LECTURE - Adrenal Hormones Flashcards
mineralocorticoid hormones act on kidneys to:
- increase Na+ reabsorption into blood
> increase blood volume so increase blood pressure by synthesis of Na+ channels, Na+/K+-ATPase and ATP - increase K+ excretion into the urine
- increase H+ excretion into urine
T or F. the hypothalamus and pituitary regulate aldosterone regulation
F! no role; the renin-angiotensin aldosterone system is what regulates this
renal baroreceptors detect decrease in BP and blood volume to turn on RAAS
adrenal primary disorder
- autonomous aldosterone production by adrenal tumor
- Cohn’s disease
secondary adrenal disorder
- renin-producing tumor
- renal artery stenosis (impaired flow to the kidney)
- drugs (some diuretics, laxatives)
consequences of aldosterone excess
- Na+ retention: blood vol expansion and hypertension
- K+ loss: muscle weakness and cardiac arrhythmias
- H+ loss: increased blood pH
Addison’s disease
- primary disorder
- the destruction of the adrenal cortex; other adrenal cortex hormones are deficient in Adison’s
- enzyme deficiency in aldosterone synthesis pathway
cause of aldosterone deficiency: secondary disorder
- renin deficiency
physiological effects of cortisol
- stress hormone
- effects carbohydrate, protein, lipid metabolism
> increase blood glucose (gluconeogenesis)
> increase protein breakdown
> increase lipolyis - facilitates catecholamine effects (increase BP)
- suppresses immune system
insulin antagonist
cortisol
Cushing’s syndrome
- diabetes; glucose cannot enter cells
- skin thinning, easy bruising, poor wound healing, muscle weakness (increase protein breakdown)
- abnormal fat distribution: moon face, buffalo hump, central obesity; glucose is stored as fat
- hypertension
- immune system suppression
- osteoporosis
T or F. bound cortisol is the active form
F! it is the free cortisol that is the active form
consequence of cortisol deficiency
- hypoglycemia
- low BP- severe weakness + fatigue
- weight loss and decreased appetite
- +/- hyperpigmentation (only if ACTH high)
- in Addison’s disease, can also see Na+ loss (dehydration); K+ retention (cardiac arrhythmias)
> due to co-existing aldosterone deficiency
lab investigation of aldosterone excess
- measure aldosterone => excess
- measure renin and aldosterone/renin ratio to differentiate primary (adrenal) vs secondary (kidney)
- deceased renin; increase in aldosterone/renin = primary
- increased renin; aldosterone/renin not drastically increased = secondary
T or F. all labs measure renin and aldosterone
F
consequences of aldosterone deficiency
- Na+ loss = dehydration, decreased BP, weakness
- K+ retention = muscle weakness, cardiac arrhythmias
- H+ retention = decreased blood pH
lab investigation of aldosterone deficiency
- measure aldosterone = decreased
- measure renin and aldosterone/renin ratio
> increased renin; decreased aldosterone/renin = primary
> decreased renin; aldosterone/renin not drastically decreased
cortisol regulation
- CRH = corticotropin-releasing hormone
- ACTH = adrenocorticotropic hormone
- undergoes diurnal variation = highest in morning and lowest at midnight
causes of cortisol excess
- adrenal/primary disorder = autonomous cortisol production by adrenal tumor
- pituitary/secondary disorder = autonomous ACTH production by pit tumor = Cushing’s
- ectopic ACTH-producing tumor (tumor somewhere else)
in serum, cortisol is highly ….
protein-bound
- cortisol binding globulin and albumin
lab tests for cortisol and their disadvanatges
- serum (total) cortisol => does not measure active form, diurnal variation
- 24 hr urinary free cortisol => difficult for patient
- salivary cortisol => not widely available (but preferred), diurnal variation
when is cortisol lowest?
midnight
lab investigation for Cushing’s
- excess cortisol? patient gives midnight saliva or 24 hr urinary free cortisol sample
- if high = Dexamethasone suppression test
> measure serum cortisol before and after administering DXM - if not cortisol not suppressed = TUMOR
- ACTH measurement can help identify cause
> adrenal 1ry if decreased ACTH
> pituitary 2ry or ectopic if increased ACTH
DXM
- a potent glucocorticoid
- normally suppresses cortisol production
lab investigation of cortisol deficiency
- AM serum cortisol (when it should be highest)
- can we stimulate the production of cortisol?
> measure serum cortisol before and after giving synthetic ACTH - if healthy = large increase in cortisol
- if primary def = no increase in cortisol
- secondary def = small increase in cortisol
- ACTH measurement can help distinguish primary and secondary
this is the only thing that varies among catecholamines
the monoamine structure
catecholamines
dopamine, norepi, epi
catcholamine synthesis
- amino acid = tyrosine
- also produced in the nervous system
- adrenal medulla = epi (80%), norepi (20%)
fight or flight
- increase in BP
- increase rate/strength of heart contraction
- bronchodilator
- increase in blood glucose
pheochromocytoma
- catecholamine-secreting tumor
- adrenal medulla
symptoms of pheochromocytoma
4 P’s
- perspiration
- palpitations (pounding/racing heart)
- pain (headache, abdominal pain)
- increased blood pressure
- severe panic attack symptoms last few seconds to an hr; sporadic or persistent hypertension*
why are epi and norepi not the preferred tests for pheochromocytoma?
- SECRETED EPISODICALLY BY TUMOR (CHROMAFFIN CELLS)
- ALSO PRODUCED IN SIGNIFICANT AMOUNTS BY NERVOUS SYSTEM (NOT SPECIFIC TO ADRENAL MEDULLA)
what do we measure when we want to investigate excess catecholamines (pheochromocytoma)?
metanephrine and normetanephrine
- methylated metabolites of epi and norepinephrine
- BEST tests for investigation
> produced continuously
> much more specific to the adrenal medulla
when does pheochromocytoma occur?
any age
- most commonly between 30-50
affected individuals (pheochromocytoma) should…
- avoid foods with tyramine (tyrosine = natural derivative)
> pickled foods, cured smoked or processed meats, fermented soy products, leftovers - avoid meds with monoamine oxidase inhibitors
> antidepressants, antianxiety=, meds for Parkinson’s
treatment for pheochromocytoma
surgery
chemotherapy
radiation therapy
