ENDOCRINE - GOLJAN Flashcards

1
Q

suppression tests

A

DMX-dexamethasone-cortisol analogue

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2
Q

low/dose DMX

A

low dose DOES NOT suppress cortisol in Cushing syndrome

high dose DOES suppress ACTH production

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3
Q

which hyper functioning endocrine disorders can be suppressed

A

MOST CAN NOT

but prolactinoma and cushing syndrome can

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4
Q

what tumors affect the hypothalamus

A
  1. pituitary adenoma MC
  2. craniopharyngioma
    * 3. midline hamartoma - not a neoplasm/produces precocious puberty in boys
  3. Langerhans histiocytosis - metastasis
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5
Q

what inflammatory disorder affect the hypothalamus

A

sarcoidosis

meningitis

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6
Q

central DI

A

2ndary hypopituitarism

no ADH from hypothalamus

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7
Q

ADH made in

A

supraoptic and paraventricular nuclei

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8
Q

hyperprolactinemia

A

loss of DA from hypothalamus causes increased prolactin release which leads to GALACTORRHEA

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9
Q

define: true precocious puberty
girls vs guys
major cause

A

due to CNS dysfunction, not peripheral (pseudoprecocious puberty)

guys - puberty before age of 9
girls - puberty before age of 8

midline hamartoma
McCune-Albright syndrome

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10
Q

*Kallmann syndrome

A
X-linked AR disorder that affects males
embryological defect in migration
anosmia b/c loss of olfactory bulb
and decrease in GnRH from hypothalamus ( less estrogens + androgens )
-underdeveloped genitals
-sterile gonads
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11
Q

pineal gland

  • location
  • production
A

located at the quadrigeminal plate aka tectum
melatonin - sleep/mood/circadian rhythms

http://www.radpod.org/wp-content/uploads/2007/10/quadrigeminal_plate_lipoma.jpg

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12
Q

pineal gland

-disorders

A

dystrophic calcification - beings in childhood
used as a marker for midline shift

tumors:

  • majority are GERM CELL that resemble SEMINOMA
  • teratomas
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13
Q

a pineal gland tumor causes what clinical findings

A
  • PARINAUDs syndrome - inability to perform upward conjugate gaze
  • obstructive hydrocephalus- b/c of aqueduct of sylvius
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14
Q

MC of hypopituitarism is adults

A

nonfunctioning ( null ) pituitary

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15
Q

MC of hypopituitarism in kids

A

*craniopharyngioma

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16
Q

craniopharyngioma is derived from*
located where?
features?
sequela?

A

rathke pouch - SURFACE ECTODERM
above the sella turcica
cystic tumor w/ hemorrhage and calcification
bitemporal hemianopia + CDI

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17
Q

MEN I syndrome

A

parathyroid - hyperPTH
pancreas - zollinger Ellison or insulinoma
pituitary - adenoma

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18
Q

Sheehan postpartum necrosis

A

hypovolemic shock causes infarction of pituitary

loss of prolactin leads to no lactation

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19
Q

located of pituitary in relation to sella turcica

A

below

craniopharyngioma is above

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20
Q

empty sella syndrome

types

A

radiograph shows empty sella turcica

Primary type - anatomic defect. CSF invades space and pushes on pituitary leading to atrophy ** seen in obese woman w HTN

Secondary type - regression in size due to trauma, radiation, etc

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21
Q

what happens to pituitary during pregnancy

A

increases double in size due to prolactin synthesis

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22
Q

how does progesterone relate to prolactin

A

inhibits release of prolactin

seen during pregnancy

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23
Q

autoimmune destruction of pituitary gland seen in women

A

lymphocytic hypophysitis

seen during or after pregnancy

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24
Q

oxytocin produced primarily where

function

A

paraventricular nucleus

uterine contractions + milk ejection

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25
Q

MC pituitary tumor

A

prolactinoma

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26
Q

prolactinoma can also secrete

A

GH

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27
Q

clinical features of prolactinoma

women vs men

A

WOMEN

  • 2ndary amenorrhea b/c prolactin inhibits GnRH which decreases FSH/LH
  • NO galactorrhea present

MEN

  • loss of libido b/c of less LH ( less testosterone )
  • decrease estrogen and progesterone
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28
Q

prolactinoma tx

A

bromocriptine or cabergoline

surgery if microadenoma <10mm

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29
Q

effects of GH

A
  1. stimulate gluconeogenesis and AA uptake in muscles
  2. cause increase in IGF-1 production
  3. antinatriuretic action (retains sodium)
30
Q

*functions of IGF-1

A

stimulate bone (lateral, linear) cartilage and soft tissue growth

31
Q

MCC of death in acromegaly

A

dilated cardiomyopathy

32
Q

big clinical features of acromegaly

A
  1. DM - hyperglycemia from increased gluconeogenesis
  2. HTN - GH retains Na+ / hyperglycemia causes increased insulin which acts on mineralocorticoid rec.
  3. macroglossia
33
Q

*steps in thyroid hormone synthesis

A
  • everything is mediated by TSH / w/o it = atrophy
    1. iodide is trapped
    2. thyroid peroxidase mediates oxidation of iodide to iodine ( inhibited by propylthiouracil )
    3. organification
    a. iodine + tyrosine = MIT ( monoiodotyrosine )
    b. MIT + DIT = T3
    c. DIT + DIT = T4
    4. hormones stored as colloid
    5. proteolysis by lysosomal proteases
    6. released and bind to TBG
34
Q

thyroid hormone synthesizes what 2 things

A
  1. Beta adrenergic receptors for catecholamines

2. LDL receptors

35
Q

interrelation between total serum T4, FT4, and TSH

A
  • if TSH increases, then total serum T4 increases \ and vice versa
36
Q

how does estrogen affect TSH

A
  1. increases TSH production by the liver
  2. increases TBG which binds with free T4
  3. thyroid makes more T4 to compensate for loss

total serum T4 is increased
FT4 is normal = normal TSH

37
Q

what causes a decrease is TSH

A

anabolic steroids + nephrotic syndrome

total serum T4 is decreased, because lower TBG
but FT4 and TSH remain normal

38
Q
TBG normal + FT4/FT3 increased
TBG normal + FT4/FT3 decreased
TBG decreased + FT4/FT3 normal
TBG increased + FT4/FT3 normal
*******************************************
A

graves disease or thyroiditis
hypothyroidism
anabolic steroids or nephrotic syndrome
estrogen and during pregnancy

39
Q

what is used to measure synthetic activity of the thyroid gland

A

123 Iodine uptake

40
Q

marker for thyroid cancer

A

thyroglobulin

41
Q
  • decreased uptake of 123 I
A
  1. inactivity of thyroid gland ( patient taking thyroid hormone - decreases TSH )
  2. inflammation of gland ( acute, subacute, chronic thyroiditis - interferes w normal function of gland )
42
Q
  • increased uptake of 123 I
A

indicates increased synthesis of T4

graves disease and toxic nodular goiter

43
Q

” cold “ thyroid nodule

A

decreased 123 I uptake

cyst, adenoma, cancer

44
Q

” hot “ thyroid nodule

A

toxic nodule goiter

45
Q

decreased serum TSH is seen in

A

thyrotoxicosis
hypothalamic dysfunction
hypopituitarism

46
Q

mass at the base of the tongue

A

lingual thyroid

47
Q

cystic midline mass

A

thyroglossal duct cyst

48
Q
  • different types of THYROIDITIS
A
  1. acute thyroiditis
  2. subacute granulomatous thyroiditis
  3. hashimoto thyroiditis
  4. Riedel thyroiditis
  5. subacute painless lymphocytic thyroiditis
49
Q

describe : ACUTE THYROIDITIS

A
bacterial infection
fever
painful tender gland
increased T4, decreased TSH
adenopathy is present 
decreased 123 I uptake
tx is penicillin or ampicillin
50
Q

describe : subacute granulomatous thyroiditis

A
MCC painful thyroid*
viral infection
usually follows URI
women 40-50
no fever of adenopathy
decreased T4, increased TSH
decreased 123 I uptake
self limiting
51
Q

HLA subtypes for Hashimoto thyroiditis

A

HLA-Dr3 + Dr5

52
Q

type of HSR in Hashimoto thyroiditis

A

mainly type 4 - cytotoxic T and helper T destroy parenchyma

also type 2- antibodies against TSH receptor

53
Q

what autoantibodies are in Hashimoto thyroiditis*

A

anti-microsomal and anti-thyroglobulin

54
Q

morphology seen in Hashimoto thyroiditis

A

enlarged, gray gland

lymphocytic infiltrate with prominent germinal follicles

55
Q

Hashimoto has increased risk for *

A

primary B-cell malignant lymphoma of thyroid

56
Q

describe : Riedel thyroiditis

A

“Riedel REPLACES thyroid with fibrous tissue”

and surrounding tissue

57
Q

hypothyroid disorder seen POSTPARTUM*

A

subacute painless lymphocytic thyroiditis

58
Q

describe : subacute painless lymphocytic thyroiditis

A
autoimmune destruction postpartum
NO germinal follicles 
slightly enlarged and painless 
antimicrosomal antibodies 
can progress to primary hypothyroidism
59
Q

hypothyroidism in infancy or early childhood

A

cretinism

60
Q

brain requires which thyroid hormone for maturation

A

thyroxine during 1st year of life *

61
Q

what is MYXEDEMA COMA

A

causes include :

  • idiopathic / cold exposure
  • infection
  • sedatives/opiates

clinical features include :

  • stupor *hypothermia
  • hypoglycemia, hypocortisolism
  • bradycardia, hypoventilation
62
Q

define : thyrotoxicosis

A

increase in hormones regardless of cause

63
Q

HLA subtypes of GRAVES disease

A

HLA- Dr3 + B8

64
Q

etiology of GRAVES disease

A

female dominant!

65
Q

GRAVES disease HSR

A

type 2

IgG autoantibodies against TSH receptor

66
Q

autoantibodies in GRAVES disease

A

anti-microsomal and anti-thyroglobulin

67
Q

unique features in GRAVES disease

A

pretibial myxedema, thyroid acropachy, exophthalmos

68
Q

define thyroid acropachy *

A

digital swelling and clubbing of fingers

separating of nail bed from nails - onycholysis

69
Q

describe : toxic multinodular goiter

A

one or more HOT nodules - TSH independent

LACKS exophthalmos and pretibial myxedema

70
Q

GRAVES disease in the elderly AKA

A

apathetic hyperthyroidism

  • thyromegaly
  • AFib + CHF
  • muscle weakness