Endocrinology

Question 1

Calcium physiology

Answer 1

Low Ca -> increases PTH
-> Bone -> increased resorption of Ca
-> Kidney
     -> Increases Ca reabsorption
     -> Reduces PO4 reabsorption
     -> Increased Vit D -> Gut -> Increase Ca absorption
Thus increases Ca

Low Ca -> PTH -> Increases Ca + PO4

Question 2

Calcium physiology 2

Increase Ca + PO4

Answer 2

Stimulate by LOW Ca, LOW PO4, HIGH PTH

Question 3

Calcium physiology 3

Answer 3

Vit D3 (cholecalciferol - sun, fish, plants
Vit D2 (ergocalciferol) - plants, fungi, yeast
D2 + D3 -> 25OH (liveR)
-> kidney via 1a hydroxylase
-> 1, 25 (OH)2 active form (Calcitriol)
     -> Intestinal Ca + PO4 absorption
     -> Bone mobilises Ca stores
     -> Kidney PCT + DCT resorbs Ca
     -> Inhibits PTH

Question 4

Vitamin D deficiency

Answer 4

Vit D deficiency:
LOW Ca, PO4, 25-D (liver)
HIGH 1, 25D (kidney), PTH

Renal Disease:
LOW Ca, 1,25D (kidney)
HIGH PO4, PTH ++
Normal 25-D (liver)

Vit D dependent Rickets Type 1 (1a hydroxylase mutation):
LOW Ca, PO4, 1,25D
HIGH PTH, ALP
Normal 25D

Vit D dependent Rickets Type 2 (Vit D receptor mutation):
LOW Ca, PO4
HIGH 1,25D++, PTH, ALP
Normal 25 D

Vitamin D resistant Rickets:
LOW PO4, Ca, PTH
HIGH ALP
Normal 25D, 1,25D

X-linked hypophosphataemic rickets (PO4 renal tubular loss):
LOW PO4
HIGH ALP
Normal 25D, 1,25, PTH

Question 5

PTH

Answer 5

PTH
Increases Ca, reduces PO4
Stimulated by: LOW Ca, LOW 1,25D, HIGH PO4

Hyperparathyroidism:
Primary: HIGH Ca, N/H PTH, LOW PO4, HIGH ALP
Secondary: LOW Ca, HIGH PTH/PO2/ALP (e.g. Vit D def, CRF)

Hypoparathyroidism:
LOW PTH, LOW Ca, HIGH PO4 (e.g. DiGeorge)

Pseudohypoparathyroidism:
HIGH PTH/PO4, LOW Ca
Short stature, short 4th/5th metacarpal

Question 6

Pituitary

Answer 6

POSTERIOR: ADH, oxytocin

ANTERIOR: (hypothalamus -> pituitary -> end organ)
TSH (TRH -> TSH -> T3, T4)
ACTH (CRH -> ACTH -> corticosteroids (adrenal cortex))
GH (somatocrinin -> GH -> bone growth, Somatostatin inhibits GH -> slows bone growth)
FSH, LH (GnRH -> FSH, LH -> testosterone, eostrogen/progestins. GnIH inhibits -> FSH, LH)
Prolactin (prolactin releasing peptide -> prolactin. Prolactin inhibiting factor (e.g. dopamine) inhibits prolactin)

Question 7

Congenital adrenal hyperplasia

Answer 7

21-hydroxylase deficiency: 90%
Classical - salt wasting crisis (low Na, high K), females virilised, gender ambiguity rare
Non-classical - mild, symptomatic, amenorrhoea. More in Ashkenazi Jews
HIGH 17OH progesterone/K+/renin/sex hormones, LOW Na/aldosterone/cortisone, LOW BP

11b-hydroxylase deficiency: females virilised
HIGH BP, HIGH sex hormones. LOW K+/aldosterone/low cortisol/renin

17a-hydroxylase deficiency: males ambiguous genitalia. undescended testes. Females lack sexual development
HIGH aldosterone, BP. Low K+/cortisone/sex steroids

Primary adrenal insufficiency: loss of gland function
HyPerPigmentation, LOW Na/Cortisol/BSL, HIGH K/ACTH
Causes: CAH, autoimmune (APES, Addison)

Secondary adrenal insufficiency: low pituitary aCTH production. Skin Spared.
Causes: tumour, radiotherapy, surgery
LOW ACTH/Na/cortisole/BSL, HIGH K

Tertiary adrenal insufficiency: from Treatment (exogenous steroid use)

Addisons: primary adrenal insufficiency, low cortisol

Conn: HIGH aldosterone, LOW renin