Endocrine Flashcards
Embryology of thyroid
First and second pharyngeal pouches
Forms from base of tongue
In 3rd week - endoderm cells of primitive pharynx proliferate creating thyroid diverticulum
Proliferation of cells bifurcates and descends into neck as two-lobed diverticulum
7th week - anterior neck forms 2 lateral lobes connected by central isthmus
Results for primary hyperthyroidism
Low TSH
High T3 T4
Results for secondary hyperthyroidism
High TSH
High T3 T4
Results for Primary hypothyroidism
High TSH
Low T3 T4
Results for secondary hypothyroidism
Low TSH
Low T3 T4
Causes of hyperthyroidism
Grave’s disease
Toxic multi nodular goitre
Drugs - amiodarone
Causes of hypothyroidism
Drugs - lithium
Hashimoto’s thyroiditis - autoiminue, ass/ T1DM
Subacute thyroiditis - De Quervain’s
Iodine deficiency
Embryology of parathyroid
Inferior parathyroid comes from 3rd pharyngeal pouch
Superior comes from 4th pharyngeal pouch
Blood supply to parathyroid
Thyroid arteries
What stimulates release of PTH
Hypocalcemia, hypomagnesium, hypophosphate
Actions of PTH
Increased levels of serum calcium by
Increasing osteoclasts to increase calcium reabsorption from bone to blood
Increases calcium reabsorption in distal convuluted tubule - less excreted in urine
Convert vit d to calciférol in kidneys to promote calcium absorption in the intestines
Hypothalamus-pituitary axis
Dopamine inhibits prolactin
TRH stimulates TSH + T3 T4
CRH stimulates ACTH + cortisol
Somatostatin - GH
GHRH + GH + IGF’S
GnRH + FSH LH + Andogrens estrogen and progesterone
What causes congenital adrenal hyperplasia
Defect in 27 hydoxylase enzyme
Physiology of CAH
27 Hydoxylase enzyme converts progesterone to aldosterone and cortisol
Progesterone also is converted to testosterone
Defect in 27 hydoxylase causes more conversion to testosterone
Blood results for CAH
High testosterone
Low aldosterone and cortisol
HYPONATRAEMIC HYPERKALAEMIC HYPOGLYCAEMIA
How is CAH inherited?
Autosomal recessive
Signs and symptoms of CAH
Female - tall, deep voice, early puberty, facial hair, absent periods
Male - tall, deep voice, large penis, small testicles, early puberty
ACTH and melatonin
Byproduct of production of ACTH is melanocyte stimulating hormone
Ant. pit. releases more ACTH in response to low cortisol more converted to MSH
MSH caused hyperpigmentation by melatonin
Management of CAH
Replace glucocorticoid (Cortisol) with hydrocortisone
Replace mieralcorticoid (aldosterone) with fludrocortisone
Embryology of gonads
5th weeks - gonadal ridge develops
6th week - primordial germ cells migrate from yolk sac to gonadal ridge
7th week - primordial Ferm cells promote sexual differentiation
8th Week - Wolfian and Mullerian duct differentiate into rest of reproductive system
Male development
Gene expression in sex-determining region of Y choromosome (SRY) is prompted
Promotes testis determining factor production - gonadals transform to testis
Wolffian ducts transform to internal male reproductive system
What types of cells do testes form?
Germ cells - produces spermatogonia
Leydig cells - synthesis of testosterone
Sertoli cells - synethesis anti-mullerian hormone
Female development
No SRY
Development of ovaries doesn’t being until week 9
10th week - ovarian cortex and inner medulla distinguishable
Mullerian dust -> female genitalia
Lack of testosterone degenerates Wolffian duct
Lack of anti-mullerian hormone allows mullein duct to persists
Type of Ovarian cells
Germ cells - produce oogonia
Granulosa cells - synthesis estradiol
Theca cells - produce synthesise progesterone
What is gonadranche
Gonadal activation by LH and FSH
Males - LH works on leading cells to produce testosterone, FSH works of Sertoli cells to produce sperm
Females - LH works on ovarian follicles to produce progesterone and androstenedione
What is adrenarche
Adrenal gland activated
Pubic hair, oily skin and hair, body odour
What is thelarche
Breast development
Precedes menarche by 2 years
What stage is Menarche?
Usually Tanner stage 4
Central causes of precious puberty
GnRH -dependent -
-Idiopathic
-Hypothyroidism
- Obesity
-Silver-rusell syndrome
Peripheral causes of precious puberty
GnRH independent
- Congenital adrenal hyperplasia
-Gonadal tumour
-HCG secreting tumours in liver
When would you say someone has delayed puberty
Girls - no breast development by 13
Boys - testicular not filled to 4mls by 14
Primary amenorrhea by 16
How is Kellman’s Syndrome inherited
X-linked recessive trait
What Is Kellman’s syndrome
Delayed puberty secondary to hypogonadatrophic hypogonadism
Failure of GnRH secreting hormone to hypothalamus
What does Kellman’s syndrome cause
Delay in puberty
Anosmia
Action of cortisol
Stress response
Insulin counter-regulatory hormone
Increased gluconeogenesis, hepatic glycogenolysis and ketogenesis
Normal puberty in girls - Tanner Stages
Stage 1 - pre-adolescent
Stage 2 - breast bud formation, sparse growth of pubs hair
Stage 3 - Further enlargement and elevation of breast and papilla with no separation of their contours , hair spreads over junction of pubis and becomes darker, axillary hair - adult in quantity and type
Stage 4 - Projection of areola and papilla to form a secondary mound
Stage 5 - mature stage with projection of papilla only, adult hair in quantity and type
Tanner stages in Males
S1 - pre-adolescent
S2 - Enlargement of scrotum and testes and changes in scrotal skin
S3 - Further growth of testes and scrotum, enlargement of penis
S4 - Increase in breadth of penis and development of glans
S5 - Adult genitals
What does vasopressin / ADH do?
Increases water permeability of collecting ducts
Increases water reabsorbed back into the circulation
What illnesses do you see SIADH in?
Pneumonia
Lymphoma
Meningitis
Cranial abscess
Trauma
SIADH
High levels of ADH
Hyponatreamia
Pass small amount of concentrate urine
Serum osmolality is less than urine osmolality
Water retention due to water reabsorption in distal collecting tubules
High sodium con. in urine
Signs of diabetes insipidus
Polyuria
Polydipsia
Increase freq and nocturnal enuresis
What is nephrogenic diabetes insipdus
Insensitivty to ADH at the collecting duct In kidney
-Desmopressin has no affect on urinary concentration
What is cranial diabetes insides
lack of production of ADH (vasopressin)
What is nephrogenic diabetes insipdus
lack of response to ADH
Where is ADH produced
hypothalamus
Where is ADH released
posterior pituitary
Causes of nephrogenic diabetes insipdus
Medications - lithium
Genetic mutations - X-linked inheirtance
Hypercalcamia
Hypokalaemia
Kidney disease
Causes of cranial diabetes insipidus
Brain tumours
Brain injury
Brain surgery
Wolfram syndrome - genetic condition optic atrophy, deafness and diabetes mellitus
What do investigation show
low urine osmolality
High/ normal serum osmolality
>3 litres in collection in 24 hours
Water deprivation test
How does water deprivation test work? Desmopressin deprivation test
Avoid fluid for 8 hours
Test urine osmality - if low, give ADH (Desmopressin)
What result rules of diabetes insidious
high urine osmality in Desmopressin deprivation test
Results of cranial disipidus
Urine osmality low pre Desmopressin
High post Desmopressin
Kidneys can respond to ADH
Results of nephrongenic
Low urine osmality pre
Low post
Kidneys can’t respond to aDH
where is renin secreted from
Juxtaglomerular cells in afferent arterioles in kidney
When is renin secreted
in response to Low blood pressure
How does renin increase blood pressure
Converts angiotensin to angiotensin I in liver
Moves to lung to be converted to angiotensin II
how does angiotensin II act on blood pressure
causes vasoconstriction
Stimulates release of aldosterone
Three functions of aldosterone
Increases sodium reabsorption in distal tubule
Increase potassium secretion in distal tubule
Increase hydrogen secretion in collecting tubule
When Na is reabsorbed, water follows by osmosis, = increase intravascular volume = increase blood pressure
what is the most common cause for primary testicular failure
Kleinfelter’s syndrome
Features of Kleinfelter’s syndrome
47 XXY
Caused by nondisjunction at stage 1 or 2 of meiosis
Blood results in Addison’s
hyponatreamic
hyperkalemia
Lack of cortisol
