Overview of hypothalamic-pituitary regulation Flashcards
1
Q
Primary dysfxn vs secondary dysfxn 1
A
- If there is low amount of a hormone, and the stimulating hormone level is nl or low, then the dysfxn is secondary (the problem is not with the gland, but either in the pituitary or hypothalamus or elsewhere)
- This is b/c when there is low levels of a hormone the controlling centers should be increasing the release of their controlling hormones (if not-> inappropriate relationship/secondary dysfxn)
2
Q
Primary dysfxn vs secondary dysfxn 2
A
- If there is low levels of a hormone and the stimulating hormone is high then the problem is primary (dysfxn in the gland)
- If there is high levels of a hormone and the stimulating hormone is low there is either a primary dysfxn or there is a mimicking compound
3
Q
Overview of adrenal zones
A
- Going from superficial-> deep in the adrenal gland: cortex-> medulla
- Cortex (releases steroids) is divided into: glomerulosa (aldo), fasciculata (cortisol- largest layer), reticular is (androgens)
- Medulla (releases catecholamines): secretes epinephrine and NE
- Adrenal glands do not store steroid hormones; they are released immediately after synthesis (induced by increased cAMP)
4
Q
Glucocorticoid vs mineralocorticoid activity
A
- Mineralocorticoid: Na and H2O retention, K depletion
- GCC: regulation of organic matter, amplification/inhibition of other hormones
- Aldo-secreting tumor: causes retention of Na/loss of K, however serum Na levels do not rise due to pressure natriuresis (water retention->HTN-> Na excretion) and ANP (Na excretion)
- Cortisol can bind to both GCC and MCC receptors, but the inactivate form cortisone has reduced affinity for both
- Cortisol transported on the plasma protein transcortin
5
Q
Regulation of GCC effects at MCC targets
A
- In MCC target tissues (kidney, colon, sweat glands) there is 11BHSD2 nz, which inactivates cortisol into cortisone so that aldosterone is the only hormone that can activate the MCC receptor
- In GCC target tissues (everywhere else- liver, adipose, CNS) there is 11BHSD1, which converts cortisone into cortisol so there is maximum activation of the GCC receptor
- Glycyrrhizic acid (licorice) inhibits 11BHSD2 and can cause a hyper-aldo phenotype due to GCC activation (cortisol) of the MCC receptor
6
Q
GCC effects in various tissues 1
A
- During the absorptive state cortisol promotes the storage of glc as glycogen in the liver (amplifies insulin’s effect)
- This is so the body is prepared for the next stressor (i.e. epinephrine/glucagon)
- However, cortisol inhibits uptake and metabolism of glc in other tissues (except brain and heart), and thus cortisol is DIABETOGENIC (raises blood glc levels)
- Furthermore, cortisol increases GNG and can contribute to hyperglycemia (esp. when pts lack insulin sensitivity)
- Cortisol causes lipolysis in some areas, and fat deposition in others (is weakly lipolytic), but it is critical for the lipolytic effects of other hormones
- It is required for the survival of stress, and its purpose is to prepare the body for the next stress
7
Q
Effects of GCCs in various tissues 2
A
- Cortisol decreases number of circulating T cells and decreases their effectivity
- Cortisol leads to thinning of skin and capillary walls-> more prone to injury
- Leads to SkM breakdown and muscle wasting during cortisol excess
- Vascular system: maintains blood pressure and capillary dilation/permeability
- Cortisol maintains bone mass, excess cortisol leads to bone resorption
- Cortisol is highest in the morning and slowly decreases over the day
8
Q
Regulation of GCC release
A
- GCCs are release from the zone fasciculata under the control of ACTH from the pituitary
- Rx w/ exogenous GCCs causes suppression of ACTH release and thus atrophy of fasciculata
- ACTH released in response to CRH (corticotropin releasing hormone) from the hypothalamus
- Cortisol negatively feedsback to inhibit CRH and ACTH
- Excess cortisol = cushing’s syndrome
- Deficient cortisol = addison’s disease
