Extras Flashcards
PTH acts on what
OSTEOBLASTS!!!
Where does leptin act
receptors in hypothlamus and choroid plexus where initiates appetite by counteracting the effects of neuropeptide Y (potent appetite stimulator) and promoting synthesis of alpha melanocyte stimulating hormone- an appetite supressant
Ghrelin does what
stimulates growth hormone secretion
produced by stomach and pancreas
stimulates appetite
REDUCD GHRELIN may partially account for the effect of some obesity surgery
glucagon achieves what
Glucagon increases gluconeogenesis and glycogenolysis
what is the transporter for glucose reuptake in kidney?
SGLT
1 is low capacity high affinity (in S3)
2 (in S1) is low affinity high capacity- 90%
in type 2 DM this capacity is increased!
Once in the ep cells, uses GLUT to get into blood
NOT GLUT!!!!
Role of PPAR gamma
adipocyte differentiation and prolif, fatty acid uptake and storage
What is HNF?
hepatocyte nuclear factors
transcription factors in the liver
mutation leads to MODY 3 and renal cysts
important in pancreatic beta cells to regulate expression of the insulin gene and genes involved in glucose transport
IN MODY there is no problem with actual insulin, but glucose sensing and secretion impaired
what converts vitamin D to active and where
1 alpha hydroxylase in prox tubule cells
What happens to vit D and calcium in preg
increase 1,25 and 25 vitamin D
placenta has 1 alpha hydroxylase activity
hence increase calcium in preg
GLP-1 actions
decreases glucagon
increases insulin
reduces gastric emptying
reduces appetite
FIRST thing that happens with hypoglycaemia
reduced insulin secretion
next increase glucagon
third adrenaline (which also blocks more insulin secretion via alpha 2 adrenergic effects)
GH begins to rise after hours, cortisol too
glucagon does what
gluconeogenesis glycogenolysis lipolysis ketosis increase satiety and decrease food intake thermogenesis and energy expend increase increase bile acid synthesis
How does primary adrenal insuff cause low sodium
cortisol def–>By increasing CRH–>stimulates ADH release
If aldosterone low–>renal sodium loss, hypovolaemia adn baroreceptor mediated ADH release
what does amoiodarone do peripherally
reduces conversion of T4 to T3
thyroglobulin good in what cancers
papillary
follicular
If thyroglobulin is detectable on thyroxine treatment, it will increase after thyroxine has been withdrawn
adrenal incidentaloma over 4cm, think
cancer- even if not doing anything, prob resect
How do you define dexameth supression test
failure to fall to less than 50% baseline value
Suppress on 2mg dex sup test…
No suppress on 2mg but suppress on 8mg…
No suppress on 8mg,,,,,
no cushing
cushing disease
ectopic ACTH or adrenal tumour (look at ACTH- adrenal tumour will have low ACTH, etopic ACTH will be high)
If 8mg suppresses and suspect cushing and see tumour or MRI vs no tumour
operate vs inferior petrosal sinus sampling
look for basal ratio central to periph of 2:1 or after CRH of 3:1
what predicts DM in indigenous
age and BMI
lean is protective
some communities have been able to improve insulin resistance, increase red cell folate and reduce homocysteine levels
obestity and thyroid
can look like subclin hypothyroid
TSH up and borderline upper T3
reverses with weight loss
micro or macro more likely to be cured in acromeg
micros- 80% cured
use octreotide and lanreotide pre op in macro to shrink
if no cure, can use octreotide WITH dopamine agonist post to supress
if looks like acromegaly but MRI normal, do CT chest and abdo to look for ectopic
What is pegvisomant
GH receptor antagonist
use where not cured by surgery and not responding to somatostatin analogues
What is KALLMAN syndrome
Anosmia + deficient LH/FSH From HYPOTHALAMUS Usually X linked or AR Usually at puberty diagnosed MRI to exclude hypothalamic causes Hormone replacement Can become fertile
