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SFM5 > Pituitary Pathophys > Flashcards

Pituitary Pathophys Flashcards

1
Q

pituitary gland location and nearby nerves

A

in sella turcica of sphenoid bone
suspended from hypothalamus by pituitary stalk

nearby:

  • optic chiasm, superiorly
  • cavernous sinus
  • CN 3, 4, 6 (all involved in eye movement)
  • opthalmic and maxillary branches of CN 5
  • internal carotid artery, laterally

clinical implications w/ pituitary tumor or bleed:

  • bitemporal hemianopsia (vision loss)
  • cranial nerve palsies, especially involving extraocular movement
  • transsphenoidal surgery to avoid ICA
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2
Q

origin/makeup of anterior vs posterior pituitary

A

anterior pituitary

  • adenohypophysis
  • non-neuronal tissue
  • formed from Rathkes pouch (ectodermal evagination of oropharynx)
  • 5 subtypes of secretory cells:
    • corticotropes (ACTH)
    • gonadotropes (LH and FSH)
    • somatotropes (GH)
    • thyrotropes (TSH)
    • lactotropes (prolactin)

posterior pituitary

  • neurohypophysis
  • nervous origin
  • axons of hypothalamic and paraventricular origin
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3
Q

corticotroph axis

A
  1. ht: CRH, corticotropin-releasing hormone
  2. ap: ACTH, adrenocorticotropic hormone
  3. medulla of adrenal gland: cortisol
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4
Q

somatotroph axis

A
  1. ht: GHRH, growth hormone releasing hormone
  2. ap: GH, growth hormone
  3. liver (mainly): IGF-1
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5
Q

gonadotroph axis

A
  1. ht: GnRH, gonadotropin-releasing hormone
  2. ap: FSH and LH, follicular stimulating and luetenizing hormones
    3f. ovaries: estradiOL, indirectly stimulates progesterone
    3m. testes: testosterone
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6
Q

thyrotroph axis

A
  1. ht: TRH, thyrotropin releasing hormone
  2. ap: TSH, thyroid stimulating hormone
  3. thyroid: T3/T4
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7
Q

lactotroph axis

A
  1. ht: dopamine
  2. DOWNREGULATES ap: prolactin

when ht signalling is interrupted, all ap hormones except prolactin go down, prolactin goes up

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8
Q

cortisol stimuli

A
  • circadian (morning, just before waking)
  • inflammation
  • hemorrhage
  • hypoglycemia, fasting
  • etc
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9
Q

cortisol suppression

A
  • circadian (night)
  • exogenous glucocorticoids, e.g. therapeutics
  • pathophys e.g. primary adrenal insufficiency
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10
Q

LH and FSH stimuli

A
  • pulsatile GnRH (continuous results in suppression)
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11
Q

LH and FSH suppression

A
  • continuous GnRH (pulsatile stimulates)
  • pathophys e.g. secondary hypogonadism
  • negative feedback from estradiol or testosterone
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12
Q

GH suppression

A
  • hypothalamic somatostatin
  • IGF-1 negative feedback
  • circadian (daytime)
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13
Q

GH stimuli

A
  • pulsatile, circadian (night/sleep)

- GHRH

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14
Q

GH/IGF-1 functions

A

lipolysis –> FFA
amino acid uptake, protein synth –> muscle and soft tissue mass
growth plate chondrocytes –> skeletal linear growth
insulin antagonism –> hyperglycemia

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15
Q

prolactin stimuli

A
  • estrogen
  • sucking
  • ht TRH

pathophys/hyperprolactinemia:

  • prolactinoma
  • hypophyseal stalk compression, lesion (interruption of ht dopamine)
  • dopamine inhibitors
  • enhanced TRH, e.g. primary hypOthyroid
  • breast stimulation, e.g. chest wall injury
  • reduced clearance (hepatic, renal insufficiency)
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16
Q

prolactin suppression

A

ht dopamine

17
Q

arginine vasopressin (AVP)

A
  • aka ADH
  • posterior pituitary
  • osmoreceptors in ht trigger in supraoptic and paraventricular nuclei (SON and PVN)

stimuli

  • most sensitive: increased plasma osmolality
  • also: RAAS system following 10-20% change in plasma volume or bp

suppressors
- baroreceptors in heart and lung (i.e. high bp shuts down production)

18
Q

central diabetes insipidus etiology

A
  • too little AVP (ADH)

caused by any of:

  • lesion must destroy both PVN and SON (large lesion, they are far apart)
  • lesion interrupting communication b/w PVN/SON and pp (i.e. directly above diaphragm sella/pituitary stalk)
  • AVP gene mutations (autosomal recessive)
  • pregnancy d/t placental vasopressinASE
19
Q

central DI tx

A
  • drink lots of water (but usually not sufficient in itself as demand could be upward of 18-20 L intake per day in absence of any AVP to concentrate urine)
  • DDAVP (desmopressin) replacement therapy
20
Q

SIADH etiology, labs

A
  • too much ADH

caused by any of:

  • ectopic production e.g. cancer
  • drugs, esp psychotropes
  • disruption of baroreceptor pathway (thorax or brain)

labs:

  • concentrated urine: low volume, high Osm
  • hyponatremia d/t continued water consumption despite decreased output
  • potential volume overload
21
Q

tx chronic vs acute hyponatremia

A

acute: treat fast
chronic: treat slow d/t risk of osmotic demyelination syndrome

22
Q

only ____ hormones can be made ectopically (e.g. in tumors)

A

peptide

steroid hormones require too much machinery

23
Q

basis for oral administration of sex steroid administration to lower sex steroids

A

tonic low-level GnRH (versus pulsatile GnRH) inhibits FSH/LH

24
Q

Laron syndrome

A

GH insensitivity
high GH, low IGF-1

sx:

  • short stature
  • truncal obesity
  • hypogonadism
  • prominent forehead
  • depressed nasal bridge
  • underdeveloped mandible
  • reduced susceptibility to cancer (tumors rely on IGF-1)

tx:
- IGF-1 injections help

25
Q

pseudohypOparathyroidism

A

PTH resistance
high PTH
low Ca++
high PO4-

most common subtype: Albright’s hereditary osteodystrophy
- includes resistance to other hormones

26
Q

McCune albright syndrome

A

Gs protein subunit activation
enhanced sensitivity to many hormones
mosaic pattern

sx:

  • cafe au lait pigmentation d/t mosaic hypersensitivity to MSH
  • fibrous dysplasia (fibrous, weak, uneven bone growth) d/t FGF hypersensitivity
  • precocious puberty, F>M d/t GnRH production and ovarian cysts (F) or autonomous testosterone production (M)
  • in males, macroorchidism (large testes) and/or testicular lesions
  • hypophosphatemia
  • other peptide hormone hypersensitivities may also occur, e.g. hyperthyroidism, growth hormone excess, neonatal Cushing’s syndrome (ACTH)

tx:

  • hormone antagonists
  • (including puberty blockers)
27
Q

acidophils

A

pink-staining cells of anterior pituitary
somatotrophs: GH
mammotrophs/lactotrophs: prolactin

28
Q

basophils (pituitary)

A

dark staining cells of anterior pituitary

thyrotrophs: TSH
gonadotrophs: FSH and LH
corticotrophins: ACTH

29
Q

chromophobes

A

non-staining cells of anterior pituitary
degranulated/dying cells
stem cells

30
Q

posterior pituitary histology

A

mostly storage cells

storage only, ADH and oxytocin

31
Q

monotonous appearance on AP histology

A

indicates an adenoma (overgrowth of one cell type)

H&E (acidophilic/basophilic), IHC, clinical picture can identify hormone

32
Q

prolactinoma

A

eosinophilic monotonous AP adenoma
most common pituitary adenoma

hypogondadism
amenorrhea
galactorrhea

SFM5 (14 decks)

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