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CLINICAL EXAMINATION OF
ENDOCRINE SYSTEM
 Diabetis mellitus
 Osmotic symptoms
 Hyperglycemia-renal threshold-glycosuria
 despite hyperglycaemia,people with an increased renal
threshold for glucose may have no osmotic symptoms
 D/D
 Diabetis Inspidus
 Central
 Nephrogenic
▪ Inherited
▪ impairment of antidiuretic hormone
action by hypercalcaemia or hypokalaemia
 Psychogenic polydipsia
 Hyperthyroidism
 Type 1 insulin-dependent diabetes mellitus
 Hypopituitarism
 Adrenocortical failure (Addison’s disease)
 Anorexia nervosa
 Simple obesity: energy intake/expenditure
imbalance
 Primary hypothyroidism
 Cushing’s syndrome
 Hypothalamic lesions
 Leptin defciency
 Symmetrical proximal weakness, mainly involving the
shoulder and hip girdle musculature.There is usually
associated muscle wasting
 diffculty in climbing stairs, boarding a bus or rising from a
sitting/squating position
 Painless
 Hyperthyroidism
 Cushing’s syndrome, including iatrogenic steroid myopathy
 Acromegaly
 Painful
 Vitamin D defciency
 Osteomalacia
 Hypothyroidism
 Cold intolerance
 hypothyroidism
 Heat Intolerance
 hyperthyroidism
 constitutional abnormality
 Anxiety
 Hyperthyroidism
 Phaeochromocytoma
 acromegaly
 fine rapid resting tremor- thyrotoxicosis
 D/D
 Tremor frequency:
 low frequency < 4 Hz (cerebellar tremor)
 medium frequency, 4-7 Hz (parkinsonian tremor,
physiological tremor, essential tremor,dystonic
tremor,drug-induced tremor, psychogenic tremor)
 high frequency > 7 Hz (essential tremor,
physiological tremor)
 Palpitations are a heightened, unpleasant
awareness of the heart beat.
 Thyrotoxicosis
 D/D
 paroxysmal tachyarrhythmias
 Dizziness, or a sensation of faintness on
standing
 Postural hypotension – SBP fall >20 mmhg,
DBP fall > 10 mmhg within 3 minutes
 Adrenal insufficiency (exclude Bleeding/GI blood
loss)
 Autonomic neuropathy (Diabetis)
 Drug therapy for essential hypertension
 Decreased visual acuity- spaceoccupying lesions
compressing the optic nerve
 severe dysthyroid eye disease and orbital
or retro-orbital tumours
 Bitemporal hemianopia
 Suprasellar extension of pituitary adenomas compressing
the optic chiasm
 Double vision (diplopia) on lateral or upward gaze
 Medial,lateral, inferior rectus muscle tethering in
dysthyroid eye disease.
 Apparent magnifcation of vision (macropsia)
 hypoglycaemia
 Tachycardia, sweating and tremor -
hypoglycaemia.
 Decreased consiousness
 Autonomous insulin production - insulinoma.
 Glucocorticoid defciency, with or without
thyroxine and growth hormone defciency
(e.g.primary adrenal failure or hypopituitarism)
 Inappropriate insulin or excessive sulphonylurea
drug administration in a diabetic patient
 hepatic failure
 decreased level of circulating ionized calcium
 Hypoparathyroidism
 fall in the ionized component of serum
calcium, owing to an increased extracellular pH
(alkalosis)
▪ respiratory alkalosis - hyperventilatory states
▪ metabolic alkalosis - hypokalaemia
 Hypomagnesaemia
 adrenal insuffciency
 hypercalcaemia
 D/D
 Exclude GI causes
 multinodular thyroid enlargement with
retrosternal extension
 viral subacute thyroiditis (de Quervain’s
thyroiditis)
 autoimmune thyroiditis
 bleeding into a pre-existing thyroid nodule
 Painless enlargement of the thyroid gland (goitre)
presents either with pressure effects- dysphagia,
tracheal compression and stridor, or cosmetic
disturbance
 Reduced erectile potency
 Decreased blood supply to the penis (e.g.
atherosclerosis).
 Neural dysfunction (e.g. autonomic neuropathy
complicating diabetes)
 Testosterone defciency (e.g. hypopituitarism
and primary testicular failure)
 Hyperprolactinaemia
 Drug therapy (e.g. certain antihypertensives (diuretics, beta
blockers, central acting – methyl dopa)
 Psychological factors
 total erectile failure and the absence of nocturnal and morning
erections suggest a physical cause
 “Gynaecomastia” means “woman’s breast” refers to a smooth, firm, mobile,
often tender disc of breast tissue under the areola in the male
Increased oestrogen/testosterone ratio
 Chronic liver disease
 Thyrotoxicosis
 Phenytoin therapy
 Androgen receptor antagonists
 Spironolactone, digoxin
 Inherited androgen receptor defects
 Testicular feminization syndrome
 Testosterone defciency or oestrogen excess
 Primary and secondary hypogonadism
 Tumour production of human chorionic gonadotrophin
(hCG)
 Oestrogen production by Leydig cell tumour of testis
 Congenital and hereditary
 X-linked spinal muscular atrophy (Kennedy syndrome)
 Klinefelter’s syndrome (karyotype XXY)
 primary amenorrhoea - failure of onset of
menses
 hypothalamic–pituitary dysfunction (e.g. due
to tumours)
 ovarian failure (e.g. failure of normal ovarian
development or cytotoxic chemotherapy)
 thyroid dysfunction
 defects in lower genital tract development.
 Secondary amenorrhoea (cessation of previously
established menses
 Idiopathic galactorrhoea, in which there is an
apparent increased sensitivity to normal levels
of serum prolactin.
 Prolactin-secreting tumours of the pituitary
gland.
 Hyperprolactinaemia due to hypothyroidism.
 Hyperprolactinaemia due to dopamine
antagonist drugs.(typical antipsychotics)
 Hyperprolactinaemia due to lactotroph
disinhibiting lesions of the hypothalamopituitary
region.
 Sexual hair – face, Axilla, Pubis
 growth of facial and body hair in adult females -
increased circulating androgens.
Normal
 Pathological causes of hirsutism
include:
 polycystic ovary syndrome
 late presentation of congenital adrenalhyperplasia
 androgen-secreting ovarian or adrenal tumours
 Constipation and abdominal distension -
hypothyroidism or panhypopituitarism.
 Diarrhoea – autonomic neuropathy involving
the gut in diabetes mellitus.
 Peptic ulceration
 Zollinger–Ellison syndrome
 Pigmentation
 Acne
 Pretibial myxedema
 measure weight and height
 Calculate BMI
 Distribution of fat
 cushing syndrome
 Buccal fat pads
 increased fullness and
coarsening of soft
tissues,including the lips and
tongue overgrowth of the
zygoma, orbital ridges and
mandible (prognathism)
 Acromegaly in young
people occurring
before epiphyseal
fusion causes
abnormally tall stature
gigantism
 skeletal proportions should be noted
 Lower segment > Upper segment
& Arm span> height – delayed epiphyseal
fusion
 Eunuchoidism
 Marfan syndrome
 short stature
 failure of secondary sexual
development
 decreased or absent
secondary sexual hair
 an increase in the normal
angulation between
the humerus and the
lower arm
 a low posterior hairline
and an exaggerated fold
of skin between the neck
and shoulder
 Excessive pigmentation occurs in
adrenocorticotrophic hormone (ACTH)-
dependentCushing’s syndrome
 Increased sebum
production causing
greasy skin and acne
on the face and
shoulders may
occur in all causes
of glucocorticoid excess
 hypothyroidism, the skin appears dry, pale,
sallow or even slightly yellow, scalp hair is
coarse and lateral eyebrow hair is thinned
 patchy
depigmentation
of the skin
autoimmune
disorders,
autoimmune
hypothyroidism
& vitamin B12
defciency.
 skin, mostly in the
axillae and nape of
the neck becomes
dark, soft, and
velvet-like with
delicate fold
 acromegaly
 hyperprolactinemia
 diabetes mellitus
 Cushing’s syndrome
 excessive androgen
production
 anterior tibia and dorsum
of the feet and toes,
consisting of nonpitting,
thickenning and induration
of the skin
 Glycosaminoglycans
deposition in the reticular
dermis
 excess hair growth in
an androgen-
dependent
distribution
(hirsutism)
 hair loss in a male
pattern
 indicate increased
circulating androgen
 examination for
evidence of
virilization
 Inspection
 Palpation
 Diffuse enlargement
 Multinodular goitre
 Single nodule
 consistency
 Pubertal development
10 and 11 and takes 3
to 4 years to
complete.
 growth spurt starts
about 1 year before
breast development,
peak height velocity is
reached on average 1
year later, and
menarche follows in
an average of 1 year.
 In males, pubertal
development usually
commences between the
ages of 11 and 12, takes
approximately 3 years to
complete
 testicular development,
beginning of pubic hair,
beginning of growth
spurt and peak height
velocity
 Genital examination in the male should document
testicular volume
 Prepubertal testicular volume is less than 4 ml
 pubertal growth spurt in boys is associated with a
testicular volume of 10 ml
 normal adult testicular volume is in the range
of 15 to 25 ml
 Testicular atrophy in the adult male indicates
hypogonadism, due either to primary testicular
failure, hypothalamopituitary dysfunction or chronic
liver disease
 Visual aquity
 visual fields
 Fundus examination
 corneal calcifcation – hypercalcemia
 exophthalmos (proptosis)
 Lid retraction
 Lid lag
 Fine tremor – thyrotoxicosis
 Proximal muscle weakness - thyrotoxicosis,
glucocorticoid excess and vitamin D defciency
 Hypocalcaemia – neural excitability -Chvostek’s sign
 Tendon reflexes
 abnormally brisk - thyrotoxic patients
 slow relaxation – hypothyroidism
 nerve entrapment syndromes - median nerve at the
wrist (carpal tunnel syndrome)
 Hypothyroidism
 acromegaly

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Clinical examination of endocrine system

  • 2.  Diabetis mellitus  Osmotic symptoms  Hyperglycemia-renal threshold-glycosuria  despite hyperglycaemia,people with an increased renal threshold for glucose may have no osmotic symptoms  D/D  Diabetis Inspidus  Central  Nephrogenic ▪ Inherited ▪ impairment of antidiuretic hormone action by hypercalcaemia or hypokalaemia  Psychogenic polydipsia
  • 3.  Hyperthyroidism  Type 1 insulin-dependent diabetes mellitus  Hypopituitarism  Adrenocortical failure (Addison’s disease)  Anorexia nervosa
  • 4.  Simple obesity: energy intake/expenditure imbalance  Primary hypothyroidism  Cushing’s syndrome  Hypothalamic lesions  Leptin defciency
  • 5.  Symmetrical proximal weakness, mainly involving the shoulder and hip girdle musculature.There is usually associated muscle wasting  diffculty in climbing stairs, boarding a bus or rising from a sitting/squating position  Painless  Hyperthyroidism  Cushing’s syndrome, including iatrogenic steroid myopathy  Acromegaly  Painful  Vitamin D defciency  Osteomalacia  Hypothyroidism
  • 6.  Cold intolerance  hypothyroidism  Heat Intolerance  hyperthyroidism
  • 7.  constitutional abnormality  Anxiety  Hyperthyroidism  Phaeochromocytoma  acromegaly
  • 8.  fine rapid resting tremor- thyrotoxicosis  D/D  Tremor frequency:  low frequency < 4 Hz (cerebellar tremor)  medium frequency, 4-7 Hz (parkinsonian tremor, physiological tremor, essential tremor,dystonic tremor,drug-induced tremor, psychogenic tremor)  high frequency > 7 Hz (essential tremor, physiological tremor)
  • 9.  Palpitations are a heightened, unpleasant awareness of the heart beat.  Thyrotoxicosis  D/D  paroxysmal tachyarrhythmias
  • 10.  Dizziness, or a sensation of faintness on standing  Postural hypotension – SBP fall >20 mmhg, DBP fall > 10 mmhg within 3 minutes  Adrenal insufficiency (exclude Bleeding/GI blood loss)  Autonomic neuropathy (Diabetis)  Drug therapy for essential hypertension
  • 11.  Decreased visual acuity- spaceoccupying lesions compressing the optic nerve  severe dysthyroid eye disease and orbital or retro-orbital tumours  Bitemporal hemianopia  Suprasellar extension of pituitary adenomas compressing the optic chiasm  Double vision (diplopia) on lateral or upward gaze  Medial,lateral, inferior rectus muscle tethering in dysthyroid eye disease.  Apparent magnifcation of vision (macropsia)  hypoglycaemia
  • 12.  Tachycardia, sweating and tremor - hypoglycaemia.  Decreased consiousness  Autonomous insulin production - insulinoma.  Glucocorticoid defciency, with or without thyroxine and growth hormone defciency (e.g.primary adrenal failure or hypopituitarism)  Inappropriate insulin or excessive sulphonylurea drug administration in a diabetic patient  hepatic failure
  • 13.  decreased level of circulating ionized calcium  Hypoparathyroidism  fall in the ionized component of serum calcium, owing to an increased extracellular pH (alkalosis) ▪ respiratory alkalosis - hyperventilatory states ▪ metabolic alkalosis - hypokalaemia  Hypomagnesaemia
  • 14.  adrenal insuffciency  hypercalcaemia  D/D  Exclude GI causes
  • 15.  multinodular thyroid enlargement with retrosternal extension
  • 16.  viral subacute thyroiditis (de Quervain’s thyroiditis)  autoimmune thyroiditis  bleeding into a pre-existing thyroid nodule  Painless enlargement of the thyroid gland (goitre) presents either with pressure effects- dysphagia, tracheal compression and stridor, or cosmetic disturbance
  • 17.  Reduced erectile potency  Decreased blood supply to the penis (e.g. atherosclerosis).  Neural dysfunction (e.g. autonomic neuropathy complicating diabetes)  Testosterone defciency (e.g. hypopituitarism and primary testicular failure)  Hyperprolactinaemia  Drug therapy (e.g. certain antihypertensives (diuretics, beta blockers, central acting – methyl dopa)  Psychological factors  total erectile failure and the absence of nocturnal and morning erections suggest a physical cause
  • 18.  “Gynaecomastia” means “woman’s breast” refers to a smooth, firm, mobile, often tender disc of breast tissue under the areola in the male Increased oestrogen/testosterone ratio  Chronic liver disease  Thyrotoxicosis  Phenytoin therapy  Androgen receptor antagonists  Spironolactone, digoxin  Inherited androgen receptor defects  Testicular feminization syndrome  Testosterone defciency or oestrogen excess  Primary and secondary hypogonadism  Tumour production of human chorionic gonadotrophin (hCG)  Oestrogen production by Leydig cell tumour of testis  Congenital and hereditary  X-linked spinal muscular atrophy (Kennedy syndrome)  Klinefelter’s syndrome (karyotype XXY)
  • 19.  primary amenorrhoea - failure of onset of menses  hypothalamic–pituitary dysfunction (e.g. due to tumours)  ovarian failure (e.g. failure of normal ovarian development or cytotoxic chemotherapy)  thyroid dysfunction  defects in lower genital tract development.  Secondary amenorrhoea (cessation of previously established menses
  • 20.  Idiopathic galactorrhoea, in which there is an apparent increased sensitivity to normal levels of serum prolactin.  Prolactin-secreting tumours of the pituitary gland.  Hyperprolactinaemia due to hypothyroidism.  Hyperprolactinaemia due to dopamine antagonist drugs.(typical antipsychotics)  Hyperprolactinaemia due to lactotroph disinhibiting lesions of the hypothalamopituitary region.
  • 21.  Sexual hair – face, Axilla, Pubis  growth of facial and body hair in adult females - increased circulating androgens. Normal  Pathological causes of hirsutism include:  polycystic ovary syndrome  late presentation of congenital adrenalhyperplasia  androgen-secreting ovarian or adrenal tumours
  • 22.  Constipation and abdominal distension - hypothyroidism or panhypopituitarism.  Diarrhoea – autonomic neuropathy involving the gut in diabetes mellitus.  Peptic ulceration  Zollinger–Ellison syndrome
  • 23.  Pigmentation  Acne  Pretibial myxedema
  • 24.
  • 25.  measure weight and height  Calculate BMI  Distribution of fat  cushing syndrome  Buccal fat pads
  • 26.  increased fullness and coarsening of soft tissues,including the lips and tongue overgrowth of the zygoma, orbital ridges and mandible (prognathism)  Acromegaly in young people occurring before epiphyseal fusion causes abnormally tall stature gigantism
  • 27.  skeletal proportions should be noted  Lower segment > Upper segment & Arm span> height – delayed epiphyseal fusion  Eunuchoidism  Marfan syndrome
  • 28.  short stature  failure of secondary sexual development  decreased or absent secondary sexual hair  an increase in the normal angulation between the humerus and the lower arm  a low posterior hairline and an exaggerated fold of skin between the neck and shoulder
  • 29.  Excessive pigmentation occurs in adrenocorticotrophic hormone (ACTH)- dependentCushing’s syndrome
  • 30.  Increased sebum production causing greasy skin and acne on the face and shoulders may occur in all causes of glucocorticoid excess
  • 31.  hypothyroidism, the skin appears dry, pale, sallow or even slightly yellow, scalp hair is coarse and lateral eyebrow hair is thinned
  • 32.  patchy depigmentation of the skin autoimmune disorders, autoimmune hypothyroidism & vitamin B12 defciency.
  • 33.  skin, mostly in the axillae and nape of the neck becomes dark, soft, and velvet-like with delicate fold  acromegaly  hyperprolactinemia  diabetes mellitus  Cushing’s syndrome  excessive androgen production
  • 34.  anterior tibia and dorsum of the feet and toes, consisting of nonpitting, thickenning and induration of the skin  Glycosaminoglycans deposition in the reticular dermis
  • 35.  excess hair growth in an androgen- dependent distribution (hirsutism)  hair loss in a male pattern  indicate increased circulating androgen  examination for evidence of virilization
  • 36.  Inspection  Palpation  Diffuse enlargement  Multinodular goitre  Single nodule  consistency
  • 37.  Pubertal development 10 and 11 and takes 3 to 4 years to complete.  growth spurt starts about 1 year before breast development, peak height velocity is reached on average 1 year later, and menarche follows in an average of 1 year.
  • 38.  In males, pubertal development usually commences between the ages of 11 and 12, takes approximately 3 years to complete  testicular development, beginning of pubic hair, beginning of growth spurt and peak height velocity
  • 39.  Genital examination in the male should document testicular volume  Prepubertal testicular volume is less than 4 ml  pubertal growth spurt in boys is associated with a testicular volume of 10 ml  normal adult testicular volume is in the range of 15 to 25 ml  Testicular atrophy in the adult male indicates hypogonadism, due either to primary testicular failure, hypothalamopituitary dysfunction or chronic liver disease
  • 40.  Visual aquity  visual fields  Fundus examination
  • 41.  corneal calcifcation – hypercalcemia
  • 42.  exophthalmos (proptosis)  Lid retraction  Lid lag
  • 43.  Fine tremor – thyrotoxicosis  Proximal muscle weakness - thyrotoxicosis, glucocorticoid excess and vitamin D defciency  Hypocalcaemia – neural excitability -Chvostek’s sign  Tendon reflexes  abnormally brisk - thyrotoxic patients  slow relaxation – hypothyroidism  nerve entrapment syndromes - median nerve at the wrist (carpal tunnel syndrome)  Hypothyroidism  acromegaly

Notes de l'éditeur

  1. Lid retraction, evident as a wide-eyed staring expression, and lid lag, in which depression of the upper lid lags behind the eye in a downward gaze, are due to increased activity of the sympathetic innervation of levator palpebri superioris