Endocrinology Flashcards
(72 cards)
Where would a paracrine hormone act?
in local ECF to neighbouring cells
What controls neuroendocrine cells?
synaptic transmission
Where embryologically do the
- ant pituitary
- post pituitary
develop from?
ant - from oralpharynx ectoderm - rathke’s pouch
post - from neural ectoderm, extension of infundibulum
In floor of 3rd ventricle
Where do the hypothalamic parvocellular neurosecretatory cells release hormones?
into the capillaries of the median eminence to ant pituitary
Where do the hypothalamic magnocellular nuclei project to?
post pituitary
Name 3 parameters that cause increased release of GH.
- Hypoglycaemia, starvation
- low FA
- excercise
- sleep
Name 2 parameters that cause decreased release of GH.
- hyperglycemia
- high FA
Outline GH action.
- stimulates liver IGF1 production
- increases lipolysis so increases FA
- increases gluconeogenesis
- stimulates chondrogenesis (more linear growth) up to 20yrs
- stimulates somatic/organ growth
Acromegaly symptoms in adults may include…
…insulin resistance, diabetes and hyperglycemia
-increased mass/thickness of bones
Name whats made in these adrenal cortex layers:
zona glomerulosa -
zona fasiculata -
zona reticularis -
z glomerulosa - mineralocorticoids
z fasiculata - cortisol
z reticularis - testosterone
Explain 2 steps in screening for Cushing’s?
- cortisol levels at night (loss of dinural rhythm)
- dexamethasone 11pm, measure cortisol in morning (los s of negative feedback)
What patient groups might be suspected to have Cushing’s, (but have pseudocushing’s)?
-depressed, alcoholics, anaorexics
baseline higher cortisol level individuals
How do you confirm a diagnosis of Cushing’s/rule out pseudocushings?
Low dose 48hr Dexamethasone Supression Test
should be <50 at end, if not it is true Cushings
How can you determine if Cushing’s is caused by excess ACTH from the pituitary/adrenal or an ectopic site?
High Dose 48hr Dexamethasone Supression Test
if pituitary/adrenal, ACTH should fall to 50% baseline-neg feedback, if ectopic will stay high
What metabolic results may you see in Cushing’s regarding:
- K+ levels
- Glucose
- pH
- hypokalemia
- hyperglycemia
- metabolic alkalosis
Why may you have the following in Cushing’s?
-hypokalemia
-metabolic alkalosis
The mineralocortidoid receptors in kidney respond normally to aldosterone, how does cortisol (usually inactivated as cortisone) have action here?
The enzyme 11BHSD2 which turns cortisol to cortisone can become saturated in cushings so cortisol can act in the same way as aldosterone…
- by retaining Na+ (and lose K+ in return)
- if K+ is depleted, when bringing in Na+ we lose H+ in return (–>low K+, high pH)
Which enzyme turns cortisol to cortisone?
11BHSD2 - 11 B Hydroxysteroid Dehydrogenase 2
Why can you have skin hyperpigmentation in Cushing’s?
-ACTH is a precursor of a-MSH which forms melanin.
Some of the ACTH forms this
How does the CRH test differentiate between all types of Cushing’s Syndrome?
(Results measure ACTH levels…)
- an exaggerated ACTH response will be die to a pituitary tumour. It is sensitive to CRH levels.
- an adrenal adenoma will be low. As its system is sensitive to ACTH levels, not CRH, so v low (no ACTH)
- ectopic will be high, no neg feedback
Give 5 symptoms of Addison’s disease?
- weight loss, hypoglycemia
- postural hypotension
- hyponatremia, salt craving
- hyperkalemia, acidosis
- nausea (steroids close pores that allow BBB to detect toxins, low steroids -> open pores -> more nausea)
Name 3 causes of Addison’s disease.
- autoimmune condition (e.g. from TB)
- steroid withdrawal (adrenal cortex had shrunk/reduced production)
- enzyme defect e.g. congenital adrenal hyperplasia
One way to test for Addison’s is to illicit a huge stress response and measure the cortisol response. What is used to illicit this?
-Insulin
insulin tolerance test
2 Treatments for Addison’s disease
- Hydrocortisone
- Fludrocortisone (also increases aldosterone)
What is the common enzyme deficiency in CAH-congenital adrenal hyperplasia? What is the result?
21-Hydroxylase
- so cant convert progesterone-deoxycorticosterone-corticosterone to aldosterone
- cant convert 17OH progesterone to 11-deoxycortisol-cortisol
- so only pathway that can be maintained is testosterone production
