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
at what serum osmoloatlity level does max antidiuresis occur?
295
26
at what serum osmolaltiy does thirst kick in?
290
27
what specifica gravity do DI pts hang out around?
1.00
28
what is primary DI?
genetic or sporadic
29
what can secondary DI be caused by?
hypothalamic or pituitary pathology caused by tumor, anoxic encephalopathy, surgery, accidental head trauma, infxn, sarcoidosis, multifocal langerhangs cell granulomatosis or metastatic dz
30
what are the four types of DI?
hypothalmaic, nephrogenic, transient, primary polydipsia
31
what are the clinical features of DI?
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
what are features of central (hypothalamic) DI?
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
what are features of nephorogenic DI?
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
what is transient DI?
- pregnance and puerperium | - rapid destruction/breakdown of vasopression
35
what is primary polydipsia?
disorder of thirst mechanism- ADH levels low
36
dx studies of DI
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
tx of DI
desmopressin acetate in central DI or transient DI
38
mild cases of DK?
none
39
what else can central and nephrogenic DI respond to?
HCTZ, K or amiloride supplementaion
40
what does nephrogenic DI respond to?
indomethacin +/- desporessin, HTZ, amiloride