Pituitary Gland Flashcards

1
Q

what is the infundibulum?

A

the stalk that attaches the hypothalamus to the pituitary gland (sits in the sella turcica)

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2
Q

what hormones does the anterior Pit secrete?

A

ACTH, TSH, LH, GH, FSH, PRL

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3
Q

what hormones does the posterior pit secrete?

A

oxytocin and ADH

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4
Q

what does the intermediate lobe produce?

A

melanocyte-stimulating hormone that controls skin pigmentation

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5
Q

GH excess

A

benign pituitary adenoma, a mixed cell tumor, or ectopci tumors (islet cell type) or MEN type I

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6
Q

what does a pit. adenoma secrete?

A

> 1 cm, stimulates GH release that then stimulates the relase of insulinlike growth factors from the liver

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7
Q

what accounts for 10-15% of pituitary tumors?

A

somatotrph-producing tumors

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8
Q

what are mixed cell tumors often associated with?

A

PRL secretion

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9
Q

what is gigantism?

A

occurs in children prior to closure of the epiphyses and causes excess growth of long bones (super rare)

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10
Q

what is acromegaly

A

causes enlargement and elongation of the hands, feet and jaw and internal organs

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11
Q

when is the onset of acromegaly?

A

in the 30s so it doesn’t affect long bones

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12
Q

what are other features of acromegaly?

A
  • increased risk of DM. HTN, CAD
  • doughy, moist hands
  • macroglossia
  • carpal tunnel syndrome,
  • deep, coarse voice
  • obstructive sleep apnea
  • goiter
  • HTN and cardiomegaly
  • weight gain and insulin resistance
  • arthralgias and arthritis
  • colon polyps
  • hyperhidrosis
  • cystic ance
  • acanthosis nigrican
  • HA
  • spinal stenosis
  • tmeproal hemainopsio
  • decreased libido
  • ED
  • menstural abnormalites
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13
Q

what is a common organ finding upon dx of acromegaly?

A

overt heart failure w/ dilated left ventricle and reduced EF

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14
Q

dxof GH excess

A

if IGF-1 is elevated fivefold, them suggests adnemoa

PRL levles are also measure

-randome GH levels aren’t accurate

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15
Q

what would a 1 hour glucose tolerance test show?

A

failure of GH to decrease to 2 ug/L after 75 g loading dose

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16
Q

what is the modality of choice when dx GH excess?

A

MRI- negative scan virtually r/o GH pit adenoma

skull radography often shows enalarged sella and thickened skull

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17
Q

what might an xray of the hands and feet reveal?

A

tufting of the terminal phalanges

18
Q

tx of GH excess?

A

somatostatin analogs

ocreotide and lanreotide are inhibiory and may decrase tumor size

19
Q

what can be used for pts that fail surger?

A

DA agonist like cabergoline or bromocriptine 9supress GH levels)

20
Q

what is the most successful surger in pts w/ GH blood levels below 50 and tumors no larger than 2 cm?

A

transphenoidal microsurger

21
Q

what ist he best measure of surgical success in GH excess?

A

normilization of IGF-I

22
Q

what is pegvisomant?

A

a GH receptr antagonist that blocks hepatic IGF-1 production- sx relieft

23
Q

Diabetes Inspidus

A

-insipid- tasteless (as opposed to sweet0mellitus)

24
Q

what is DI caused by?

A

deficiency of or resistance to vasopressin (ADH)

25
Q

at what serum osmoloatlity level does max antidiuresis occur?

A

295

26
Q

at what serum osmolaltiy does thirst kick in?

A

290

27
Q

what specifica gravity do DI pts hang out around?

A

1.00

28
Q

what is primary DI?

A

genetic or sporadic

29
Q

what can secondary DI be caused by?

A

hypothalamic or pituitary pathology caused by tumor, anoxic encephalopathy, surgery, accidental head trauma, infxn, sarcoidosis, multifocal langerhangs cell granulomatosis or metastatic dz

30
Q

what are the four types of DI?

A

hypothalmaic, nephrogenic, transient, primary polydipsia

31
Q

what are the clinical features of DI?

A

polydipsia, polyuria, and a dilute urine

  • intense thrist w/ fluid intake of 2 to 20 L/da
  • craving for ice water
  • large volume polyuria
  • hypernatreumoa
  • dehydration

-unremitting enuresis

32
Q

what are features of central (hypothalamic) DI?

A

inability to produce and secrete vasopression (levels will be low)

  • commonly occurs after head trauma or brain surgery
  • can be inhertited
  • may lack “osmostat”
  • repsoneds to desmopressin
33
Q

what are features of nephorogenic DI?

A

kidney unalbe to respond to vasopressin (levels are high)

  • associated w/ CKD, lithium toxcicity, hypercalcemia, hypokalema
  • may be inheroted
  • abnormal receptors in kidneys
  • NO response to desmopressin
34
Q

what is transient DI?

A
  • pregnance and puerperium

- rapid destruction/breakdown of vasopression

35
Q

what is primary polydipsia?

A

disorder of thirst mechanism- ADH levels low

36
Q

dx studies of DI

A

clinical judgement

  • serusm osmolality high, urine osmolality low
  • BUM may be low,
  • uric acid elevlabed
  • serum sodium can be N or high
  • may need supervised vasopressing challenge test
  • MRI- mass lesion
37
Q

tx of DI

A

desmopressin acetate in central DI or transient DI

38
Q

mild cases of DK?

A

none

39
Q

what else can central and nephrogenic DI respond to?

A

HCTZ, K or amiloride supplementaion

40
Q

what does nephrogenic DI respond to?

A

indomethacin +/- desporessin, HTZ, amiloride