PHYS Endocrine Response to Stress - Week 12 Flashcards
What does the adrenal cortex synthesise? What are its layers? What do each of these layers specifically secrete?
Steroids.
Glomerulosa - aldosterone
Fasciculata - cortisol
Reticularis - DHEA,
What does the adrenal medulla synthesise?
Catecholamines - A & NA.
Remember: Adrenal medulla derived from neural tissue, thus it makes sense that it can synthesise & secrete A & NA.
Describe how NA/A are produced. Where are they produced? What is the rate-limiting step? When are they secreted?
Tyrosine -> L-Dopa -> Dopamine -> NA -> A w conversion of tyrosine -> L-Dopa the ‘rate-limiting step’ @ chromaffin cells of the medulla -> storage in vesicles -> neuronal stimulation -> depolarisation of the cell membrane -> Ca2+ influx -> exocytosis of A /NA .
A vs NA targets?
A - acts on both a & B adrenergic receptors.
NA - specifically targets a adrenergic receptors.
Describe feedback mechanism & HPA axis involved in cortisol secretion. State what it is stimulated by? Where feedback loop begins? What reduces further cortisol production?
HPA axis – stimulated by circadian rhythm & stress -> parvocellular neurone stimulation @ PVN -> CRH (cortisol-releasing hormone) secretion into hypophyseal portal blood vessels -> ACTH production -> ACTH binds to adrenal cortex cell receptors -> stimulates steroid hormone production via increasing activity of steroidogenic enzymes -> cortisol feeds back to the pituitary & hypothalamus to suppress ACTH & CRH production via -ve feedback mechanism.
When & why do cortisol levels peak?
Peak in the few hrs post awakening to increase appetite and prepare body for potential stressors during the day.
Actions of cortisol
- Increases plasma glucose levels during fasting states via stimulating protein metabolism -> increase in circulating amino acids & lactate AND via gluconeogenesis AND via promoting lipolysis -> fatty acid & glycerol release AND increase hepatic glucose production btw meals.
- Increases adrenergic receptor expression
- Increases pro-inflammatory cytokines
- Increases inflammatory mediators (e.g., PPGs & leukotrienes)
- Suppresses growth & function of key immune cells (e.g., lymphocytes)
- Stabilises lysosomal membranes in damaged cells, preventing the release of their proteolytic contents
- Decreases capillary permeability in injured areas
- Decreases function of the reproductive axis at the hypothalamic, pituitary & gonadal levels.
Symptoms experienced by pts w Addison’s disease.
- Weakness
- Fatigue
- Loss of appetite
- Loss of weight
- Increase skim pigmentation
- Low BGL
Symptoms experienced by pts w Cushing’s syndrome.
- Diminished bone strength
- Muscle weakness
- Easy bruising
- Abdominal obesity
- Hypertension
- High BGL.
Most common cause of Cushing’s syndrome.
Pharmacological use of exogenous corticosteroids.
Seyle’s 3 x stages of general adaptation to stress.
- Alarm reaction (6-48hrs) - modulated by A @ adrenal medulla & NA via SYMP.
- Resistance (>48hrs) - via cortisol @ adrenal cortex.
- Exhaustion (>1-3mths) - cortisol secretion continues, as well as increasing A & NA again.
Describe mechanism of A & NA release in response to stress & its effect on the body. Repeat for cortisol.
Stress -> HPA axis activation -> SYMP activation -> stimulates adrenal medulla -> secrete A & NA -> increased heart rate, BP, liver gluconeogenesis, bronchiole dilation, metabolic rate, changes in blood flow patterns leading to decreased digestive system activity, reduced urine output.
AND
HPA axis activation -> CRH stimulates production of ACTH -> promotes steroid production by cells of adrenal cortex -> cortisol & aldosterone secretion -> protein & fat conversion to glucose, increased BGL, immune suppression, sodium & water retention by kidneys, increased blood volume, increased BP.
