Initiating event
↑Na retention ↓Renin

↑Aldosterone
production ↓Blood volume

Initiating event
↑Na retention ↑Renin

↑Aldosterone
production

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5. Investigation :
a. Investigations for the cause : suprarenal gland imaging : US , CT , MRI
b. Assay of the hormone level :
i. In blood :
1. ↑aldosterone in serum ( n = 3 -15 ngm%).
2. ↓plasma renin activity (due to -ve feed back )
ii. In urine :
↑metabolite of the hormone (tetrahydroaldosterone)
c. Investigation for the function of aldosterone :
i. Blood :
1. ↓K. ( hypokalemia) [ n : 3.5 - 5 mEq/L ].

2. ↑Na. ( hypernatremia ) [ n : 140 mEq/L ].

3. alkalosis : ↑serum HCO3 [ n: 22 - 26 mEq/L ].
ii. Urine :
1. ↓Na.
2. ↑K.
3. ↑H +.

6. Treatment :
a. Surgical removal of the tumor.
b. Irradiation.
c. Antagonism :
i. Aldosterone antagonist : spironolactone ( aldactone 400 mg/d )
ii. ACE inhibitors : captopril in 2ry hyperaldosteronism. MCQ

d. Symptomatic treatment : excess K & low Na.

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Cushing’s syndrome
1. Physiology :
a. Hormone : ↑Cortisol .
b. Gland : Suprarenal gland ( Zona fasiculata )
c. Function of the hormone : 10
i. CHO : hyperglycemia.
ii. Protein : catabolic.
iii. Fat :
1. lipolytic.
2. Redistribution of fat in abnormal sites ( face, back of neck, trunk)

iv. Water & electrolyte : ( aldosterone like )

1. ↑H2O & Na.
2. ↓K & H+.
v. Stomach : ↑HCl
vi. Bone : anti-vitamin D action.
vii. Blood : (2↑
↑ & 3↓
↓) MCQ
1. ↑RBCs.
2. ↑neutrophils.
3. ↓lymphocytes.
4. ↓esinophils & basophilis.
viii. Psychosis.
ix. Androgenic action.
x. Anti-inflammatory & anti-allergic.

d. Regulation of the hormone : stimulated by ACTH.

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2. Etiology :
a. 1ry ( adrenal Cushing or Cushing syndrome ) : adenoma or
adenocarcinoma of zona fasiculata → secreting cortisol [ 20 % ].
b. 2ry ( pituitary Cushing or Cushing disease ) : adenoma or
hyperplasia of pituitary gland → secreting ACTH [ 70 % ].
c. paramalignant syndrome e.g. oat cell carcinoma.
d. Exogenous intake ( Cushinoid picture ).
3. Clinical picture :
a. C / p of the cause : Pituitary tumor , Paraneoplastic syndrome.
b. C / p of the hormone :
i. CHO : hyperglycemia & may be secondary DM in 15 %.
ii. Protein : catabolic
1. muscle wasting , weakness & fatigue.
2. Capillary fragility : vascular purpura.

3. osteoprosis.
4. thinning of skin, stria rubra , delayed wound healing.
iii. Fat : abnormal deposition of fat in :
1. face : moon face with acne.

2. inter-scapular area : buffalo hump.

3. trunkal obesity with thin limbs ( samboxa shaped obesity
iv. Water & electrolyte : ↑Na , H2 O & ↓K , H+
1. HTN ( due to ↑Na & ↑the action of catecholamines )

2. manifestations of hypokalemia.
3. alkalosis.
v. Stomach : peptic ulcer ( perforation ).

vi. Bone : osteomalacia & osteoporosis.

vii. Blood : polycythemia (plethoric face) , Recurrent infections

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viii. Psychiatric : depression & suicidal tendency.

ix. Androgenic action :

1. female : amenorrhea, hirsutism.
2. male : ↓libido , impotence & ↑body hair.
x. Skin pigmentation only in 2ry ( pituitary) Cushing due to ↑ACTH
Causes of death : Cardiovascular disease & infections.

4. Differential diagnosis :
I. DD of the cause : 1ry & 2ry Cushing.
II. Pseudo Cushing :
a. Obese hypertensive diabetic patients.
b. Females taking oral contraceptive pills.
c. chronic alcoholism → impaired liver function → impaired
metabolism of corticosteroids.

5. Investigation :
a. Investigations for the cause :
i. Imaging for suprarenal gland : abdomen X-ray , U/S , CT & MRI

ii. Imaging for pituitary gland : Skull CT & MRI .

iii. Imaging for oat cell carcinoma : X-ray , CT chest.

b. Assay of the hormones level :

i. In blood :
1. cortisone : ↑ ( N : 5 – 20 μgm % )

a. early : loss of circadian rhythm ( no ↓of cortisol level by night).

b. later : persistent high level .
2. ACTH : ( N : 60 pg/ml )
a. ↑ → pituitary Cushing or Paramalignant syndrome.
b. ↓ → adrenal Cushing.

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ii. In urine :

urinary free cortisol excretion on 24-hour : ↑, this is the single best

biochemical marker of Cushing syndrome. MCQ

c. Investigations of the function of cortisone :

i. Biochemical changes :
↑
↑Na.  ↓
↓K.
↑
↑NaHCO3 .  ↑
↑glucose.
ii. Blood picture :
↑RBCs  ↑neutrophils.
↓lymphocytes.  ↓esinophils.
iii. Urine : ↓Na , ↑K , ↑H+.

d. Suppression test : ( dexamethazone test ).

1. Low dose : 0.5 mg / 6h → for 2days.
i. +ve ( ↓cortisol level ) → normal.
ii. –ve ( no suppression ) → Cushing.
2. High dose : 2 mg / 6h → for 2days.
i. +ve (↓cortisol level ) → 2ry ( pituitary ) Cushing.

ii. –ve ( no suppression ) → 1ry Cushing.

6. Treatment :
a. Treatment of pituitary Cushing :
i. Surgical removal or Pituitary irradiation.
ii. Antagonist : Bromocriptine.
Nelson syndrome : big pituitary adenoma with very high ACTH & hyperpigmentation
after bilateral adrnalectomy in a case of pituitary Cushing.

b. Treatment of adrenal Cushing :

i. Surgery : removal of adenoma followed by cortisol & ACTH.
ii. Adrenocrtical inhibitor : Metyrapone ( ↓cortisol synthesis ) MCQ

c. Paramalignant syndrome : surgical removal of the tumor.

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Adrenogenital syndrome
( Congenital adrenal hyperplasia )

1. Physiology :
a. Hormone : Sex hormone ( androgen ).
b. Gland : Suprarenal gland ( zona reticularis ).
c. Function of the hormone : Gametogenesis & 2ry sex characters.
d. Regulation of this hormone : ACTH.

2. Etiology :
Enzyme deficiency in the cortical synthetic pathways ( 21 hydroxylase enzyme ) → ↓
cortisol level → ↑ACTH → act on zona reticularis → ↑sex hormone secretion

3. C / P : depends on age & sex of the patient.

a. Pre-natal : Female pesudohermaphrotidism :

( small vagina, big fused labia majora simulating scrotum)
b. Post-natal & before puberty :
i. In males : pesudo-precocious puberty ( musculinization, deepening of
voice, but with small testis & no spermatogenesis
ii. In females : virilism (amenorrhea, musculinization & hirsutism)
N.B. : Hirsutism before menarche is suggestive for congenital adrenal hyperplasia.
c. After puberty : there is virilism in females.

4. Investigation :
a. Investigations for the cause : Imaging for the gland.
b. Assay of the hormones level :
i. In blood : ↑testosterone , ↑ACTH.
ii. In urine : ↑metabolite of testosterone (17-hydrotestosterone).

5. Treatment : Cortisone → Suppress ACTH → ↓Androgens.

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Addison’s disease
( 1ry Chronic adrenal failure )

1. Physiology :
a. Hormone : ↓Cortisol , Aldosterone , Sex hormones.
b. Gland : suprarenal gland ( 3 zones).
c. Function of the hormones : see before.
d. Regulation of the hormone : see before.
2. Etiology :
a. Autoimmune → 80%
b. Tuberculosis → 15%
c. Surgery. d. Irradiation.
e. Sarcoidosis & Heamochromatosis. ♫♫

3. C / P :
a. C / p of the cause : TB , Surgery.
b. C / p of the hormone :

i. Hypoglycemia : ( due to ↓cortisone )

1. drowsiness, lack of concentration, hunger pain, coma.
2. There may be absence of the usual warning signs due to
lack of adrenaline ( notice that ↓cortisone →↓action of catecholamine )

ii. Hypotension : (due to ↓cortisone & aldosterone )

1. ↓Cortisol & aldosterone → ↓Na → Hypovolemia &
decreased response of the blood vessels to the action of
catecholamines → hypotension.
2. postural hypotension is common due to ↓action of
catecholamines.

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iii. Hyper-pigmentation : ( due to high level of ACTH )

1. ↑
↑ACTH → direct action on melanocytes.
2. It is not present in secondary adrenal failure.
3. sites :
a. sun exposed areas : face & neck.
b. friction areas : elbow.
c. pigmented areas : areola.
d. scars .
e. mucous membrane : mouth & tongue.

iv. GIT manifestations :

1. diarrhea → 85%.
2. constipation → 15%.
3. anorexia, nausea, vomiting.
4. abdominal pain : due to↓Na , tender renal angle due to TB.

v. Asthenia : marked muscle weakness & loss of weight due to :

1. ↓aldosterone → hyperkalemia & hyponatremia.

2. ↓cortisol → hypoglycemia.
3. ↓androgens → -ve nitrogen balance.

vi. Others
1. polyuria : due to Na diuresis.
2. neuropathy.
3. infertility in males & amenorrhea in females.
4. Associated autoimmune diseases.

vii. Addisonian crisis : see later

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4. Differential diagnosis :
a. 2ry adrenal insufficiency :
- Hypopituitarism → ↓ACTH → ↓cortisone & ↓androgen with no ↓aldosterone.
- In 2ry adrenal failure there are :
 No skin pigmentation. ( due to ↓ACTH )
 Minimal hypotension ( due to normal aldosterone ).
 Manifestations of panhypopituitarism.
b. Skin pigmentation :
- Endocrinal diseases : 1ry Addison , 2ry Cushing , DM , thyrotoxicosis.
- Chronic renal failure.
- Malignancy. - Pregnancy. ♫♫
- Heamochromatosis. - 1ry biliary cirrhosis. ♫♫
- skin diseases.

5. Investigation :
a. Investigations for the cause :
i. Imaging for suprarenal gland : Abdominal U/S , CT, MRI.

ii. Adrenal antibodies : in autoimmune cases.

b. Assay of the hormones level :
1. Cortisol level : low [ n. 5 -20 µgm%]
2. ACTH level : ↑in 1ry adrenal failure , ↓in 2ry adrenal failure
c. Investigations of the function of i hormone :
i. Biochemical changes :

1. ↓( Na & glucose).
2. ↑( K , Ca & H+ ).
ii. Blood picture :

1. ↓ ( RBCs & neutrophils )

2. ↑( lymphocytes & esinophils ).
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d. Stimulatory test : ( ACTH stimulation test )

Synacthen ( synthetic ACTH ) is given IM or IV & plasma cortisol levels
are estimated at 0 , 30 , 60 minutes.
 +ve ( ↑cortisol level ) → 2ry adrenal failure.
 –ve ( no stimulation ) → 1ry Adrenal failure.

6. Treatment :
a. Treatment of the cause e.g. TB.
b. Diet : ↑( Na , CHO & protein ).
c. Replacement therapy :
i. Oral cortisone ( predinsolone : 7.5 mg/d ).
ii. Flurocortisone : 0.1 mg/d to replace aldosterone, especially

in severe hypotension.

Addisonian crisis
( Acute adrenal failure )

Etiology :
i. Acute on top of chronic :
1. Addison’s disease subjected to : surgery , infection, bleeding.
2. Panhypopituitarism : if treatment is initiated with thyroxin

without cortisol.

ii. Acute from the start :

1. surgery : bilateral adrenalectomy.
2. sudden withdrawal of chronic cortisone therapy.
3. meningococcal septicemia (Waterhouse-Freidrichon’s syndrome)
4. massive thrombosis of adrenal vein.

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C/P:
a. C / p of the cause : Surgery, Infection.
b. C / p of the hormone :
1. Sever hypoglycemia → coma.
2. Sever hypotension → shock.
3. Sever asthenia → confusion.
4. Sever skin pigmentation → desquamation.
5. Sever diarrhea → dehydration & acute abdomen.

Investigation : As Addison’s disease.

Acute adrenal failure should be suspected in any patient in the ICU who develops
hypotension of unclear etiology or has refractory hypotension ( hypotension not
corrected by saline & vasopressors)

Treatment : medical emergency

i. IV fluids :

 1 - 2 L of normal saline ( 0.9 % NaCl ).

 1 - 2 L of 10% glucose.

ii. Cortisone is started immediately as follow :

 Hydrocortisone , 50 - 100 mg /6 h IV until the patient is

clinically stable then shift to oral cortisone.

 Dexamethasone ( Decadron ) can be given before or during
the ACTH stimulation test. It will not interfere with plasma
cortisol assay.
iii. Treatment of the precipitating factors : e.g. infection or DIC.

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Pheochromocytoma
(Hyperfunction of adrenal medulla)

 It's the commonest tumor arising from the adrenal medulla.

 Rule of 10 :
 10 % familial.
 10 % bilateral.
 10 % malignant.
 10 % extra-adrenal ( in the sympathetic chain ).
C/P: 
a. Paroxysmal hypertension.
b. Paroxysmal headache.
c. Paroxysmal sweating.
d. Paroxysmal tachycardia (palpitation)
e. Anxiety & psychiatric disturbance.
Investigation : 
a. Urinary ↑↑VMA ( Valenyle Mandelic Acid ) : ↑
b. Urinary catecholamine : ↑
c. Plasma catecholamine : ↑
d. CT scan , MRI for abdomen.
e. Radioisotope scanning : scanning with Meta Iodo Benzyl Guanidine
( MIBG ) produces specific uptake in sites of sympathetic activity.

Treatment :
a. Surgery is the treatment of choice.
b. Medical : combined α& βblockers.
If you start with βblocker → unopposed αaction → Hypertensive crisis.

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Steroid preparations
Uses :
1. Replacement therapy :
a. Addison’s disease.
b. Congenital adrenal hyperplasia.
2. Supplementary therapy in non endocrine diseases :
a. Anti-inflammatory & anti-allergic :
i. CNS :
1. cerebral edema with neoplasm.
2. ↑ICT.
ii. CVS :
1. rheumatic fever.
2. Post infarction syndrome ( Dressler’s syndrome )
3. hemolytic anemia.
4. ITP.
iii. GIT :
1. ulcerative colitis & Crohn’s disease.
2. chronic hepatitis.
iv. Respiratory :
1. bronchial asthma .
2. COPD.
3. sacroidosis.
v. Renal : certain types of GN.
vi. Collagen disease : SLE , polymyositis ,PAN , Rh.arthritis.
vii. Allergic disease : anaphylaxis.
viii. Inflammatory conditions :
1. eye → conjunctivitis.
2. skin → eczema.
b. Anti-stress & anti-shock.
3. Suppression therapy :
a. Tissue transplantation.
b. Lymphoma & leukemia.

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Side effects & contraindications :

Side effect Contraindication

1. From prolonged treatment

a- Metabolism :
 CHO - Hyperglycemia. - D.M.
 Fat - Moon face. - Cushing
- Buffalo hump. syndrome.

 Protein - Osteoporosis. - Myopathy.

- muscle weakness. - Wasting.
 Electrolytes - Na & water - Hypertension.
retention. - Hypokalemia.
- Hypokalemia. - Rickets &
- Hypocalcaemia. osteoporosis.
b- Systems :

 General - Delay healing of - Uncontrolled

wound. infection.
 Eye - Cataract. - Cataract.
- Glaucoma. - Glaucoma.
 CNS - Nervousness. - Psychosis.
- Insomnia.
- Psychosis.
 CVS - HTN. - HTN.
- HF. - HF.
- Thrombosis.
 Respiratory - Chest infections. - T.B.
 GIT - ↑Gastric acidity. - Peptic ulcer.
 Genital - Teratogenecity. - Pregnancy.
- Menstrual
disturbance.
- Hirsutism.

2. From sudden withdrawal of steroids

- Addisonian crisis. - Sudden
withdrawal.

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Diabetes mellitus
Definition:
It’s a clinical syndrome in which there is an error of CHO metabolism ;
due to insulin deficiency, resistance or both, ending in : chronic
hyperglycemia ± glucosuria, vasculopathy & neuropathy.

Etiology : ( 1ry → 95% & 2ry → 5% )

I. Primary : ( includes 3 types : )

a. Type 1 : previously called Insulin-Dependant DM (IDDM) or juvenile-onset DM.

b. Type 2: previously called non insulin-dependant DM (NIDDM) or adult-onset DM
c. MODY : mature onset diabetes in young patient.
- intermediate between type 1 & type 2.
- Treatment : oral anti-diabetic drugs.

The old classification of insulin dependant & non-insulin dependant DM is misleading

because many patient type 2 DM eventually require insulin for control hyperglycemia.

II. Secondary D.M. :

a. Pancreatic causes e.g. Chronic pancreatitis .
b. Endocrinal : Cushing , Acromegaly , Thyrotoxicosis.
c. Drugs : Cortisone, Thiazide , Contraceptive pills.
d. Others : Gestational diabetes , DIDMOAD syndrome.
Pathogenesis :

Type 1 : 10%.

 An autoimmune destruction of the pancreatic β-cells leads to

absolute insulin deficiency.

 Genetic factor play an important role ( the combination of HLA DR3
& DR4 makes a person more likely to develop type 1 DM )

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viral infection may play a role.

without insulin, these patients are prone to develop ketoacidosis.
Although typically diagnosed before age 30, it can present at any
age due to variability in rate of β-cell destruction.
Type 2 : 85%
 It’s characterized by peripheral insulin resistance, so
hyperglycemia develops despite above average level of insulin.
 In addition, it may be due to abnormal structure of insulin or
due to anti-insulin hormones e.g. glucagons.
 Factors that may play a role in pathogenesis include : genetic

predisposition & obesity.

Type 1 Type 2
 Incidence : 10 % 85%
 Pathogenesis : Insulin deficiency due to Insulin resistance.
damage of β-cells.
 Insulin level : ↓↓ Normal or even ↑ ↑
 Age of onset : Younger (usually < 30y). Older (usually > 30y).
 Body weight : Thin. Obese (usually 80 %).
 Hereditary : - 30% in identical twins - Near 100%
- usually no family history. - strong family history.
 C/P:
- Severity : Sever. Mild or moderate.
- Ketoacidosis : Common. Rare, need ppt factors.
- Complication : More common. Less common.
 Treatment :
- Oral hypoglycemic Ineffective. Effective.
- Insulin : Necessary (essential for life ) Usually not required

Stages of DM :

I. Pre diabetes : ( impaired glucose tolerance )

a. It refers to a group of people who have glucose values too
high to be considered normal but not fit the criteria for the
diagnosis of DM (fasting blood glucose > 110 & < 126 mg%)

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b. It’s an intermediate category between normal & DM.

c. There is risk factor for future diabetes & CVS diseases.
d. This group includes :
i. +ve family history. ii. obesity.
iii. ♀with bad obstetric history → macrosomia.
iv. renal glucosuria.

II. Latent diabetes :

Diabetes appears only on exposure to stress & disappears
after removal of stress e.g. pregnancy.
III. Chemical diabetes : Raised blood glucose with no symptoms.
IV. Clinical diabetes :
a. Uncomplicated : Classic triad of symptoms : 3 p
 polyuria : due to osmotic diuresis induced by sugar.
 polydepsia : due to loss of fluid.
 polyphagia with weight loss : ↓insulin → no glucose can enter
satiety center → ↑ ↑of satiety center. While loss of weight is
caused by fluid depletion , fat & muscle breakdown.
b. Complicated : May be the 1st presentation. see later

Investigations of DM : 
I. Blood :
1. Blood sugar tests :
i. Fasting blood glucose : ( no caloric intake for at least 8 hours)
 70 - 110 mg % → normal.
 > 126 mg % → DM.
 110 - 126 mg % → impaired glucose tolerance.
ii. 2 h. post-prandial : ( after ingestion of 75 gm glucose).
 < 140 mg % → normal.
 > 200 mg % → DM.
 140 - 200 mg % → impaired glucose tolerance.

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i. Random ( casual ) glucose level : it means glucose level

during any time of day regardless to last meal.
2. Oral glucose tolerance test : ( OGTT )

i. Patient should be fasting over night.

ii. Fasting blood sugar is done.
iii. The patient is fed 75 gm glucose orally.
iv. Take blood & urine samples every 1/2 h. for 2 h.
v. Normal curve : 3 criteria
1) Fasting : 70-110 mg %
2) Reach maximal point in 1h. but still under 180 mg %
3) Return to normal within 2 h.
3. Cortisone glucose tolerance test :

i. Dexamethazone 3 mg is given before OGTT.

ii. It will induce hyperglycemia in latent & pre diabetes.

II. Urine :
1. Glucosuria : occurs when glucose serum level exceeds 180 mg %
( renal threshold ); but it's not a good indicator for DM diagnosis.
2. Ketonuria : for diagnosis of diabetic ketoacidosis.
III. Monitoring of treatment :
1. Plasma glucose monitoring.
2. Glycosylated hemoglobin ( HBA1c )
i. Normally it's less than 7 % of total HB.
ii. > 12% → poor glycemic control in the past 3 months.
IV. Investigations for complication :
1. Plasma lipids. 2. Urine analysis.
3. ECG. 4. Chest X-ray .

V. Investigations for the cause : If 2ry diabetes is suspected ( < 5 % )

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New WHO diagnostic criteria : 2 of these 3 criteria :

1- Fasting plasma glucose > 126 mg %.
2- Random plasma glucose > 200 mg %.
3- Classic triad of diabetic symptoms ( 3p ).

Pathogenesis of diabetic complications :

1. Glycosylation :
This may lead to thickness of basement membrane of capillaries
with narrowing of their lumen → leading to vasculopathy.
2. Sorbitol pathway :
Glucose is reduced to sorbitol by aldose reductase →  of ATPase
activity → leading to neuropathy & nephropathy.

Complications of DM

Cutaneous :
1. Infection : carbuncles & recurrent abscesses.
2. Pruritis : pruritis vulvae.
3. Delayed healing of the wounds.
4. Xanthelasma ; due to hyperlipidemia.
5. Necrobiosis diabeticorum :
a) Red painless papules with yellow center.

b) usually over the anterior surface of the legs.

c) due to cutaneous blood vessels occlusion.
6. Cutaneous features of diabetic foot.
7. Acanthosis nigricans : black patches due to insulin spillover
into the skin in type 2 DM. MCQ

8. Lipodystrophy : at the sites of insulin injection.

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Cardiovascular :
1. Microangiopathy :

a) Diabetic retinopathy → retina.

b) Diabetic nephropathy → glomeruli.
c) Diabetic neuropathy → vasa nervosa.

2. Macroangiopathy :

a) cerebral : thrombosis & ischemia.

b) coronary : angina & MI ,may be painless due to neuropathy
c) peripheral : gangrene & intermittent cludication.
d) renal : reno-vascular hypertension.

3. Cardiomyopathy : due to microangiopathy.

4. Blood pressure :
a) systemic hypertension.
b) postural hypotension due to autonomic neuropathy.

Causes of HTN in diabetic patient :

1- Diabetic nephropathy.
2- Endothelial dysfunction.
3- Insulin → retention of Na.
4- 2ry diabetes : Cushing & acromegaly.
5- Type 2 DM may be a part of metabolic syndrome X which consists of :
( DM , hypertension , Hyperlipidemia, obesity ).

Chest :
1. Recurrent chest infection e.g. T.B. ( T.B. follows DM as its shadow ).
2. Kussmaul respiration ( air hunger ) & acetone smell in DKA.

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Gastrointestinal : Diabetics never have normal bowel habits

1. Mouth : gingivitis , loosening of teeth.

2. Stomach :
o gastroparesis .
o Nausea , vomiting & abdominal pain in DKA.
3. Intestine :
o Diarrhea : due to sympathetic neuropathy , vasculopathy
& GIT infections.
o Constipation : due to vagal neuropathy.
4. Liver : fatty liver.
5. Gall bladder : chronic cholecystitis , gall stones.

Genital :
1. In ♂ : impotence ( psychological, neuropathy, vasculopathy )
2. In ♀ : infections & pruritis vulvae.
3. Effects of DM on pregnancy :
- On mother :
i. Eclampsia.
ii. post Partum hemorrhage.
iii. puerperal sepsis.
- On fetus :
iv. High birth weight.
v. Hypoglycemic baby.
vi. Congenital anomalies.
4. Effects of pregnancy on DM :
i. ↑needs for insulin due to ↑anti-insulin : estrogen.
ii. ↓renal threshold for glucose.
iii. ↑incidence of complications.

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Eye :
1. Lids : infection ( chalazion , conjunctivitis ) , Xanthelasma.

2. Iris : New vessels formation in iris ( rubeosis iridis )

3. Lens :
 Senile cataract ( occur at an earlier age )

 Repeated error of refraction secondary to osmotic lens changes

with fluctuating glucose level :
- Hyperglycemia leads to myopia.
- Hypoglycemia leads to hypermetropia.
4. Nerves :Optic neuritis , Cranial nerve palsy ( 3, 4 & 6 nerves).

5. Diabetic retinopathy :

a. It’s the most characteristic form of diabetic eye diseases.

b. It is related to the duration & control of the disease.
c. It eventually occurs in nearly all patients of type 1 DM 10 years after
diagnosis. It is present in 10% of type 2 DM at diagnosis, 50% after 10
years and 80 % after 20 years.
d. It is usually accompanied by nephropathy & neuropathy.
e. Detected by fluorescin angiography.
f. There are 2 important types :
- Non proliferative ( background retinopathy) :
 Characterized by ↑capillary permeability, Microaneurysms
, hemorrhage , exudates .
 During this stage of diabetic retinopathy, no local treatment
required , except in a case of diabetic maculopathy, just
good control of diabetes and of any coexisting
hypertension and stopping smoking ,

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- Proliferative :
Characterized by neovascularization, retinal detachment. this type
must be treated as early as possible by laser photocoagulation.
 without treatment 50% of proliferative patients become blind within 5 – 10 years.
 Proliferative retinopathy : more common in type 1 DM.
 Diabetic maculopathy : more common in type 2 DM.

Renal :

1. Interstitial injury :
- Pyelonephritis : Fever  Pain. Dysuria. 
- Acute necrotizing papillitis : fever , pain , dysuria and hematuria.

2. Diabetic nephropathy : (Diabetic glomerulosclerosis)

Definition :
clinical syndrome characterized by ↑in urine albumin excretion ,↑BP
up to end stage renal failure with progressive rise in CV risk.
Incidence :
o long standing DM ( 30% type1 , 20 % type2 ) .
o Genetic factor may play a role.

Pathogenesis : Glomerular sclerosis :

i. Early Thickening of basement membrane of glomeruli &

mesangial expansion .
ii. Hyalinization of afferent & efferent arterioles.
Glomerular hyperfilteration  proteinuria  end stage renal disease.

DM affects efferent more than afferent arterioles . So ; there is more narrowing in efferent than in
afferent, this ↑↑intra-glomerular pressure  this will allow plasma proteins to escape into the urine
 Some of these proteins will be taken up by the proximal tubular cells, which can initiate an
inflammatory response that contributes to interstitial scarring eventually leading to fibrosis.

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Types :

i. Diffuse : 80 %.
ii. Nodular : 20 % ( Kimmelestiel-Wilson’s syndrome ).

Clinical picture :

i. Long standing DM especially poorly controlled diabetes after about

10-20 years .
ii. Proteinurea : the early clinical sign of diabetic nephropathy
1. micro-albuminuria : 30-300 mg/day It is reversible by ACEIs .
2. macro-proteinuria : > 300 mg/day
3. heavy proteinurea ( nephrotic syndrome )
Nearly 100% with gross proteinuria will progress to End Stage CRF in 5 – 15 y 
iii. Lately, progressive loss of renal function ( CRF ) .
iv. Hypertension, diabetic retinopathy& neuropathy are usually present.
Stages of diabetic nephropathy : for postgraduates
A) Incipient nephropathy :

o Stage I : nephromegally , ↑GFR.

o Stage II : stage I + microalbuminuria on exercise.
o Stage III : as stage 2 but persistent microalbuminuria > 30 mg/d.
This stage may remain silent for up to 10 – 15 years.
B) Overt nephropathy :

o Stage IV :
 Macro proteinuria > 300 mg/d . ( rarely the proteinuria
exceed 5 gm /d )
 ↓GFR.
 Hypertension is common.
o Stage V : End stage CRF.

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Investigation :

1- Urinalysis : Screening of microalbuminuria is a mandatory .

It should be performed in type 1 patients who have had diabetes > 5 years
and all type 2 diabetic patients starting at diagnosis (In type 2 DM ,
microalbuminuria can be present at the time of diagnosis ).
2- Blood : urea & creatinine.
3- U/S : normal or large kidney. ( not shrunken as usual CRF ) MCQ

4- Biopsy : may be done if there is any doubt in the diagnosis. It is not

always necessary if the case is straightforward, with a documented progression
of proteinuria over time and presence of diabetic retinopathy.
Treatment : 
1- Diabetic control can reverse the microalbuminuria.
2- Control of hypertension is a mandatory by ACEIs & ARBs which
decrease the albuminuria even in normotensive patients.
3- Treatment of CRF : 3D + T see nephrology
o Diet : low protein diet
o Drugs : symptomatic treatment.
o Dialysis.
o Transplant : treatment of choice in young patients.

Diabetic foot :
Definition : Trophic changes in foot of diabetic patients ( ulcers,
falling of hair & gangrene ).
Etiology : vasculopathy, neuropathy & infection combine to produce
tissue necrosis.
Treatment :
a) Control of diabetes.
b) Careful foot cleaning & careful nail cutting.
c) For infection : strong antibiotic & drainage of pus.
d) For ischemia : revascularization & amputation in gangrene.

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Diabetic infections :

1. skin : staph & candida .

2. urinary tract : pyelonephritis & perinephric abscess.
3. Chest : T.B. & pneumonia.
4. Genital : pruritis vulva.
5. GB : cholecystitis.

Neurological :

I. Diabetic macroangiopathy
II. Diabetic neuropathy.
III. Diabetic comas.

I. Diabetic macroangiopathy : ( due to atherosclerosis )

a. Cerebral hemorrhage.
b. Cerebral thrombosis.
II. Diabetic neuropathy :
Pathogenesis : unknown but there are 4 important theories :
1. Hypovitaminosis : polyuria washes water soluble B complex.
2. Microangiopathy of vasa nervosa.
3. Metabolic ketosis : toxic effect of keton bodies.
4. Transformation of glucose to sorbitol by aldose reductase enzyme.
C/P : ( may precede the discovery of DM )
1. mononeuropathy or mononeuropathy multiplex, affecting :
a. Peripheral nerves : femoral , ulnar & median nerves.
b. Cranial nerves : 3 , 4 , 6 . MCQ

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2. polyneuropathy :
a. Sensory affection is more than motor affection.
b. Superficial sensation : Symmetrical parasthesia especially in
LL followed by stock & glove hyposthesia.

c. deep sensations : nocturnal calf spasm is common.

d. Motor weakness is late.
3. Autonomic neuropathy :
- CVS :
 Postural hypotension.
 Painless myocardial infarction.
 Persistent tachycardia .
- GIT :
 Gastroparesis : delayed gastric empting.
 Diarrhea : severe, nocturnal & alternating with constipation.
- Genito-urinary :
 Impotence.
 Incontinence.
- Skin :
 Generalized sweating.
 Edema of the feet due to loss of the vasomotor tone.
 Trophic ulcers.

Treatment :
 Strict control of DM : diet, oral hypoglycemic or insulin.

 Reassurance may be all that needed.

 Physiotherapy if motor weakness is present.
 Drugs : Low benefit

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a. Analgesics of neurotic pain : carbamazepine ( Tegretol )

b. Vit. B complex ( Tri B ) & ATP ( adenoplex ).
c. Aldose reductase inhibitors : sorbinil.
d. Cerebrolysin. ( nerve growth factor )
III. Diabetic comas :
1. Hypoglycemic coma. ( insulin reaction )
2. Diabetic ketoacidosis. ( DKA )
3. Hyperglycemic hyperosmolar non ketotic coma.
4. Diabetic lactic acidosis.
5. Other causes of coma : uremic, hepatic, ………

Hypoglycemic coma

a. Etiology :
Missed meal or severe exercise after insulin or oral hypoglycemic drugs.
Over dose of insulin or decreased elimination of insulin as in cases of
renal failure.

b. C/P : severity of symptoms can vary with the individual.

i. Adrenergic symptoms : ( warning signs ) 

due to ↑catecholamines when blood glucose < 50 mg %
1- Tachycardia ( palpitation ).
2- Sweating.
3- Tremors.
4- Anxiety.
5- Hunger pain.

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ii. CNS symptoms : 

due to cerebral dysfunction when blood glucose < 30 mg %
1- Headache.
2- Blurring of vision.
3- Lack of concentration.
4- Convulsion may occur.
5- Coma.
Masked symptoms of hypoglycemia may occur in the following
conditions : ( not associated with adrenergic symptoms )
 During night.
 β-blockers.
 Old age.
 Recurrent hypoglycemia.

c. Investigation :
Low blood glucose < 50 mg % in male & 45 % in female.
d. Differential diagnosis :
o From diabetic ketoacidosis : see later.
o From other causes of hypoglycemia : see later.

e. Treatment : Recovery is very rapid except in irreversible brain damage

i. If patient is conscious : oral glucose in the form of candy.

ii. If there is coma : IV glucose 50 gm 50 % .
iii. Hypoglycemia due to oral hypoglycemic drugs ( sulphonylurea ) : may
persist for long time ( days ) so glucose has to be infused for long time.

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Diabetic ketoacidosis “ DKA ”

a. Definition :
DKA is an extremely serious metabolic complication of DM due to sever
insulin deficiency, it’s characterized by triad of : 
- Acidosis. - Ketosis. - Hyperglycemia ( usually >250 mg % ).
NB : There is no relation between the severity of hyperglycemia & the severity
of ketoacidosis.
b. Etiology : ketONE bodies are seen in type ONE DM ☺

 Occurs mainly in type 1 DM, due to sever insulin deficiency e.g :

 Previously un diagnosed DM
 Missed insulin ( neglected treatment ).
 Precipitating factors :
 Infections ( lead to increased insulin requirements ).
 Infarction ( I mean myocardial infarction ).
 Intoxication ( Alcohol ).

In type 1 DM : DKA occurs with or without Precipitating factors.

In type 2 DM : DKA occurs with Precipitating factors only.

c. Pathogenesis & C/P : sever insulin deficiency leads to : 

i. Glucose can’t enter the cells → hyperglycemia > 250 mg %.
ii. Fat : ↑↑lipolysis to produce energy → ↑production of ketone
bodies ( β-hydroxy buteric acid, acetoacetic acid & acetone ) →
ketoacidosis ( PH < 7.3 )
iii. Effects of ketoacidosis : gradual onset of : X 2
1- Muscles :
a. generalized weakness.
b. muscle pain.
2- Kidney : ketonuria together with glucosuria lead to sever
a. polyuria.
b. dehydration.
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3- GIT :
a. Anorexia , nausea & vomiting.
b. abdominal pain.
4- Respiration :
a. Kussmaul respiration ( deep rapid )
b. acetone odour of breath.
5- CVS :
a. depressed contractility & low blood pressure.
b. rapid weak pulse.
iv. Hyperkalemia due to Shift of K outside cells in absence of insulin.
v. Coma due to combined effect of :
1. ketone bodies.
2. dehydration.
3. electrolyte disturbance.
d. Investigations :
i. Blood examination :
o ↑glucose > 250 mg %.
o ↑ketone bodies.
o Acidosis ( PH < 7.3 ) with high anion gap.
o ↑FFA.
o Electrolytes : ↑↑K & ↓↓Na .
ii. Urine examination : Polyuria , glucosuria & ketonuria.

e. Treatment : 
i. Insulin :
 short acting soluble insulin.
 Regimen : 2 methods
a. IV insulin infusion : 5 – 10 u/ h infusion . when blood
glucose < 250 mg /dl → reduce insulin to 2 – 4 u/h
b. Repeated IM : 20 U at the start then 6 U/ h
 The goal is to decrease the blood glucose by 75 mg % / hour.

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ii. Fluid therapy :

 4 – 8 L is usually required.

 1 L / hour for the first 2 hours followed by 1/ 2 L / hour until the

deficit is replaced.
 At first normal saline is given, then change to dextrose saline
when blood glucose < 250 mg/dl.

iii. K therapy :
The serum K falls during insulin therapy ( intracellular shift ), and this
fall may be dramatic. so add ( 20 – 40 mEq ) to each 1L saline.
iv. Na bicarbonate : in sever acidosis [ PH < 7.1 ]
v. Treatment of precipitating factors e.g. infection : antibiotics.

Hypoglycemic coma DKA

 History : - Missed meal. - Missed insulin.
 Onset : - acute. - gradual.

 Pulse : - Strong . - Weak & rapid.

 Bl.P. : - ↑ - ↓
 Skin : - Sweaty. - dry.
 Pupils : - dilated. - normal.
 Respiration: - normal. - Rapid , deep.
 Urine : - normal. - +ve sugar & acetone.

 Coma : - Irritable. - not irritable.

 IV glucose : - rapid recovery. - no effect.

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Hyperglycemic hyperosmolar non ketotic coma ( HHNK )

 There is low insulin level which is enough to prevent ketosis , but not enough
to inhibit hyperglycemia, so there is hyperglycemia without ketosis.
 It occurs in old type 2 DM.
 Patients typically having sever hyperglycemia ( > 600 mg/dl ), sever
dehydration . plasma osmolarity > 340 mOsm/L ( N : 290 ) is the landmark
of this condition.
 Clinical picture :
o Severe hyperglycemia : polyuria , polydepsia.
o Severe dehydration  renal failure & thrombotic complications.

o severe hyperosmolarity  CNS symptoms (convulsions , coma ).

 Treatment : The same as DKA but
o Aggressive fluid replacement. ( the most important measure )
o Low rate of Insulin infusion ( 3 U/h ).
o S.C. heparin to prevent thrombotic complications.
o Na bicarbonate is not given.

Lactic acidosis

o It occurs in diabetics using high dose of biguanides e.g. metformin

o Biguanides  tissue hypoxia  anaerobic glycolysis  accumulation of
lactic acid.
o C/P :
a. Rapid deep respiration ( Kussmaull respiration ).
b. Confusion , coma.
o Treatment : NaHCO3

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Diagnostic criteria of diabetic comas

DKA HHNK Lacctic acidosis

 Hyperglycemia > 250 mg/dL.  Hyperglycemia > 600 o Severe acidosis with
 Acidosis with blood pH < 7.3. hyperventilation.
mg/dL.
 Serum bicarbonate < 15
 Serum osmolality > 310 o Blood pH below 7.30
mEq/L.
 Serum positive for ketones. mosm/kg. o Serum bicarbonate < 15
 No acidosis; blood pH mEq/L.
above 7.3. o Anion gap > 15 mEq/L (
 Serum bicarbonate > 15 high anion gap )
mEq/L. o Absent serum ketones.
 Normal anion gap (< 14 Serum lactate > 5
mEq/L). mmol/L

 Acute diabetic complications : diabetic coma + infections.

 Micro-vascular complications : diabetic triopathy.
 Hyperglycemic coma : DKA , HHNK.

Treatment of DM :
I. General measures.
II. Diet.
III. Oral hypoglycemic.
IV. Insulin.
V. Treatment of complications.

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I. General measures :
a. Reassurance.
b. Education about nutrition & lifestyle modifications.
c. Exercise.

II. Diet :
a. It’s an important item in control of D.M.
b. Diet alone can control mild cases of type II D.M.
c. Total calories/day : depending on weight & physical activity
i. Mild activity → 1500 cal/d.
ii. Moderate activity → 2500 cal/d.
iii. Severe activity & pregnancy → 3500 cal/d.
d. Food components :
i. CHO : 50% of calories . avoid simple sugars.
ii. fat : 30% of calories . avoid saturated fat.
iii. protein : 20% of calories.
iv. vitamins : B-complex & vit. A
v. ↑↑fibers : ↑satiety.
e. Number of meals :
3 main meals + 2 snacks in between, to avoid hyperglycemia
or hypoglycemia .

III. Oral hypoglycemic

a. Sulphonylureas :

- mechanism of action :
1. ↑↑insulin secretion from pancreas.
2. ↑↑peripheral action of insulin.
3. ↓↓hepatic production of glucose.

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- preparations :
Drug Trade name Dose ( mg/d ) Duration of action
 Old generation :
- Cholropropamide Pamidine 100 - 500 long acting
- Tolbutamide Diamol 500 - 3000 short
 New generation :
- Glibenclamide Doanil. 2.5 - 15 long acting
- Glimepiride Amaryl. 1-6 long acting
- Gliclazide Diamicron. 80 - 480 intermediate
- Glipizide Minidiab 2.5 - 30 short

- Indication :
type 2 DM not controlled by diet alone especially in non obese patients.
- Side effect :
- Allergy. - Aplastic anemia.

- Hypoglycemia. - Hepatitis.

- Hyponatremia due to increased ADH by cholropropamide.

b. Biguonides :
- Mechanism of action :
1. ↑anaerobic glycolysis.
2. ↓
↓intestinal glucose absorption. 3. ↓
↓appetite.
- preparations : Metformin ( Cidophage ) 500 - 850 mg t.d.s.
- Indications :
1. type 2 DM not controlled by diet alone esp. in obese patients.
2. combined with suphonylurea or insulin to achieve control.
- Side effects :
- GIT irritation. - lactic acidosis.

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a. Biguonides :
- Mechanism of action :
1. ↑anaerobic glycolysis.
2. ↓↓intestinal glucose absorption. 3. ↓
↓appetite.

- preparations : Metformin ( Cidophage ) 500 - 850 mg t.d.s.

- Indications :
1. type 2 DM not controlled by diet alone esp. in obese patients.
2. combined with suphonylurea or insulin to achieve control.
- Side effects :
- GIT irritation. - lactic acidosis.
b. Recent drugs :
i. Alpha Glucosidase inhibitors : Acarbose ( Glucobay ) 50 mg t.d.s.
prevent breakdown of CHO in intestine  ↓glucose absorption.
ii. Pioglitazone ( Diabetin ) : ↑tissue sensitivity to insulin (insulin sensitizer)

A physician without differential diagnosis is like a soldier without his gun,

like a clown without his fun.
Dr/Alsayed Dawoud
Kasr Alainy School of medicine

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I. Insulin

- Action :
i. Rapid action : Insulin stimulates 2 things to go Into the cells : glucose & K
ii. Gradual action :
1. CHO : hypoglycemia
a. ↑glycogensis.
b. ↓gluconeogenesis.
c. ↑peripheral utilization of glucose.
2. fat : - ↑
↑lipogenesis. - ↓
↓lipolysis.
3. protein : anabolic.

- Preparations : was discovered in 1921.

Type Trade names Duration of action

1- Short-acting : - Neutral ( regular ). Onset : < ½ h.

( soluble ) - Humulin R Peak : 2 – 4 h.
- Semilent. Duration : 6 – 8 h.
2- Intermediate : - Isophane (NPH) Onset : 2 h.
- Humulin N Peak : 6 – 8 h.
- Lente. Duration : 12 – 24 h.

3- Long-acting : - Protamine zinc insulin Onset : 6 – 8 h.

- Humulin L Peak : 12 – 24 h.
- Ultralente Duration : up to 36 h.

4- Insulin mixture : 30% short + 70% NPH ( mixtard )

- Indications :
i. All type 1 DM.
ii. Type 2 DM not controlled with diet & oral hypoglycemic.
iii. During pregnancy, infection & surgery.
iv. DKA & HHNK .
v. ↑
↑K ( Hyperkalemia ).

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vi. Insulin stimulation test in pan-hpypopituitarism.

- Dose : trial & error ( s. c. , 1 cm mixtard = 40 u )
i. Start with 20 – 30 U / d ( 20 U in non obese , 30 U in obese patient )
ii. The dose is gradually ↑( by 5 u /d ) until blood glucose is controlled.
iii. 2 /3 of dose before breakfast & 1 / 3 of dose before lunch.
iv. 2 /3 of dose intermediate & 1 /3 of dose short acting insulin (mixtard)

- If mixtard is not available → 1/3 regular insulin + 2/3 NPH can be mixed in
the syringe & injected as rapid as you can.

- Multiple SC insulin injection ( MSII ) : in cases of poor glycemic control

o 75% of the dose is given as regular insulin before each meal.
o 25 % of the dose is given as intermediate insulin before sleep.

- Administration :
i. S.C.
ii. Insulin pump ( Continuous S.C Insulin Infusion , CSII ) .
iii. IV infusion or IM : in case of DKA , HHNK
iv. Insulin pens.
v. Oral , nasal & rectal insulin → under trial ?
- Side effects :
i. Hypoglycemia & hypoglycemic coma.
ii. Allergy : use human insulin.
iii. Insulin resistance :
o obesity → mild resistance.
o antibodies against insulin.
iv. Insulin lipodystrophy : atrophy or hypertrophy of s.c. fat at
the site of insulin injections.
v. Insulin edema : Na & H2O retention  Hypertension.
vi. Weight gain.
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vii. Pseudo insulin resistance ( Somogi effect ) : nocturnal

hypoglycemia due to over insulin dose at night → ↑↑anti-
insulin hormones → rebound hyperglycemia in the
morning. This condition is treated by reduction of the
evening insulin dose.

II. TTT of complication : See complications.

Q : criteria for good diabetic control ?

 Lab. :
- Fasting plasma glucose ( 90 - 130 ) mg/dl
- Post prandial plasma glucose : < 180 mg/dl.
- HbA1c < 7%.

 Clinical :
- No symptoms of DM : …….

Secondary causes of hyperglycemia

I . Hyperglycemia due to tissue insensitivity to insulin :

- Hormonal tumors (acromegaly, Cushing's syndrome, glucagonoma,
pheochromocytoma)
- Pharmacologic agents (Cortisone, sympathomimetic drugs )
- Liver disease (cirrhosis, hemochromatosis)
- Muscle disorders (myotonic dystrophy)
- Adipose tissue disorders (lipodystrophy, truncal obesity)
- Insulin receptor disorders (acanthosis nigricans syndromes )
II. Hyperglycemia due to reduced insulin secretion :
- Hormonal tumors (somatostatinoma, pheochromocytoma)
- Pancreatic disorders (pancreatitis, hemochromatosis)
- Pharmacologic agents (thiazide diuretics, phenytoin, pentamidine)

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Scheme for treatment of DM :

Diabetic patient

Type 1 Type 2

Diet & insulin Diet

controlled uncontrolled

Oral hypoglycemic

obese Non obese

Biguanides sulfonylurea

uncontrolled controlled controlled uncontrolled

Add sulfonylurea Add biguanides

Uncontrolled

Insulin

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Hypoglycemia

Causes :
I. Fasting hypoglycemia :
o Iatrogenic : insulin , sulfonylureas.
o Insulinoma : tumor of pancreatic βcell that produce too much
insulin.
o Extrapancreatic tumor( fibrosarcoma , mesothelioma ) that
produce Insulin like growth factor-I ( IGF-1)
o Starvation.
o Hepatic dysfunction.
o Chronic renal failure.
o Hormonal deficiency : hypopituitarism , hypothyroidism , Addison
disease.
II. Postprandial ( reactive ) hypoglycemia :
o Alimentary hypoglycemia : gastrectomy. this is due to rapid glucose

absorption with excessive insulin release  glucose metabolized

rapidly but insulin level remains high resulting in hypoglycemia.
o Idiopathic type.
o Early type II DM : The peak value of insulin occur after 2 hours or
later when the absorption of CHO from the intestine has been
completed.
Clinical picture : see hypoglycemic coma 5&5

Investigations :

1- Fasting plasma glucose : < 50 mg% in males , < 45 mg% in females.

2- Plasma level of insulin , thyroxin , cortisol.

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3- The insulin / plasma glucose ratio : normally < 0.4 . It is higher in patients
with insulinoma.
4- Liver & renal function tests.
5- Abdominal US & CT for tumors.
Treatment :
I. Fasting hypoglycemia :
 The acute attack : see hypoglycemic coma.
 Insulinoma : MCQ

 Surgical removal .
 Medical to prevent insulin release e.g. diazoxide , octreotide.
II. Postprandial hypoglycemia :
 Diet : Frequent small meals & avoid simple CHO.
 Drugs :
 Probanthine : 7.5 mg 2 h before meals.
 Phenytoin : it inhibits insulin secretion.

We think so because all other people think so, or … because we were told to think so, and
think we must think so …

Rudyard Kipling

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Hirsutism

Definition : ↑↑growth of body hair in androgen dependant areas.

Etiology :
a. Ovarian :
1. polycystic ovary syndrome > 90% of cases.
2. ovarian tumors secreting androgens.
b. Adrenal :
1. congenital adrenal hyperplasia ( CAH ).
2. Cushing's syndrome.
c. Drugs :
- minoxidil. - phenytoin.
- androgens. - diazoxide.
-------------------------------------------------------------------------------------------------------------

Gynaecomastia

Definition:
 Enlargement of the male breast, this is due to a decreased
androgens : estrogen ratio.
 It should be differentiated from fatty breast which lacks the
glandular element.
 It's unrelated to galactorrhea, breast enlargement is not
necessary to make milk.

Etiology : mnemonic : gynecomastia

- Genatic : Klinefelter syndrome
- Young boy ( puberty )
- Neonate.
- Estrogen.
- Cirrhosis , cimetidine.
- Old age.
- Marijuana.
- Acromegaly.
- Spironolactone.
- Tumor ( testis , adrenal & bronchogenic carcinoma )
- INH.
- Alcoholism.

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Obesity
Definition :
Obesity is an increase of body adipose (fat tissue) mass.

Etiology :
 Genetic factors.
 Excessive caloric intake.
 Diminished caloric consumption : physical inactivity.
 Endocrinal :
- Cushing's syndrome.
- Hypothyroidism.
- Hypogonadism.
- Insulinoma.
 Hypothalamic disorders : ( DI , polyphagia , obesity , hypersomnia )
 Drugs : Cortisone , Contraceptive pills , Insulin , sulfonylureas , anti-psychotics.

Diagnosis of obesity :

- Body Mass Index ( BMI ) : BMI Classification

18.5 – 25 normal weight
25 – 30 overweight
30 – 35 class I obesity
35 – 40 class II obesity
Over 40 class III obesity

- Skin fold thickness e.g. over triceps ( N : 20 mm in ♂, 30 mm in ♀).

- Estimation of body fat : ( Waist / hip ratio )

a. Central obesity : more fat in the upper body ( Apple

shaped ) , associated with more morbidity .

b. Peripheral obesity : more fat in lower body ( pear

shaped ) , associated with less morbidity .
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Complications : ( Hazards of obesity )

Cardiovascular :
○ Hypertension.
○ Atherosclerosis & coronary heart diseases.
○ DVT & pulmonary embolism.
Neurological :
○ Stroke. ○Migraine.
Endocrinology :
○ Type 2 DM. ○Menstrual disorders.
GIT :
○ Cholecystitis & gall stones. ○ Fatty liver.
○ GERD. ○ Hernias.
Respiratory :
○ Dyspnea (restrictive hypoventilation )
○ Sleep apnea syndrome.
Joints :
○ Osteoarthritis. ○ Back pain. ○ Gout.
Psychological : depression & social stigmatization.
Malignancy : Increased incidence of : cancer colon , breast , prostate.
Metabolic syndrome : ( syndrome X )
▪Obesity. ▪Hyperlipidemia. ▪Hypertension. ▪DM.

Treatment :
 Life style & diet modification : Low caloric , balanced diet with mild exercise.
 Drugs :
Orlistat ( Xenical ) : inhibits the pancreatic lipase so decrease fat absorption.
Sibutramine ( Meridia ) : Appetite suppressant.
 Surgery e.g. Gastric plication , liposuction : indicated with BMI > 40
 Treatment of the cause & complications.
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Loss of weight

Etiology :

I. Loss of weight inspite of good appetite :

i. Increased caloric utilization :
○ Thyrotoxicosis.
○ Anexity.
○ Severe exercise.
ii. Decreased intestinal absorption : malabsorption syndrome & diarrhea. ( see GIT )
iii. Diabetes mellitus.
iv. Parasitic infection : Ascaris.

II. Loss of weight associated with decreased appetite :

i. Psychological disorders :
○ Depression.
○ Anorexia nervosa.
ii. Gastro-intestinal disorders : e.g.
○ Esophageal diseases.
○ Peptic ulcer.
○ Inflammatory bowel diseases.
○ Hepatobiliary diseases.
iii. Systemic disorders : e.g.
○ Malignancy.
○ Cardiovascular diseases.
○ Infection.
iv. Iatrogenic : Alcohol , Amphetamines : cause appetite suppression leading to
weight loss.
v. Smoking.

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Endocrinology MCQ
1- Which one of the following inhibits growth hormone secretion from the anterior
pituitary gland?
a. Somatostatin.
b. GH releasing hormone.
c. Hypoglycemia.
d. Arginine.
e. Serotonin.
2- In hypertensive individual , which one of the following is the likely finding in a
patient with renal artery stenosis and is helpful in distinguishing the condition from
Conn's syndrome ?
a. A high aldosterone level
b. A high renin and a high aldosterone level
c. A high renin level
d. A low aldosterone level
e. A low renin and a high aldosterone
3- A 45-year-old obese man without known medical problems complains of feeling very
sleepy during the day and often falling asleep while listening to friends. The most likely
cause of this patient’s problem is
a. narcolepsy
b. upper airway obstruction at night
c. glucocorticoid excess
d. growth hormone excess
e. estrogen excess
4- Obese persons are at an increased risk for which of the following disorders?
a. Hypothyroidism
b. Cholelithiasis
c. Type 1 diabetes mellitus
d. Elevated levels of HDL cholesterol
e. Central sleep apnea
5- Which of the following regimens is best for the preoperative management of a
patient with a known pheochromocytoma?
a. Propranolol alone
b. Propranolol followed by phenoxybenzamine
c. Phenoxybenzamine followed by propranolol
d. Prazosin alone
e. Propranolol followed by prazosin
6- Which of the following may be a direct consequence of severe magnesium
defciency?
a. Hypophosphatemia
b. Hypercalcemia
c. Hypokalemia
d. Hyponatremia
e. Shortening of the QT interval

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7- A 55-year-old woman presents to her physician with mild fatigue. Her past medical
history is unremarkable. She is taking no medication. No abnormalities are detected
on physical examination. The only abnormality detected on routine blood testing is an
elevated calcium (11.9 mg/dL) and a serum inorganic phosphorus of (2 mg/dL). An
immunoreactive parathyroid hormone level is undetectable. The most likely etiology
for this patient’s high serum calcium is
a. primary hyperparathyroidism
b. malignancy
c. hypervitaminosis
d. hyperthyroidism
e. familial hypocalciuric hypercalcemia
8- The most common presentation of primary hyperparathyroidism is
a. bone fracture
b. increased serum creatinine
c. osteitis fibrosa cystica
d. calcium kidney stones
e. asymptomatic hypercalcemia
9- Which of the following medications is known to cause hyperprolactinemia?
a. Metoclopramide
b. Levothyroxine
c. Glucocorticoids
d. Propanolol
e. Cigarette use
10- A 23-year-old woman is diagnosed with Graves’disease shortly after discovering she
is pregnant. Appropriate therapy includes
a. radioactive iodine to ablate her thyroid gland
b. propylthiouracil with the goal of maintaining her thyroid function tests in slightly high range.
c. methimazole therapy
d. a beta blocker
e. propylthiouracil with care taken to maintain her thyroid function tests in the mid normal range
11- A 19-year-old man with type 1 diabetes mellitus presents to the emergency room
with nausea and vomiting. His arterial pH is 7.16 with potassium of 5.4 mEq/L ,
bicarbonate of 7 mEq/L, sodium of 132 mEq/L, phosphate of 3.0 mg/dL, and glucose of
475 mg/dL. In addition to intravenous saline & insulin, which electrolyte should be
considered in treatment of this case?
a. Bicarbonate
b. Potassium
c. Dextrose
d. Phosphate
e. None of the above
12- The diagnosis of diabetes mellitus is certain in which of the following situations?
a. Abnormal oral glucose tolerance in a 24-year-old woman who has been dieting
b. Successive fasting plasma glucose 147, 165, and 152 mg/dL in an asymptomatic woman
c. A serum glucose level 100 mg/dL in a woman in her twenty-fifth week of gestation after a 50
g oral glucose load
d. Persistent asymptomatic glycosuria in a 30-year-old woman
e. Persistently elevated nonfasting serum glucose levels
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13- A 46-year-old woman arrives in your clinic for routine examination. She has no
specific complaints, and a full review of systems is unrevealing. On physical
examination she has normal vital signs and a 1.5 cm thyroid nodule is palpated in the
right lobe of her thyroid; there
are no other abnormal findings. A laboratory test reveals a serum TSH level of 2.3
mU/L. Which of the following would be the most appropriate recommendation?
a. Fine-needle aspiration biopsy
b. Unilateral thyroid lobectomy
c. Thyroxine suppressive therapy
d. Radioiodine therapy
e. No intervention needed; a wait and watch approach is recommended
14- Which of the following has been associated with an effective approach towards the
prevention of diabetic retinopathy?
a. A reduction in the serum triglyceride level
b. Improved control of blood glucose concentrations
c. Use of an ACE inhibitor
d. Use of aspirin therapy
e. Smoking cessation

15- Which of the following medications is known to cause hypoglycemia?

a. Acetaminophen
b. Pentamidine
c. Epinephrine
d. Verapamil
e. Thiazides
16- Causes of fasting hypoglycemia that are due primarily to overutilization of glucose
include
a. acromegaly
b. hepatoma
c. alcohol ingestion
d. congestive heart failure from cor pulmonale
e. Hypopituitarism
17- Manifestations of hypothyroidism include
a. prolongation of the QT interval
b. depressed serum cholesterol
c. microcytic anemia
d. increased serum creatine phosphokinase
e. decreased serum lactate dehydrogenase level
18- Which of the following is most sensitive for detecting diabetic nephropathy?
a. Serum creatinine level
b. Creatinine clearance
c. Urine albumin
d. Glucose tolerance test
e. Ultrasonography
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19- Which of the following statements regarding adrenal insufficiency is true?

a. The most common cause of adrenal insufficiency is tuberculosis
b. The critical test for the diagnosis of chronic adrenal insufficiency is Synthetic ACTH test
c. Chronic secondary adrenal insufficiency is treated with hydrocortisone and fludrocortisone,
whereas chronic primary adrenal insufficiency is treated with hydrocortisone alone
d. ACTH levels greater than normal in secondary adrenal insufficiency.
e. 2ry adrenal insufficiency is characterized by skin pigmentation.
20- Which of the following statements regarding hyperaldosteronism is true?
a. The most common causes of secondary hyperaldosteronism are congestive heart failure and
cirrhosis with ascites
b. Treatment of primary adrenal hyperaldosteronism is spironolactone
c. Patients with primary adrenal hyperaldosteronism usually present with hypertension,
hypokalemia, and metabolic acidosis
d. Diagnosis of primary adrenal hyperaldosteronism is confirmed by elevations in the levels of
both renin and aldosterone
e. Patients with primary adrenal hyperaldosteronism usually present with generalized edema.
21- A 42-year-old man with long-standing type 1 diabetes presents with gastroenteritis
that has been worsening for 5 days. His blood pressure is 90/55 mm Hg, and his heart
rate is 135 beats/min. Other laboratory findings are as follows: blood glucose: 656
mg/dl; sodium: 127 mEq/L; potassium, 4.2 mEq/L; HCO3 : 14 mEq/L; anion gap,25;
and pH, 7.05. Which of the following would not be an appropriate step in the
immediate treatment of this patient?
a. I.V. administration of 0.9% saline
b. Admission to the intensive care unit
c. I.V. administration of potassium chloride
d. I.V. administration of insulin
e. I.V. administration of sodium bicarbonate
22- As regard to secondary diabetes, which is correct ?
a. A patient can be assumed not to be ketosis-prone
b. Most patients with panhypopituitarism are diabetic
c. Classical diabetic complications do not occur
d. Thiazide diuretics and beta-blockers can both impair insulin secretion
e. Most patients with acromegaly are diabetic
23- The physiological effects of insulin include ……
a. increased glycolysis
b. increased glycogenolysis
c. increased lipolysis
d. increased gluconeogenesis
e. increased protein catabolism
24- Sulphonylurea drug therapy in diabetes mellitus ….
a. causes less weight gain than biguanide therapy
b. increases hepatic gluconeogenesis
c. decreases the number of peripheral insulin receptors
d. decreases hepatic glycogenolysis & gluconeogenesis to reduce hyperglycaemia
e. may be used alone in type 1 DM

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25- Biguanide drug therapy in diabetes mellitus ….

a. is more likely to cause weight gain
b. Increases plasma immunoreactive insulin concentration
c. Decreases pancreatic glucagon release
d. Inhibits hepatic glycogenolysis
e. Causes troublesome constipation
26- The clinical features of acromegaly include the following EXCEPT :
a. Arthropathy & myopathy.
b. Hypertension & impaired glucose tolerance.
c. Goiter & cardiomyopathy.
d. Increased sweating & headache.
e. Skin atrophy & decreased sebum secretion
27- Typical results of investigations in a patient with acromegaly include :
a. Failure of the plasma GH to rise during glucose tolerance test
b. Decreased serum prolactin
c. Increased serum IGF-1
d. Abnormality of the pituitary fossa on plain x ray
e. Tumor shrinkage in response octerotide therapy
28 - Which one of the following is true of atrial natriuretic peptide?
a. It causes increased thirst.
b. It causes salt retention.
c. It causes vasodilatation.
d. It is secreted by the juxtaglomerular apparatus.
e. It suppresses the release of aldosterone.
29- Features of multiple endocrine neoplasia (MEN ) type 1 include which one of the
following ?
a. Adrenal nodules
b. Hyperparathyroidism
c. Hyperthyroidism
d. Hypothyroidism
e. Pheochromocytoma
30- The most likely etiology for the eating disorder anorexia nervosa is
a. decreased levels of luteinizing hormone– releasing hormone (LHRH)
b. decreased levels of growth hormone
c. decreased levels of insulin-like growth factor I
d. low levels of serum thyroxine
e. psychiatric disorder
31- Which of the following is most likely to be associated with increased insulin
sensitivity ?
a. Acromegaly
b. Smoking cessation
c. Pheochromocytoma
d. Polycystic ovary disease
e. Weight loss
32- In metabolic diabetic ketoacidosis ( DKA ) , the treatment of choice is :

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a. Normal saline , IV insulin , metformin.

b. Normal saline , IV insulin , potassium
c. Normal saline , insulin , heparin
d. Normal saline , IV insulin , cortisone
e. IV 5% glucose.
33- In Cushing syndrome which of the following is true ?
a. Esinopenia
b. Basophilia
c. Esinophilia
d. Lymphocytosis
e. Neutropenia
34-The following conditions produce gynecomastia EXCEPT :
a. Digoxin therapy
b. Klinefelter syndrome ( XXY syndrome )
c. Bronchogenic carcinoma
d. XYY karyotype
e. Spironolactone therapy
35- Syndrome of inappropriate ADH secretion may result from EXCEPT :
a. Meningitis
b. Bronchial carcinoma
c. Digoxin therapy
d. Head injury
e. Pneumonia
36- Causes of DI include the following EXCEPT :
a. Congenital disorder
b. Craniopharyngioma
c. DIDMOAD syndrome
d. Severe hypocalcemia
e. Sarcoidosis
37- Which of the following test would most reliably defect a deficiency of the GH axis in
a 19 year-old man ?
a. ACTH stimulation test
b. Arginine test
c. Glucose test
d. Insulin tolerance test
e. TRH administration test
38 - Causes of nephrogenic DI include the following EXCEPT :
a. Lithium
b. Hypokalemia
c. Congenital disorder
d. Chlorpropamide & carbemazepine therapy
e. Renal amyloidosis

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39- A 20 year old lady with a six month history of sweating and diarrhea . She is
otherwise well. Her father and grandmother died in middle age but she is unsure of the
reason why. On examination, no abnormality could be found. Which one of the
following diagnoses would it be important to exclude?
a. Cushing's disease
b. Grave's disease
c. Acromegaly
d. Medullary thyroid carcinoma
e. Premature menopause
40- hypogonadotrophic hypogonadism is typically associated with :
a. Atrophy of the testicular interstitial ( Leydig ) cells
b. Klinefelter's syndrome ( XXY )
c. Isolated GnRH deficiency ( Kallmann's syndrome )
d. Hemochromatosis
e. Hepatic cirrhosis
41- A patient comes in for a fasting plasma glucose test .On two separate occasion , the
result has been 115 and 120 mg/dl which of the following is the most appropriate next
step ?
a. Reasurance that these are normal blood sugar
b. Recommend weight loss and exercise.
c. Diagnose DM and start a sulfonylurea agent
d. Recommend cardiac stress test
e. Hospitalize him urgency
42- A 45 year-old obese woman presents for follow up of her diabetes. She currently
take glipizide ( sulfonylurea) 10 mg twice per day, and her fasting morning glucose is
180 mg/dl. Her last HbA1c was 7.9 . She states that she conscientiously follows her diet
and that she walks 45 minutes daily. What is the best next step in her care ?
a. Add an insulin pump
b. Add metformin
c. Add NPH insulin
d. Hospitalize her urgency
e. Add antibiotic
43- The finding of reduced free T4 & TSH is compatible with :
a. Hypopituitarism
b. 1ry hypothyroidism
c. Nephrotic syndrome
d. Pregnancy
e. 2ry hyperthyroidism
44- The following factors are most likely to cause hyperprolactinemia EXCEPT :
a. Breast stimulation
b. Levo dopa
c. Antipsychotics & antiemetics.
d. Renal failure
e. hypothyroidism

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45- A 33-year old woman is noted to have Grave's disease .Which of the following is the
best therapy ?
a. Long term propranolol.
b. Lifelong oral propylthiouracil ( PTU )
c. Radioactive iodine ablation
d. Surgical thyroidectomy
e. Lifelong SC insulin
46 - The clinical features of thyrotoxicosis include the following EXCEPT :
a. atrial fibrillation
b. weight loss & amenorrhea
c. proximal myopathy
d. exophthalmos
e. decreased insulin requriments in type 1 DM
47- Causes of hypercalcemia include EXCEPT
a. bone metastases
b. carcinomas secreting PTH like peptides
c. Addison's disease
d. severe hypothyroidism
e. chronic sarcoidosis
48- In 1ry hyperaldosteronism ( Conn's syndrome) …
a. peripheral edema is usually present
b. proximal myopathy is due to hypokalemia
c. severe hypertension is characteristic
d. DM is often present
e. hypertension is associated with hyperreninemia
49 - Which one of the following is characteristic of insulin resistance ?
a. acanthosis nigricans
b. nephropathy
c. retinopathy
d. hypoglycemia
e. peripheral neuropathy
50 – In diabetic patient , clinical feature suggesting hypoglycemic coma rather than
DKA include …
a. systemic hypotension
b. air hunger
c. abdominal pain
d. moist skin & tongue
e. hyporeflexia

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Answers
1- a ) somatostatin.
GHRH , Hypoglycemia , insulin , arginine , serotonin → ↑GH.
2- c) A high renin level
Renal artery stenosis results in high renin and high aldosterone levels in contrast to Conn's
syndrome in which the aldosterone level is high but the renin is characterisitically suppressed.
3-b) upper airway obstruction at night.
Grossly obese patients are more likely than are the nonobese to have high blood pressure, peripheral
vascular disease, cerebrovascular disease, diabetes, and hyperlipidemia. The so-called Pickwickian
syndrome, which is characterized by hypersomnolence during the day, is thought to be due to nocturnal
upper airway obstruction that leads to hypoxemia and hypercapnia and causes arousal with each
episode.This chronic arousal pattern at night causes sleep deprivation and daytime somnolence.
Hyperinsulinemia, insulin resistance, diabetes, and hyperlipidemia may all be more common in obese
persons but are not believed to play a role in the obesity-hypoventilation syndrome or in daytime
somnolence.
4- b) Cholelithiasis
5- c) Phenoxybenzamine followed by propranolol
Pheochromocytomas produce and secrete catecholamines, which may lead to paroxysmally high
blood pressure. It is important to prepare the patient for surgery by preventing the effects of
catecholamine release through treatment with phenoxybenzamine, a long-acting-adrenergic
blocker. Beta blockers should not be given before alpha blockade has been established because of
the potential for hypertension as aresult of the antagonism of beta-mediated vasodilation in
skeletal muscle beds. However, propranolol is useful in treating the reflex tachycardia induced by
phenoxybenzamine. While prazosin is an effective agent for the treatment of hypertensive crises
associated with pheochromocytoma, its use as a primary agent in the management of this disorder
has not been established.
6- c) Hypokalemia
About half of patients with hypomagnesemia may become hypokalemic (the mechanism is unclear,
but secondary hyperaldosteronism may play a role). This hypokalemia is refractory .
Hyponatremia is not a known consequence of hypomagnesemia. Because of QT prolongation,
dangerous arrhythmias are more likely to occur.
7- b) malignancy.
hypercalcemia and hypophosphatemia without elevated levels of PTH are likely to have the
hypercalcemia of malignancy. Patients with excessive levels of vitamin D would
not be expected to have a low serum phosphate. Second, patients with familial hypocalciuric
hypercalcemia, an autosomal dominant trait, often have normal or slightly low levels
of immunoreactive parathyroid hormone. It is now clearly recognized that many solid tumors,
including carcinomas of the lung and kidney, may produce (PTH like) that will not be
identified by the currently available assays that detect true parathyroid hormone elaborated
from the parathyroid gland.

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8- e) Asymptomatic hypercalcemia.
At present, this is the most common source of diagnoses of hyperparathyroidism. A solitary
parathyroid adenoma is the most common cause of asymptomatic hypercalcemia.
9- a) Metoclopramide
Medications are important causes of hyperprolactinemia include dopamine-blocking drugs (e.g.,
phenothiazines, , metoclopramide, methyldopa and reserpine)
10- b) propylthiouracil therapy with the goal of maintaining her thyroid function
tests in the high-normal or slightly high range.
Radioactive iodine should never be given to a pregnant woman. In addition, both methimazole and
beta blockers should be avoided in pregnant women. Antithyroid drugs, including
propylthiouracil, cross the placenta and affect fetal thyroid function Studies have shown that when
a treated pregnant woman’s thyroid function is in the mid-normal range, the fetus is hypothyroid.
When the mother’s thyroid tests are maintained in the high-normal or slightly hyperthyroid range,
the fetus is likely to have normal thyroid function.
11- b) potassium.
The mainstay of therapy for diabetic ketoacidosis (DKA) is insulin and intravenous fluids. DKA
cannot be reversed without insulin. Although the serum K concentration is high,. The K
concentration will drop quickly due to insulin therapy (due to intracellular shift) .
Because glucose levels drop more quickly than ketones disappear from the plasma, it is usually
necessary to give intravenous dextrose when the blood glucose level drops below about (250 to
300 mg/dL). This allows continued administration of insulin to clear the ketones from the blood..
Bicarbonate therapy is not recommended unless the arterial pH falls below 7.10 or 7.00 because
the rapid alkalinization may impair oxygen delivery to tissues and impair left ventricular function.
In addition, insulin therapy is effective in reversing the acidemia without the assistance of
bicarbonate therapy.
12- b) Successive fasting plasma glucose 147, 165, and 152 mg/dL in an asymptomatic woman
persistent fasting hyperglycemia even if it is asymptomatic, has been recommended by the
National Diabetes Data Group as a criterion for the diagnosis of diabetes.
Abnormal glucose tolerance—whether after eating or after a standard “glucose tolerance test”—can
be caused by many factors (e.g., anxiety, infection or other illness) Similarly, glycosuria may have
renal as well as endocrinologic causes. Therefore, these two conditions cannot be considered
diagnostic of diabetes. Gestational diabetes is diagnosed in women between the 24 – 28 weeks of
gestation, first using a 50-g oral glucose load , if the 1-h glucose level 140 mg/dL; a 100-g oral
glucose test is performed after an overnight fast. Gestational diabetes is initially treated with
dietary measures; if the postprandial glucose level remains elevated, insulin therapy is often
started. About 30% of women with gestational diabetes will eventually develop true DM.
13- a) Fine-needle aspiration biopsy
Fine-needle aspiration biopsy is indicated in all patients with solitary thyroid nodules.
Approximately 5% of all solitary thyroid nodules are thyroid carcinomas.
14- b) Improved control of blood glucose concentrations.
Improved glycemic control produced a remarkable reduction in the rate of the development of
retinopathy. It should be noted that better control of hyperglycemia lowers but does
not eliminate the risk of retinopathy and other complications of diabetes mellitus.

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15– b) Pentamidine ( Antiprotozoal )

Insulin, sulfonylureas, disopyramide, and pentamidine all cause hypoglycemia through
hyperinsulinemia. Thiazides can cause hyperglycemia.Beta agonists (e.g. epinephrine ) and calcium
channel blockers have no effect on serum glucose levels. Acetaminophen when taken in normal
dosages does not affect the serum glucose concentration; however, an overdose causing hepatic
damage could lead to severe hypoglycemia.
16- b) Hepatoma
17- d) increased serum creatine phosphokinase
Decreased QRS amplitude on ECG is common. Elevated creatine phosphokinase and lactic
dehydrogenase serum values may mimic a myocardial infarction. Hypothyroidism also is typically
associated with macrocytic anemia caused by coexistent pernicious anemia or unknown factors.
Serum cholesterol is elevated in many patients with primary hypothyroidism.

18- c) urine albumin.

Diabetic nephropathy may be functionally silent for 10 to 15 years. Clinically detectable diabetic
nephropathy begins with the development of microalbuminuria (30 to 300 mg of albumin /day).
The glomerular filtration rate actually may be elevated at this stage. Only after the passage of
additional time will the proteinuria be overt enough (0.5 g/L) to be detectable on standard urine
dipsticks. Microalbuminuria precedes nephropathy in patients with both type 1 & 2 DM. An
increase in kidney size also may accompany the initial hyperfiltration stage. Once the proteinuria
becomes significant enough to be detected by dipstick, a steady decline in renal function occurs, with
the glomerular filtration rate falling an average of 1 mL per minute per month.Hypertension
clearly is exacerbating factor for diabetic nephropathy.
19-b) The critical test for the diagnosis of chronic adrenal insufficiency is Synthetic
ACTH test
autoimmune adrenal destruction is the most common cause. The critical test for the diagnosis of
chronic adrenal insufficiency is the synthetic ACTH stimulation test. Synthetic ACTH is administered
in a 250 µg intravenous bolus, and plasma cortisol levels are measured 30 and 60 minutes afterward.
Values greater than 20 µg/dl exclude 1ry adrenal insufficiency. The differential diagnosis of adrenal
insufficiency requires the discrimination of primary and secondary causes. The most useful test for
this is measurement of the ACTH level. ACTH levels greater than normal in primary disease; below
than normal in secondary disease. Primary chronic adrenal insufficiency is treated with oral
hydrocortisone & Fludrocortisone (aldosterone). Chronic secondary adrenal insufficiency is treated in
the same way as chronic primary disease but with replacement of hydrocortisone only, not
aldosterone.
20 a) The most common causes of secondary hyperaldosteronism are congestive
heart failure and cirrhosis with ascites
Primary hyperaldosteronism is caused by benign adrenal adenomas, which are typically unilateral
and are usually less than 2.5 cm in diameter. Patients present with mild hypertension without edema
due to renal escape phenomenon. Laboratory testing shows hypernatremia , hypokalemia and
metabolic alkalosis not acidosis. Diagnosis is confirmed by elevated plasma aldosterone levels (> 14
ng/dl) & suppressed plasma renin activity .The treatment of primary hyperaldosteronism is
unilateral adrenalectomy, preferably by a laparoscopic procedure. Secondary hyperaldosteronism
may or may not be associated with hypertension.

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21- e) I.V. administration of sodium bicarbonate

Administration of bicarbonate is not generally required in most cases of DKA and is
generally reserved for treatment of severe acidosis (pH < 7.0 or HCO3 < 10)
22- d) Thiazide diuretics and beta-blockers can both impair insulin secretion
Secondary diabetes causes all the same complications as primary diabetes, including DKA.
15% of patients with acromegaly are diabetic
23- a) increased glycolysis
24- d) decreases hepatic glycogenolysis & gluconeogenesis to reduce hyperglycaemia
25- d) Inhibits hepatic glycogenolysis
Biguanide is more likely to cause weight loss than weight gain. There is no increases of plasma
immunoreactive insulin concentration , hence does not cause hypoglycaemia in non-diabetics.
Biguanide causes diarrhea which may limit drug compliance.
26- e ) skin atrophy & decreased sebum secretion.
27- c) Increased serum IGF-1
GH normally falls during the glucose tolerance test. Increased serum prolactin occurs in 30%.
Octerotide reduces GH secretion but not tumor size.
28- c) It causes vasodilatation
Atrial natriuretic peptide is a peptide hormone secreted from the myocardium & causes natriuresis
( excretion of Na ) .It is released under conditions of hypervolemia ( myocardial stretch ) and its
actions are : ↓thirst , vasodilatation & excretion of Na . It acts directly on the kidney rather than
via suppression of aldosterone.
29- b) Hyperparathyroidism
MEN type 1 : Hyperparathyroidism , pituitary tumor & pancreatic tumor ( insulinoma )
MEN type 2 : Hyperparathyroidism , medullary thyroid cancer & pheochromocytoma.
30- e ) psychiatric disorder
The disease usually begins shortly after puberty and is characterized by profound weight loss
caused by a lack of caloric intake and a high level of physical activity. Other features include cold
intolerance caused by a secondary defect in regulatory thermogenesis, hypothalamic amenorrhea,
hypokalemia, low serum immunoglobulins, normal or elevated growth hormone levels, decreased
levels of IGF 1 , and low serum T3 concentrations. All these abnormalities seem to result from,
rather than cause, the eating disorder. Most authorities favor a psychiatric etiology. Unfortunately,
the benefits of psychiatric intervention and behavior modification have been somewhat marginal.
Hospitalization may be required to save the patient’s life if the anorexia nervosa is severe.
31- e) weight loss
32- b) Normal saline , IV insulin , potassium.
33- a) Esinopenia
Cortisone increases RBCs , Neutophils & decreases esinophilis , lymphocytes , basophilis.
34- d) XYY karyotype.
35- c) digoxin therapy.
36- d) severe hypocalcemia.

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37-d) insulin tolerance test.

38- d) Chlorpropamide & carbemazepine therapy
39- d) Medullary thyroid carcinoma
Medullary thyroid carcinoma (MTC) can secrete a variety of peptides and prostaglandins ,
resulting in extra-thyroid symptoms. Diarrhea and sweating are the most common. It is an
important tumor to exclude since it can metastasise early. MTC can be inherited as part of MEN
type 2 .
Acromegaly can also cause sweating due to sweat gland hypertrophy , but usually not diarrhea.
Cushing's disease also rarely presents with these symptoms. Both these conditions also rarely show
such strong family history
40- c) Isolated GnRH deficiency ( Kallmann's syndrome )
In a case of Atrophy of the testicular interstitial ( Leydig ) cells , serum LH is elevated.
In Klinefelter's syndrome , serum FSH is elevated.
Hemochromatosis : testicular damage with hypergonadotrophic.
41- b) Recommend weight loss and exercise.
By diagnostic criteria ,this patient falls into the definition of impaired fasting glucose (pre diabetes ).
Although he does not yet meet the criteria for diabetes , he is at greater risk for developing diabetes
in the future and for macrovascular disease. Intervention such as weight loss will decrease his
insulin resistance , and following a diet lower in simple sugar and fats may place less stress on his
pancreas and increase the time to development of diabetes.
42- b) Add metformin
Because this patient is obese & young type 2 diabetic . Insulin may be associated with weight gain
,and most patients prefer to be maintained on oral agents rather than injections, if possible
43- a) Hypopituitarism
44- b) levo dopa
45- c) Radioactive iodine ablation
It is the definitive treatment for Grave's disease. Surgery is indicated for obstructive symptoms or
for women during pregnancy.
46- e ) decreased insulin requirements in type 1 DM.
47- d) severe hypothyroidism
48- b) proximal myopathy is due to hypokalemia.
49- a) acanthosis nigricans.
50- d) moist skin & tongue.

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Collections of endocrine
Endocrinal emergencies :
a. Diabetic comas.
b. Thyroid emergencies :
i. Thyrotoxic crisis.
ii. Myxoedema coma.
c. Parathyroid emergencies :
i. Acute hypercalcemia.
ii. Tetany.
d. Addisonian crisis.

Endocrinal manifestations of systemic diseases :

a. Liver cell failure : (↑ADH & ↑aldosterone )
i. In ♂: gynecomastia , ♀pubic hair , ↓libido.
ii. In ♀: breast atrophy , ♂pubic hair , ↓libido.
b. Chronic renal failure :
i. 2ry & 3ry hyperparathyroidism.
ii. Hyperprolactinemia.
c. T.B. ( miliary ) : Addison’s disease.
d. Heamochromatosis :
i. DM.
ii. Hypogonadism.
e. Sarcoidosis :
i. DI.
ii. Addison’s disease.
f. Malabsorption: 2ry hyperparathyroidism.
g. Bronchogenic carcinoma,Hepatoma& hypernephroma :
Endocrinal manifestations of paramalignant syndrome.

Endocrinal causes of HTN :

a. Pituitary : acromegaly.
b. Thyroid : - hypothyroidism → ↑diastolic Bl.P.
- hyperthyroidism → ↑systolic Bl.P.
c. Parathyroid : hyperparathyroidism.
d. Pancreas : DM.
e. Suprarenal : Conn’s , Cushing syndrome, Pheochromocytoma.

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Endocrinal causes of hyperlipidemia :

a. Hypothyroidism.
b. DM.
c. Obesity.
Endocrinal causes of osteoprosis :
a. DM.
b. Hyperthyroidism.
c. Hyperparathyroidism.
d. Cushing syndrome.
e. Osteomalacia.
Macro & micro-vascular complications of DM :
a. Macro :
i. HTN.
ii. Atherosclerosis.
iii. Non healing ulcers & amputations.
b. Micro : ( Triopathy )
i. Retinopathy.
ii. Nephropathy.
iii. Neuropathy.
Immune mediated endocrinal diseases :
a. Type 1 DM.
b. Addison’s disease.
c. Grave’s disease, Hashimoto thyroditis.
Iatrogenic endocrinal diseases :
○ Iodine → hyperthyroidism.
○ Lithium → hypothyroidism.
○ Amiodarone → thyroid dysfunction.
○ Ketoconazole → hyoadrenalism.
○ Metoclopramide → Hyperprolactinaemia.
○ Sympathomimetic → picture like thyrotoxicosis.
○ ACE s inhibitors → hypoldosteronism.
○ Steroid therapy → DM & Cushing syndrome.
○ Thyroxin therapy → thyrotoxicosis ( factitious ).
○ Vitamin D → hypercalcemia.
○ Insulin & oral hypoglycemic → hypoglycemia.
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Approach to patient with polyuria & polydepsia :

Specific gravity ↑↑ Specific gravity ↓

↓

If there is +ve sugar H2O deprivation for 12 h.

in urine

DM No response Good response

DI Psychogenic
polydepsia

Give ADH

Good response No response

Pituitary DI Nephrogenic DI

Approach to patient with hypothyroidism :

Determine TSH & free T4

Free T4 : normal Free T4 : ↓ Free T4 : ↓ Free T4 : ↑

TSH : normal TSH :↑ TSH :normal or ↓ TSH :↑

euthyroid 1ry 2ry Thyroid hormone

hypothyroidism hypothyroidism resistance
resistance

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