Clinical Approach To Pituitary/endocrine Diseases Flashcards
(37 cards)
Hypothyroidism
Low levels of thyroid hormone in blood
- causes lowered metabolic rates, HR/contractility and lowered energy levels
Most commonly is caused by autoimmune destruction of the thyroid itself
- this is primary hypothyroidism
- in this case, TSH/TRH will ALWAYS be elevated since the pituitary knows there is low T3/T4 so its trying to get the thyroid to work (but it cant)
- TSH is most clinically sensitive measure
Can be due to damage to the pituitary or hypothalamus however in which case it is secondary
- most common cause is pituitary mass
- really only tested for if patients have symptoms of cancer, hemochromatosis, sarcoidosis or sheehan syndrome. Also if new onset headache or visual changes (especially bitemporal hemianopsia) with hypothyroid symptoms
- this is noted by LOW or NORMAL TSH in blood. T4 is also ALWAYS LOW
Symptoms:
- fatigue
- weight gain
- cold intolerance
- edema
- dry skin
- menstrual irregularities
Pathway of TH release
1) hypothalamus releases Thyroid releasing hormone (TRH) to the anterior pituitary
2) anterior pituitary releases thyroid stimulating hormone (TSG) to the thyroid gland
3) thyroid gland secretes T3/T4 hormones
Causes of poor lactation in general
Two sub groups
1) poor milk extraction
- infant can latch properly or feeding techniques are improper
2) poor milk production
- stress/obesity/HTN/DM/ elevated androgens
- medications (primarily estrogen or dopaminergic agonists)
- pituitary infarction (Sheehan syndrome)
- breast reduction or radiation
How is prolactin regulated?
Is always tonically produced in the anterior pituitary
- is tonically inhibited however by hypothalamic dopamine. Most commonly seen in the action of the baby suckling the nipple
- *when dopamine is lowered = lactation**
Thyrotopin releasing hormone also plays a small role in increasing secretion as well
Serum estrogen and progesterone both also play a role
- estrogen = increases prolactin secretion
- estrogen + progesterone = inhibit production of breast milk at the mammary gland
- after giving birth, estrogen and progesterone levels drop allowing for breast milk to be produced since now it is not being inhibited
Prolactin vs oxytocin
Prolactin:
- from anterior pituitary
- function is to increase production of breast milk
Oxytocin:
- from posterior pituitary
- function is to allow for milk ejection from breast by contracting myoepithelial cells
Pituitary infarction (Sheehan syndrome)
Seen after pregnancy or during pregnancy
During pregnancy, the pituitary Hypertrophies but blood supply DOESNT. So there is less blood supply to the pituitary as needed and increases risks of infarction (due to stroke, or hemorrhages there or else where in the body)
Ovarian function broadly
Normally cyclically produces estrogen and progesterone while also holding eggs. The levels get higher through ovulation
- the cyclically nature matures and grows the endometrial lining of the uterus to prepare it for child birth
If there is no pregnancy that occurs, then estrogen and progesterone levels drop in the ovaries (but not completely) and causes the endometrial lining to “slough off” as menstrual bleeding (known as the period)
Ovarian control broadly
Is controlled by the hypothalamus, anterior pituitary and ovaries
1) hypothalamus releases GnRH which goes to the anterior pituitary
2) GnRH increases secretion of FSH and LH from the anterior pituitary gland which goes to the ovaries
3) the ovaries tonically produce estrogen and progesterone, however FSH/LH increases the rate at which these are produced
4) during menstration (or if it does) the ovaries produce estradiol which goes to the hypothalmus and anterior pituitary and lower the activity of these organs (until period is done)
How does intrauterine scarring prevent normal menstration?
The endometrial growth gets “stuck” on the scarring and prevent sloughing off during periods (or makes the timeframe irregular)
Primary Ovarian disorders and GnRH/FSH/LH production
If the ovaries are damaged or not functioning = decreases progesterone/estrogen/estradiol production
This lowers (but not completely eliminates) the inhibition on the anterior pituitary and hypothalmus as it pertains to FSH/LH and GnRH secretion respectively
Therefore, FSH/LH and GnRH will all be very elevated, but estrogen/progesterone will be low and menstrual cycle will be erratic
What are the most common causes of amenorrhea?
Pregnancy is #1
Polycystic ovarian syndrome (PCOS) is #2
Functional hypothalamic amenorrhea is 3rd most
Primary hypothalamic dysfunction effect on menstration
Is a cause of secondary ovarian dysfunction
If the hypothalamus is damaged or doesnt work properly = lowers secretion of GnRH, FSH/LH and estradiol/progesterone
- EVERYTHING IS LOWERED
Results in amenorrhea
Causes:
- actual damage to hypothalamus
- excessive exercising
- low body weight/malnutrition
- severe systemic illnesses
- severe emotional stress
will resolve after underlying issue resolves
How does prolactin decrease ovary function and amenorrhea
Prolactin levels inhibts GnRH release
This is commonly seen in breast feeding**
Pituitary primary dysfunction effects on amenorrhea and ovaries
Decreases anterior pituitary function causes a decrease in FSH/LH function and also decreases estrogen and progesterone secretion
GnRH will be VERY HIGH however**
This is a secondary disorder (secondary hypogonadism)
Causes:
- any direct damage or mass to pituitary
- TBIs and stroke history
- hemochromatosis or sarcoidosis
- systemic infections (especially TB/syphills and toxoplasmosis)
- Sheehan syndrome
How does thyroid disease cause amenorrhea?
Primary thyroid diseases results in an increase of TRH naturally
- TRH however, also increase prolactin release of the anterior pituitary
Prolactin inhibits GnRH and FSH/LH levels in the blood
- this ends up decrease progesterone/estradiol
Adrenal gland functions
Medulla layer = secretes epinephrine and norepinephrine in times of stress
- NOT controlled by pituitary
Inner Cortex layer = secretes cortisol (outer-inner/fascicular layer) in times of stress and androgens (inner-inner/reticular layer) in puberty and just tonically
- IS controlled by pituitary
Outer cortex layer = secretes aldosterone
- increases renal K+ secretion and reabsorbs Na+/H20
- focus is to keep volume levels high
- IS controlled by pituitary
Cortisol functions
Stimulates gluconeogenesis
Inhibits immune system function
- more or less just controls it (doesnt turn it off) and prevents/decreases chronic inflammation
Helps maintain vascular tone and blood pressure
Adrenal gland regulation by hypothalmus and pituitary
Mental/physical stress leads to increased hypothalamic secretion of corticotrophs releasing hormone (CRH) to the anterior pituitary
Anterior pituitary then secretes ACTH which goes to the adrenal gland and stimulates all its secretion (not much of medulla however)
- primarily secretes excess cortisol**
- does increase synthesis of aldosterone and epinephrine/NE also (but DOESNT release aldosterone and only minor releases epinephrine/NE. Secretion fo aldosterone is controlled by RAAS)
Primary adrenal insufficiency (Addison disease)
Damage to the adrenal cortex leads to decreased aldosterone/cortisol and androgens
- primarily an autoimmune cause
Also INCREASES CRH and ACTH (since the hypothalamus and anterior pituitary aren’t affected)
Symptoms vary widely but most common are
- mild hyperkalemia
- major hyponatremia and ECF fluid loss
- low glucose levels
- spontaneous fevers and mild sepsis-like conditions (especially hypotension)
- lowered sex libido in women*
- decreases pubic/axillary hair growth in women*
- increased skin pigmentation especially around palmar/elbow creases**
- in men the testes producer enough testosterone and androgens to mask this usually so these symptoms are not normally seen in men with normal testie function
** in primary adrenal insufficiency, the increased production of ACTH in response by the anterior pituitary leads to a secondary increase in melanocyte stimulating hormone release. This increase pigmentation especially in crease areas**
Adrenal crisis
Also known as acute adrenal insufficiency
- usually brought on by acute infection or severe dehydration/physical stress
Induces severe hypotension, shock, fever, coma, death
This is caused by acute severe loss of everything in adrenal gland. Much easier to see than chronic insufficiency and often can be confused with septic shock
Secondary adrenal insufficiency
Looks very similar to primary adrenal insufficiency except it is caused by anterior pituitary damage which leads to decreased ACTH production and secretion.
- remember that ACTH primarily controls secretion of cortisol (although does have minor effects on all other zones of the adrenal gland)
DOESNT show hyperpigmentation and LESS symptoms of androgen loss and hypoaldosteronism
**STILL shows symptoms of hypo secretion of cortisol (low blood sugar, hypotension and random fevers)
Why is secondary adrenal insufficiency more common than primary?
Because it is seen in rapid cessation of glucocorticoid medications after prolonged use. THIS IS WHY YOU NEED TO TAPER
- especially prednisone
Introducing exogenous prednisone causes the pituitary to think that cortisol levels are very high in the body
- so this lowers ACTH levels in the body and therefore endogenous cortisol levels
- sudden withdrawal doesn’t give the anterior pituitary enough time to “rebound” and start working again so thou will adrenal insufficiency symptoms because there is no-little cortisol in the body
How to differentiate primary from secondary adrenal insufficiency with labs
Both require measurement of morning cortisol and ACTH
If both are low OR low cortisol and NORMAL ACTH = secondary adrenal insufficiency
If cortisol is low but ACTH is very high = primary adrenal insufficiency
High yield symtpoms and words for adrenal insuffiency
Hypotension, fatigue, hypoglycemia, Hyperkalemia or hyponatremia without having clear cause = 1st adrenal insufficiency
- may also show hyperpigmentation of skin and creases
Recently stopped a corticosteroid without skin hyperpigmentation or hyperkalemia = 2nd adrenal insufficiency
- may also show visual changes and new headache
