Pituitary Disorders Flashcards
relationship between the pituitary and the hypothamlus
what homrones from the hypothamlus trigger which hormones from the pituitary (anterior and posterior)
Hypothalmus: neuronal signals trigger a release of hormones which are sent directly to the pituitary (anterior or posterior) which signal secondary hormones ot be released from the pituitary to act within the body
Posterior Pituitary: signaled by direct neuroendocrine signals from the hypothalmus for oxytocin and ADH
Anterior Pituitary: signaled by hormones through the portal system between the two
Hypothamlus secretes: GHRH, DA, TRH, CRH, GnRH
these trigger the anterior pituitary to secrete
GH, LH/FSH, TSH, ACTH, PRL
DA = prolactin
GHRH = GH = (liver) IGF-1
TRH = TSH = (thyroid) T3/T4
CRH = ACTH = (adrenals) cortiosl, androgens (NOT aldos.)
GnRH = LH/FSH = (gonads) sex hormones
Pituitary Adenomas
- general information
- majority are (cancer or not?)
- what type of hormone secreting adenomas are they (classes)
- size differentiation
Pituitary Adenomas
- majority are non-cancerous, bengin adenomas which are just overgrowth of specific types of cells within the pituitary
Types
- majority are prolactin stimulating hormones = prolactinomas
- GH-secreting
- ACTH-secreting
- non-secretory
- TSH-secreting (rare)
Size
- microadenoma if < 1 cm
- macroadenoma if > 1cm
Prolactinomas
- etiology
- who are they found earlier in
- Symptoms/signs
Etiology
- a tumor of the pituitary gland whih secretes prolactin
- most common type of pituitary adenoma
- identified in females earlier than males becuase the symptoms are more identifiable
- have the ability to secret other hormones, like mixed with GH
Symptoms (variable depending on the size of the lesion and the sex of the pt.)
- Galactorrhea = producing milk becuase of the inc. prolactin
- amenorrhea (females) because the prolactin adenoma supresses LH/FSH and thererofre suppresses estrogen/progesterone (hypogonadism)
- in men: fatigue, loss of body hair, decreased libido
- if adenoma is large: compress optic nerve at chiasm = bitemporal hemanopsia & headaches
Prolactinomas
Diagnosis
Treament
Diagnosis - labs
- check serum prolactin (high)
- imaging: MRI with and without galidium
Always R/O other causes of the symptoms and prolac.
- hypothyroidism (high TRH can trigger increase in prolactin) = get hypothyroid labs (TSH)
- check meds: risperidone, TCAs, estrogens, anti-emetics, fluoxetine)
- check liver failure, renal failure, adrenal insufficiency
- pregnancy test
- IGF-1 (rule out growth hormone related)
Treatment (restore gonadal function, reduce prolactin levels and decrease size of adenoma)
- first line treatment is medical : not surgical
- majority of pts. will need long term treatment of these (some may remit at 2-3 years)
Cabergoline (Dostinex) is FIRST LINE MEDS
- reduces prolactin with fewer side effects than bromo.
- valvular fiberosis is possible
- SE: HA, N/V/D/C, mood issues (but relatively rare)
Bromocriptine (Parlodel)
- can be given and effective but SE
- N/V is common, orthostatic hypotension
IF meds dont work, untoleraable…. surgery
- transsphenoid ressection of the prolactinoma
- rarely needed due to such success with med
- microadenoma have better surigcal outcomes
(radiotherapy is LAST line with poor poor outcomes)
Prolactinoma
Follow-up
- check prolactin levels every 3 months & taper meds accoridingly
- most clinicians will stop the med after 1-2 years, see how they do - monitor labs afte 3 months of stopping
Imaging
- if stopped med: image when prolactin levels back to normal
- if on med: wait 6mo - 1 yr. to image
- Brain MRI
NOTE: PREGNANT PTS> CANNOT BE ON THESE MEDICATIONS !!!!! need to d/c meds, and have them follow up with neurosurg. to scan periodically
ACTH secreting Adenoma
discussed elsewhere
increases cortisol = cushing DISEASE (becuase tumor)
need surgical removal
GH-secreting adenoma of pituitary
different between acromegaly and giantism
- Etiology
- pathology
Gigantism = the tumor is happening pre-puberty = thus the child is still growing and thus they become crazy tall
Acromegaly = the tumor forms after pubery (the epiphyseal clousre has happened) thus the bones grow wide not up, and happens later in life)
Etiology
- commonly missed diagnosis; by the time its caught, it is already a macroadenoma ( > 1cm)
- can see a mixed GH/prolactin adenoma
Patho
- problem is at the level of the pituitary–> so there is an increase in GH without any stimulation
- increased GH trigger the release of IGF-1 from the liver in large amounts
- normally: the secretion of GH is episodic (like cortisol) so there are sporatic spikes = more in sleep (grow big and strong if you sleep well)
- thus, you have an increase in the number of the GH hormone release spikes
- triggering: increase in IGF-1
- IGF-1 = proliferation of bone, soft tissue, cartilage and organs!!!! (heart spcifically)
Acromegaly (GH pituitary tumor)
Symptoms
because this is happening post-puberty with slow growth over time symptoms are often subtle
Symptoms
- acral (hands and feet) enlargement (think bone & soft tissue from IGF-1)
- increased hat size, ring size & dough-looking hands
- coars facial features: thickened skull, frontal sinus, enlarged nose, prominent jaw, widely spaced teeth & puffy face
- headaches!! common becuasethis are large tumors by the time we get to them, so they’re compressing
- cardiomegaly: because increased organ growth
- also - IFG-1 impacts glucose (GH is a counter-reg hormone) = thus plays a role in DM2
Signs
- visual defects (because size of tumor compressing the chiasm)
- HTN
- OSA (large features)
- hypogonadism (overtaken function by the tumor)
- can produce hypopituitary becuase the tumor gets so large it compresses all the other funtions of the pituitary
Acromegaly (GH hormone tumor)
Diagnosis
Treatment
Follow-up
Diagnosis (primarily lab based)
- GH is difficult to caputre in lab values because it peaks and falls; and doesnt ciruclate for long (can be gotten)
- IGF-1= better predictor as it remains in serum for a while
- still get IGF-1 and GH (will be high!!)
- confirmatory test after: glucose suppression of GH test: GH is a counter-reg. hormone, meaning its only utalized to increase glucose within the serum, thus when glucose is administered you want to see a DROP in GH (normally); these pts. the GH will not change (because its coming from tumor)
Imagin
- Brain MRi with and without galidolium
addition w/o
- get other pituitary abs: TSH, FT4/FT3, PRL, AM cortisol/urine cortisol, LH/FSH and testostern/estogen
always get ECHO (heart) and sleep study
Treament
- surgical removeal: transsphenodial resection of the pituitary
- larger tumor: less successful
- post -op: if GH still high octreotide can be used to suppressGH
Follow Up
- 2-4 weeks post-op get IGF-1 and GH labs
- if high- octreatide
Sheehan’s Syndrome
Etiology
Patho
Symptoms
Treatment
rare in US: most commonly found as the most common cause of hypopituiarism in developing countries
Etiology & patho
- during pregnancy, the pituitary is swollen/enlarged due to increased hormones (hyperplasia)
- if mother hemorrhages during pregnancy, this can risk necrosis to the pituitary
- because hemorrhage = volume depletion = infarction of the pituitary
Symptoms
- women will complain of inability to lactate post delivery
- can appear in days/weeks
- majority of women unfortunately will become panhypopituariism
Treatment
- hormone replacement as the pituitary is dead :(
Non-Secretory Pituitary Adenoma
- etiology
- what cell type do they mostly come from
- size consideration and impact
- what functions are lost first as a result and why
- treatment
Etiology
- a small % of the pituitary adenomas
- these do not produce any horomones; thus minial symptoms
- however; they ususally arise from the LH/FSH producing areas of the pituitary
Symptoms
- usually: the size will be large and grow to a macroadenoma = visual changes and headaches
- the pituitary; as this grows will loose gonad function first, then thyroid, last to leave will be cortisol function (because this goes from least essentail to most for survival)
pt. can develop a secondary hypothyroidism as they loose the TSH secretion, and adrenal insuff. as they loose cortisol = leading to hypopituitarism
Treatment
- surgery and raditaion
Diabetes Insipidus
Etiology (two kinds)
Patho
Eitology
- a disorder due to an imbalance of water- non-osmotic loss of water in the urine = large volume dilute urine
- due to a dimished abiity to make ADH or an inabiity to response to ADH hormone release
- nephrogenic: childhood MC (cant respond)
- central: adulthood (cant make ADH)
Central
- a posterior pituitary based issue in that there is no ability to release ADH
- in 50% of cases: it is unknown why
- tumors, infections, carcoid, CVA and trauma can cause it
Nephrogenic
- congenital, med-induced, PCKD, MM, sarcoid, etc.
Key Patho
- ADH should stimulate aquaporins to reuptake water from the colecting duct whn dehydrated (low volume)
- in DI; this process is altered: leading to high volum eurine output of DILUTE urine
- because the shear amount of water intake these pts. have will help avoid hypernatremia (because the body will try to reuptake sodium to counteract this)
Diabetes Insipidus
Symptoms
Diagnosis
Treament
Symptoms
- polyuria with DILUTE urine
- polydipsia
- nocturia
- HA/visual changes (if there is a mass on pituitary)
- orthostatic hypotension
Diagnosis
- First: get some labs to screen for DI
- BMP
- serum Osmolaity: could be normal or high
- urine osmolaity/urine sodium = will be LOW < 300
- 24 hour urine collection = > 3 L
- anyone with concentrated urine is not DI
confirmation test: Water Deprevation Test
- in-pt. deprive from water to determine if central or just thirsty
- monitor every hour: weight, plasma osmolality, serum sodium, urine osmolality, urine volume
- IF primary polydipsia = pt. will have CONCENTRATED URINE via ADH that was stimulated
- IF central DI = the pt. urine will STILL be dilute high volume
then…
- check brain MRI
- full pituitary workup if lesions found
Treament
- ADH-analong or DDAVP
- monitor for hhyponatermia on the meds
SIADH
Etiology (what pt. pop is most likely)
Patho
Etiology
- SIADH: syndrome of inappropriate anti-diuretic hormone = so reuptake of fluid when you dont need it all the time
- most commonly seen in the hospital setting
- free water retention and a secondary dilutional hyponatremia due to the free water reuptake
- known as a euvolemic, hypotonic hyponatremia
Causes : all somehow impact the nerual pathways
- CNS problems: infection, trauma, surgery
- Pulmonary: pneumoia, TB, empyema, COPD exacerbation
- Meds: DDAVP (too much), SSRIs and TCAs
- Malignancy: SMALL CELL LUNG CANCER: production of ADH from neoplasms
Patho-keys
- ADH production from other areas than just the posterior pituitary or disruption in the neural pathways
- patients will reabsrb free water , excrete sodium (in attempt to decrease fluid) and have an elevated serum osmolaitiy
SIADH
Symptoms
Diagnosis
Treatment
Symptoms
- largely depend on how quickly the hyponatremia happens
- those with abrupt changes in sodium: seizure, coma, respiratory arrest, AMS
- those with slow changes in sodium: asymptomatic, weakness, malaise
**neurologica changes wil occur with Na < 120 (ICU with Na < 110)
Diagnosis
- hypotonic hyponatremia = thus serum osmolality will be LOW
- serum os = low
- urine os = high
- urine sodium - high
- pt. will be euvolemic: because they’re excreting sodium to counter balance the increase free water so fluid overall doesnt change, the issue becomes the sodium
- rule out adrenal insuff. hypothyroidand malignancy
Treeatmnet
- self-limiting & treat underlying (CNS, lung or malignancy)
- fluid restrictionis mainstay
- if severe, acute hyponatremia: replete with hypertonic saline (3% NS)
- can be used with loop diuretic + salt tablets
- Tolvaptin: the vasopressor can be used to stop aquporins from opening
