L18- Endocrine Pathology I (pituitary) Flashcards
pituitary gland lies within (1) location of the brain
it has two components, (2) and (3)
1- Sella Turcica
2- anterior pituitary / adenohypophysis
3- posterior pituitary / neurohypophysis
Adenohypophysis is formed from (1) embryologically
Neurohypophysis is formed from (2) embryologically
1- evagination from roof of the pharynx
2- (neuroectoderm) downgrowth from floor of the 3rd ventricle of the brain
All the nerve endings of the hypothalmus going to the pituitary meet to form (1). (1) releases hormones into (2), which arised from (3) within (1). In the anterior pituitary, hormones are released into (4).
1- median eminence
2- hypophyseal portal veins
3- primary capillary network via superior hypophyseal arteries
4- secondary capillary network (formed via portal veins)
list the Anterior Pituitary hormones, include their cell type
GH, PRL- acidophiles
ACTH, TSH, FSH, LH- basophils
list the hormones released form the hypothalamus and their function in the adenohypophysis
GHRH –> (+)GH
GIH / somatostatin –> (-)GH
PIF / dopamine –> (-)PRL
TRH –> (+)TSH
CRH –> (+)ACTH
GnRH –> (+)LH/FSH
Hypopituitarism is defined as (1), where (2) defect is a rare occurrence and (3) and (4) are the main causes.
Hyperpituitarism is defined as (5- including cause).
1- underactive pituitary gland (some or all hormones)
2- panhypopituitarism (all hormones)
3- (pituitary disease) infarction, radiation, non-functioning adenoma
4- (hypothalamic disease)
5- excess pituitary hormones usually via functional pituitary adenocarcinoma
(T/F) pituitary adenomas are always hormone producing
F- can or cannot be hormone producing
Note- if does produce hormone, usually inc in one hormone leads to deficiency of the other hormones
list some local effects of pituitary disease (/tumor)
- (especially in tumor) visual disturbances, HAs, destruction of secretory cells by enlarging tumor
- possible CN involvement
- deficiency / excess of hormone(s)
Anterior Pituitary in disease status, rank the hormones most likely to be lost in descending order
- GH (not seen in adults)
- LH, FSH
- TSH
- ACTH
Name the pituitary hormone:
- (1) deficiency => growth retardation
- (2) deficiency => hypoadrenalism
- (3) deficiency => hypothyroidism
- (4) deficiency => failure of postpartum lactation
1- GH, children only
2- ACTH
3- TSH
4- PRL
describe the effect of gonadotropin deficiency in males and females
Males: (lowT) loss of libido, loss of facial and body hair, impotence
Females: amenorrhea, infertility
list the extensive number of causes for hypopituitarism
- Tumors: adenoma (functioning, non-functioning)
- Vascular: Sheehan’s, severe hypotension
- Hypothalmic disorders: tumors, isolated GHRH or GnRH deficiency
- Iatrogenic: ablation of pituitary by surgery, radiation
- Inflammatory lesions: sarcoidosis, TB
- Misc.: trauma, metastatic tumors
list the investigations used in suspected hypopituitarism
1) basal levels of pituitary gland target hormones
2) stimulation and suppression tests
3) MRI / CT scan
4) Immunostaining: IHC
describe the factors making basal level testing of the pituitary and target hormones difficult
- residual capacity in pituitary gland (if diseased)
- pulsatility of secretion
- stress
- time of day (cortisol)
- menstrual cycle: FSH, estrogen, progesterone
describe the components in pituitary stimulation and suppression tests
-simultaneous administration of insulin, TRH, GnRH
- Insulin –> induces hypoglycemia –> stress state
- stress state allows for assessment of pituitary gland capacity to secrete stress hormones: PRL, GH, cortisol (ACTH)
Essentially: insulin –> PRL, GH, ACTH release, TRH –> TSH release, GnRH –> LH/FSH
what are the main hyperpituitarisms
hyperprolactinemia (inc PRL)
acromegaly (inc GH)
list the DDxs when investigating for Pituitary adenoma
- craniopharyngiomas
- meningioma
- neurofibroma
- ectopic germinomas
- metastatic tumor (rarely)
list the causes of Hyperprolactinemia
- psychological / stress
- drugs: antipsychotics, oral contraception, antidopaminergic drugs (anything that dec DA inhibition)
- tumor: prolactinoma OR mass in suprasellar compartment disturbing normal inhibitory signal
- renal failure
- ectopic source
Hyperprolactinemia:
- (1) Sxs in women, (2) Sxs in men, (3) in both
- (4) and (5) are the main investigations
- (6) Tx
1- amenorrhea / anovulation, infertility
2- loss of libido, impotence
3- galactorrhea
4- prolactin serum levels
5- MRI, CT of head
6- medications followed by eventual surgery
(1) is the main physiological difference between Acromegaly and Gigantism. (2) is the common cause for both, as (3) is very rare.
1:
Acromegaly: excess GH after epiphyseal fusion (bones) – Adults
Gigantism: excess GH before epiphyseal fusion – Children
2- adenoma
3- ectopic production
Acromegaly:
- (1) is the direct effect
- (2) are associated Sxs
- (3) in women, (4) in men
- (5) is a disease that can develop secondarily
1- inc growth of skeletal and soft tissue
2- HTN, arthritis, HAs (local effects of tumor)
3- menstrual disturbances
4- loss of libido, loss of potency
5- DM- GH antagonizes action of insulin
describe the 2 main tests used for Acromegaly diagnosis
1) measure GH, IGF-1
- GH act on liver –> IGF-1 production
- IGF-1 is more stable, therefore more apparent, useful in acromegaly Dx
2) OGTT (oral glucose tolerance test) + GH measurment
- Normal: GH falls after given insulin to undetectable levels
- GH stable or rising suggests Acromegaly
list the Tx for Acromegaly
- surgery
- medical
- radiotherapy
ADH:
- inc secretion in response to (1) or (2)
- (3) is direct renal function, with (4) effect overall
- (5) and (6) are affected in urine
1- dec blood volume
2- raised plasma osmolarity
3- inc H2O permeability in DCT and CD in kidney
4- restore blood volume / normalize plasma osmolarity
5- dec urine volume
6- inc urine osmolarity
list the causes for DI
Diabetes Insipidus (lack of ADH or its functionality)
1) Central DI- ADH deficiency
- genetic
- hypothalamic / high pituitary stalk lesion
- head trauma, tumors, inflammatory disorders
- idiopathic
2) Nephrogenic- ADH resistance
- genetic (defective receptors)
- metabolic: hypokalemia, hypercalcemia
- drugs: lithium
describe the Process of the water deprivation test (for DI)
(diabetes insipidus)
-fluid restriction for 8hrs –> urination and throw sample away
- weight patient at 1hr intervals
- measure serum / urine osmolarity, urine volume, weight hourly for 8hrs
- STOP at 8hrs OR if weight is <5% of initial weight
-If results suggest DI –> give Desmopressin –> measure plasma osmolarity, urine volume and osmolarity
Water Deprivation Test Interpretation:
-(1) Normal Patient serum osmolarity and urine osmolarity
-(2) result indicates DI
1- serum osmolarity never >295mOsm/kg // urine osmolarity >600mOsm/Kg
2- failure to concentrate urine –> urine osmolarity remains <600mOsm/kg
Note- intermediate results and partial defects may exist
describe the results of the Water Deprication Test for Central DI and Nephrogenic DI
Central DI:
- after deprivation, urine osmolarity <300
- after vasopressin, urine osmolarity >600
Nephrogenic DI:
- after deprivation, urine osmolarity- <300
- after vasopressin, urine osmolarity <300
list the causes of SiADH
- ecoptic ADH secretion by malignant neoplasm (SCLC)
- non-neoplastic lung diseases
- local injury to hypothalamus or neurohypophysis
describe the clinical manifestations of SiADH
- hyponatremia: asymptomatic or has nonspecific Sxs
- severe hyponatremia, especially if there is a rapid fall in serum Na –> cerebral edema –> neurological Sxs –> coma –> death
