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TAS > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Embryology of thyroid

A

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

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2
Q

Results for primary hyperthyroidism

A

Low TSH
High T3 T4

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3
Q

Results for secondary hyperthyroidism

A

High TSH
High T3 T4

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4
Q

Results for Primary hypothyroidism

A

High TSH
Low T3 T4

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5
Q

Results for secondary hypothyroidism

A

Low TSH
Low T3 T4

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6
Q

Causes of hyperthyroidism

A

Grave’s disease
Toxic multi nodular goitre
Drugs - amiodarone

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7
Q

Causes of hypothyroidism

A

Drugs - lithium
Hashimoto’s thyroiditis - autoiminue, ass/ T1DM
Subacute thyroiditis - De Quervain’s
Iodine deficiency

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8
Q

Embryology of parathyroid

A

Inferior parathyroid comes from 3rd pharyngeal pouch
Superior comes from 4th pharyngeal pouch

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9
Q

Blood supply to parathyroid

A

Thyroid arteries

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10
Q

What stimulates release of PTH

A

Hypocalcemia, hypomagnesium, hypophosphate

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11
Q

Actions of PTH

A

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

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12
Q

Hypothalamus-pituitary axis

A

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

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13
Q

What causes congenital adrenal hyperplasia

A

Defect in 27 hydoxylase enzyme

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14
Q

Physiology of CAH

A

27 Hydoxylase enzyme converts progesterone to aldosterone and cortisol
Progesterone also is converted to testosterone
Defect in 27 hydoxylase causes more conversion to testosterone

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15
Q

Blood results for CAH

A

High testosterone
Low aldosterone and cortisol

HYPONATRAEMIC HYPERKALAEMIC HYPOGLYCAEMIA

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16
Q

How is CAH inherited?

A

Autosomal recessive

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17
Q

Signs and symptoms of CAH

A

Female - tall, deep voice, early puberty, facial hair, absent periods
Male - tall, deep voice, large penis, small testicles, early puberty

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18
Q

ACTH and melatonin

A

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

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19
Q

Management of CAH

A

Replace glucocorticoid (Cortisol) with hydrocortisone
Replace mieralcorticoid (aldosterone) with fludrocortisone

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20
Q

Embryology of gonads

A

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

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21
Q

Male development

A

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

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22
Q

What types of cells do testes form?

A

Germ cells - produces spermatogonia
Leydig cells - synthesis of testosterone
Sertoli cells - synethesis anti-mullerian hormone

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23
Q

Female development

A

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

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24
Q

Type of Ovarian cells

A

Germ cells - produce oogonia
Granulosa cells - synthesis estradiol
Theca cells - produce synthesise progesterone

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25
Q

What is gonadranche

A

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

26
Q

What is adrenarche

A

Adrenal gland activated
Pubic hair, oily skin and hair, body odour

27
Q

What is thelarche

A

Breast development
Precedes menarche by 2 years

28
Q

What stage is Menarche?

A

Usually Tanner stage 4

29
Q

Central causes of precious puberty

A

GnRH -dependent -
-Idiopathic
-Hypothyroidism
- Obesity
-Silver-rusell syndrome

30
Q

Peripheral causes of precious puberty

A

GnRH independent
- Congenital adrenal hyperplasia
-Gonadal tumour
-HCG secreting tumours in liver

31
Q

When would you say someone has delayed puberty

A

Girls - no breast development by 13
Boys - testicular not filled to 4mls by 14
Primary amenorrhea by 16

32
Q

How is Kellman’s Syndrome inherited

A

X-linked recessive trait

33
Q

What Is Kellman’s syndrome

A

Delayed puberty secondary to hypogonadatrophic hypogonadism
Failure of GnRH secreting hormone to hypothalamus

34
Q

What does Kellman’s syndrome cause

A

Delay in puberty
Anosmia

35
Q

Action of cortisol

A

Stress response
Insulin counter-regulatory hormone
Increased gluconeogenesis, hepatic glycogenolysis and ketogenesis

35
Q

Normal puberty in girls - Tanner Stages

A

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

36
Q

Tanner stages in Males

A

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

37
Q

What does vasopressin / ADH do?

A

Increases water permeability of collecting ducts
Increases water reabsorbed back into the circulation

38
Q

What illnesses do you see SIADH in?

A

Pneumonia
Lymphoma
Meningitis
Cranial abscess
Trauma

39
Q

SIADH

A

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

40
Q

Signs of diabetes insipidus

A

Polyuria
Polydipsia
Increase freq and nocturnal enuresis

41
Q

What is nephrogenic diabetes insipdus

A

Insensitivty to ADH at the collecting duct In kidney

-Desmopressin has no affect on urinary concentration

42
Q

What is cranial diabetes insides

A

lack of production of ADH (vasopressin)

43
Q

What is nephrogenic diabetes insipdus

A

lack of response to ADH

44
Q

Where is ADH produced

A

hypothalamus

45
Q

Where is ADH released

A

posterior pituitary

46
Q

Causes of nephrogenic diabetes insipdus

A

Medications - lithium
Genetic mutations - X-linked inheirtance
Hypercalcamia
Hypokalaemia
Kidney disease

47
Q

Causes of cranial diabetes insipidus

A

Brain tumours
Brain injury
Brain surgery
Wolfram syndrome - genetic condition optic atrophy, deafness and diabetes mellitus

48
Q

What do investigation show

A

low urine osmolality
High/ normal serum osmolality
>3 litres in collection in 24 hours
Water deprivation test

49
Q

How does water deprivation test work? Desmopressin deprivation test

A

Avoid fluid for 8 hours
Test urine osmality - if low, give ADH (Desmopressin)

50
Q

What result rules of diabetes insidious

A

high urine osmality in Desmopressin deprivation test

51
Q

Results of cranial disipidus

A

Urine osmality low pre Desmopressin
High post Desmopressin

Kidneys can respond to ADH

52
Q

Results of nephrongenic

A

Low urine osmality pre
Low post

Kidneys can’t respond to aDH

53
Q

where is renin secreted from

A

Juxtaglomerular cells in afferent arterioles in kidney

54
Q

When is renin secreted

A

in response to Low blood pressure

55
Q

How does renin increase blood pressure

A

Converts angiotensin to angiotensin I in liver
Moves to lung to be converted to angiotensin II

56
Q

how does angiotensin II act on blood pressure

A

causes vasoconstriction
Stimulates release of aldosterone

57
Q

Three functions of aldosterone

A

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

58
Q

what is the most common cause for primary testicular failure

A

Kleinfelter’s syndrome

59
Q

Features of Kleinfelter’s syndrome

A

47 XXY

Caused by nondisjunction at stage 1 or 2 of meiosis

60
Q

Blood results in Addison’s

A

hyponatreamic
hyperkalemia

Lack of cortisol

61
Q
A

TAS (18 decks)

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