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RC Peds Endo 2023 > Pituitary/H/R/Onc > Flashcards

Pituitary/H/R/Onc Flashcards

1
Q

how does PRL cause hypo hypo

A

inhibiting hypothalamic gonadotropin-releasing hormone secretion

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2
Q

how to screen for macroPRL

A

polyethylene glycol precipitation

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3
Q

PRL stimuli

A

TRH
GHRH
Estradiol
Oxytocin
VIP
Serotonin

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4
Q

inhibitors of PRL

A

dopamine
Prolactin
○ Inhibits it’s own release
○ Stimulates dopamine - likely to inhibit itself

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5
Q

PRL levels

A

50-250 ng/mL :Drug induced

<40-60 ng/mL: Venipuncture stress and breast stimulation

25-100 ng/mL: secondary to a non-functioning mass that interrupts the dopamine neurons

100-250 ng/mL: microadenomas (prolactinomas </= 1 cm)

> 500 ng/mL: macroprolactinomas

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6
Q

usually first sign in hyperPRL

A

hypogonadism
(more than lactation)

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7
Q

first labs to do when PRL high to r/o other

A

HCG and TFT and GH

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8
Q

tx hyperPRL

A

dopamine agonist
- bromocryptine
- carbergoline

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9
Q

causes of hyperPRL

A
  • Prolactinoma
  • Macroprolactinemia: due to antibodies causing a large prolactin aggregate, which is not active so has no symptoms, but only increases bound prolactin
  • Pituitary stalk disruption
    ○ Non-functioning tumours, craniopharyngiomas, granulomatous infiltration, TBI
    ○ Decreased dopamine inhibition from hypothalamus
  • Stress - surgery, exercise, hypoglycemia, acute MI
  • Breast disease, nipple stimulation, disease or injury to the chest wall, spinal cord injury, burns, herpes zoster
    ○ Neurogenic reflex: PRL secretion stimulated by activation of afferent neural pathways
  • Hypothyroidism
    ○ Hyperplasia of lactotrophs and thyrotrophs, presumably due to TRH hypersecretion
  • Dopamine receptor blockers (metoclopramide, antipsychotics): stops dopamine from inhibiting prolactin release
  • Renal failure and liver failure
    ○ Impaired renal degradation of prolactin and altered central prolactin regulation
  • Estrogen: binds to estrogen receptor (response element) that controls the prolactin gene in the lactotrophs
  • Pregnancy/lactation: physiologic increases prolactin
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10
Q

meds causing hyperPRL

A

rispiridone
olanzapine

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11
Q

size of PRLoma

A

Macroprolactinoma: >/=1cm
Microprolactinoma: <1cm

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12
Q

syndromes w PRLoma

A

MEN1’
Familial hyperprolactinemia
Familial isolated pituitary adenoma

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13
Q

most common H w pit adenoma

A

PRLoma - 66%

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14
Q

indications to treat PRLoma

A

○ Galactorrhea
○ Amenorrhea/Hypogonadism (if bothersome, could observe if isolated symptom)
○ DESIRE Planning pregnancy
○ Visual field deficits
○ If medication-induced and the med cannot be stopped or substituted and symptomatic (indication for surgery)
○ If impact on bone health (low BMD) + hypogonadotropic hypogonadism
○ Pituitary macroadenoma (not appropriate for observation alone)

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15
Q

Adv/Disadv of dopamine agonists in PRLoma

A

Bromocriptine
§ Advantage: reduces adenoma size effectively
§ Disadvantage: nausea (++), not as effective at lowering prolactin levels as cabergoline, given daily

Cabergoline
§ Advantages: only administered once or twice a week, higher rates of success suppressing prolactin, better tolerated
§ Disadvantage: risk of valvular heart disease (seen at high doses used in Parkinson’s tx)

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16
Q

TSH B subunit - genes needed

A

POUF1
GATA2

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17
Q

stimulants of TSH secretion

A
  • TRH
  • Low T3
    ○ PTU
  • Low T4
    ○ Iodine Def
  • Leptin
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18
Q

inhibitors of TSH secretion

A
  • SRIF
  • T3 > T4
  • Glucocorticoids
  • Dopamine (acutely)
  • Fasting/Starvation
  • Antiepileptics
  • Certain cytokines
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19
Q

ACTH stim by?

A

CRH
AVP

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20
Q

ACTH prod cells

A

Corticotrophs

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21
Q

key genes for ACTH

A

TBX19
TPIT

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22
Q

what R does ACTH bind

A

MC1R -> hyperpigmentation
MC2R -> adrenal steroidogenesis

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23
Q

2 neurons ADH is made

A

magnocellular -> sends ADH to post pit
parvocellular -> sends ADH to ant pit -> enhances ACTH secretion

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24
Q

2 most imp gene GnRH devel

A

KAL1
PROK2

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25
Q

hormones that are peptides

A

HT
○ TRH, CRH, GHRH, GnRH
○ AVP, Oxy
○ SRIF

PIT
○ ACTH

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26
Q

hormones that are Glycoproteins

A

LH, FSh, TSH

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27
Q

hormones that are proteins

A

GH, PRL

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28
Q

nuclear receptor hormones

A
  • cortisol
  • TH
  • E
  • Proges
  • testo
  • Aldo
  • vit D
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29
Q

Thyroid hormone receptor type and locaton

A

Nuclear R

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30
Q

Steroid hormone receptor type

A

Nuclear

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31
Q

TSH receptor type and location

A

G-protein coupled receptor = located in cell membrane

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32
Q

GPCR Gsa - list

A

TSH
LH / HCG
FSH
CRH
ACTH/MSH
GHRH
PTH

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33
Q

GPCR Gqa - list

A

GnRH
TRH
ADH
Oxytocin

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34
Q

GPCR Qia

A

Somatostatin
Dopamine

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35
Q

GOF mutations

○ Gas

○ LH receptor

○ TSH receptor

○ PTH-PTHrp receptor

○ Calcium sensing receptor

A

○ Gas
§ Mc-Cune Albright syndrome
○ LH receptor
§ Familial Male Precocious puberty
○ TSH receptor
§ Congenital hyperthyroidism
○ PTH-PTHrp receptor
§ Osteitis fibrosa cystic
○ Calcium sensing receptor
§ Familial hypercalciuric hypcalcemia

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36
Q

LOF mutations
○ TSH receptor
○ Calcium sensing receptor
○ Gas
○ Vasopressin receptor
○ LH/hCG receptor

A

○ TSH receptor
§ TSH resistance
○ Calcium sensing receptor
§ Familial hypocaluric hypercalcemia, Severe neonatal hyperparathyroidism
○ Gas
§ PHP (maternal inheritance) – AHO
□ PTH , GHRH, TRH resistance
§ PHP (paternal inheritance)
□ AHO
○ Vasopressin receptor
§ Nephrogenic diabetes insipidus
○ LH/hCG receptor
§ XY female, testicular unresponsiveness to LH

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37
Q
  • Germline GPCR activating mutations
A

§ KISS1R – precocious puberty
§ CASR – autosomal dominant hypocalcemia
§ PROKR2 – precocious puberty
§ LHCGR (LH receptor) – pseudoprecocious puberty, testotoxicosis
§ FSHR – ovarian hyperstimulation
§ TSHR – hyperthyroidism, neonatal thyrotoxicosis
§ MC2R (ACTHR) – Cushing syndrome
§ PTH1R – metaphyseal chondrodysplasia
§ AVPR2 – Nephrogenic SIADH
§ GPR101 – X-linked acro-gigantism (overgrowth syndrome, excess GH from pituitary adenoma or hyperplasia)

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38
Q

PTH-R mutation

A

§ Activating: Jansen-type metaphyseal chondrodysplasia

§ Inactivating:
Homozygous: Blomstrand’s chondrodysplasia

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39
Q

CaSR mutations

A

§ Inactivating
1. Familial benign hypocalciuric hypercalcemia (hetero)
2. Neonatal severe hyperparathyroidism (homo)

§ Activating (heterozygous)
AD hypocalcemic hypercalciuria
Bartter syndrome type V

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40
Q

MC2R mutation

A

Familial glucocorticoid deficiency type 1

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41
Q

V2 receptor type?

A

GPCR - Gqa

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42
Q

V2 mutation

A

Inactivating: X-linked Nephrogenic DI
Activating:Nephrogenic SIADH

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43
Q

Cytokine Receptors - hormones?

A

PRL
GH
Leptin

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44
Q

Inactivating mutations in Cytokine R

A

GHR - GH insensitivity
- Laron dwarfism
- Partial GH insensitivity

Leptin R
- obesity + hypohypo

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45
Q

Tyrosine Kinase Receptors

A

Insulin
IGF1
FGFR1
FGFR2
FGFR3

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46
Q

what is Ant Pit made from in development
- what is that made from

A

Rathke’s pouch from Oral ectoderm and neuroectoderm

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47
Q

what is post pit made from

A

ventral HT and 3rd ventricle

48
Q

what part of the gland is the rathe pouch come from

A

Pars intermedia: remnant tissue (Rathke pouch)

49
Q

What is GATA2 important for

A

TSH
LH
FSH

50
Q

MRI findings that can be assoc w hypopit

A
  • Absent posterior pituitary
    • Optic nerve hypoplasia
    • Ectopic posterior pituitary
    • Small anterior pituitary
    • Thin pituitary stalk
    • Pituitary stalk thickening
    • Absent corpus callosum
    • Absent septum pellucidum
    • Holoprosencephaly
    • Schizencephaly
    • Cerebellar hypoplasia
    • Chiari malformation
    • Empty sella
    • Hypothalamic hamartoma
    • Aplasia of the fornix
51
Q

Cause of thickened stalk

A

Germinoma
TB
Langerhans Cell Hypophisitis
Lymphocytic Hypophysitis
Sarcoidosis
- ectopic neurohypophysis
- Rathke cleft cyst
- Pituitary adenoma
- Craniopahryngioma

52
Q

H def w thickened stalk

A

w○ Central DI (91.3%) down
○ Growth hormone deficiency (GHD) (56.5%) down
○ Hyperprolactinemia (39%) up
○ Central hypothyroidism (34.8%) down
○ Adrenal insufficiency (9%) down
○ Precocious puberty (8.7%) up
**For pituitary stalk thickening you have deficiencies except breast development! (think prolactin and precocious puberty)

53
Q

when does ectopic PP happen?

A

when the posterior pituitary gland is incompletely descended anywhere along the path of the pituitary stalk.

54
Q

if you can see the stalk, what is most likely H def?

A

When the stalk is visualized, the clinical presentation is more often isolated GH deficiency rather than multiple pituitary hormone deficiencies

55
Q

functional adenoma - H?

A
  • Prolactinoma (66%)
  • Growth-hormone producing (9-13%)
  • ACTH-producing (4-6%)
  • TSH-secreting (0.5-3%)
  • Gonadotroph-secreting (very rare)
56
Q

pituitary is where?

A

sella

57
Q

does non functioning adenoma cause H def?

A

could cause hyperPRL from compression

58
Q

Risk of PRLoma in pregnancy

A

MicroPRLoma: <5%
MacroPRLoma: 31%

59
Q

PRL levels increasing during pregnancy normal?

A

10fold increase

60
Q

Neonatal signs of hypopit

A
  • Midline defects
    • Short
    • Cleft Lip/palate, craniofacial abnormalities
    • Central incisor
    • Micropenis (FSH, LH)
    • Cryptorchidism (FSH, LH)
    • Mutation – agenesis or CC, absent pit, etc)
  • Hypotension (ACTH)
  • Large posterior fontanel, large tongue, umbilical hernia (TSH)
  • Hypoglycemia (GH, ACTH)
  • Hyponatremia (ACTH (b/c increased AVP), TSH
  • Liver
    • Hyperbili (TSH)
    • Cholestatic jaundice
    • Giant cell hepatitis
  • Poor feeding
  • apnea
  • jitteriness
  • temp instability
61
Q

Hypothalamic problems - signs of?

A

Hypothalamus often accompanied by:
- Appetite defects (hypothalamic obesity)
- Thermoregulation defects
- Sleep defects

62
Q

Signs of SOD

A

○ Wandering gaze
○ Pituitary deficiency – hypoglycemia
○ Midline defects
○ Optic nerve hypoplasia
○ Development – normal to severely delayed
○ 30% have complete triad

63
Q

SOD H def

A

○ GH = most common
○ TSH
○ ACTH
○ GnRH = least common Ant Pit Def
○ DI = least common overall

64
Q

Psychosocial dwarfism

A
  • Triad
    ○ Short stature
    ○ Insatiable appetite
    ○ Pubertal delay / delated sexual maturation
    • Also
      ○ strange eating habits
      ○ infant feeding difficulties, sleep problems, delayed speech, malabsorption, abdominal protuberance
    • Generally reduced GH secretion
      No response to GH until psychosocial problems improve
65
Q

Pituitary apoplexy - what is it

A

caused by bleeding into and/or hypoperfusion of a hypothalamic/pituitary lesion.

Apoplexy can cause pituitary hormone deficiencies, although the presentation is often acute

66
Q

H def from infection? most likely?

when to resolve

A

somatotropin and gonadotropin deficiencies

DI rare

usually resolve w/in 6 m

67
Q

causes of acquired hypopit

A

Most common: MASSES

Other causes:
- Head trauma
- Infection
-Infiltrative
- Sarcoidosis
- LCH
○ DI first
- Inflammatory
- Lymphocytic hypophysitis (autoimmune)
- Infectious
- Meningitis, encephalitis
- Psychosocial Dwarfism

68
Q

what can insulin tolerance test test?

A

GH axis
ACTH - Cortisol axis

69
Q

TKI in cancer therapy - endo outcome

A

Tyrosine kinase inhibitors can cause varying degrees of loss of growth potential due to disruption of growth hormone signal transduction.

70
Q

Germinoma
pathophys
pres

A
  • Stalk involvement
    • DI most common
      ○ Then growth
      ○ Then puberty (may be precocious)
      Good response to XRT
71
Q

risk of DTC w RT

A

○ Risk of differentiated thyroid cancer (DTC) increases linearly until 10 Gy
○ Plateaus from 10-30 Gy
○ Decreases at doses >30 Gy

72
Q

female cancer survivors
- risk of POI
- increased risk w?

A

8% risk of developing POI
* Individuals at highest risk:
- alkylating agents
- abdominal radiotherapy
- hematopoietic stem cell transplant

73
Q

POI def’n for cancer survivor

A
  • Absence of menses for >/= 4 mos AND elevated FSH levels in the menopause range x 2

OR
- Delayed or arrested pubertal progression in girls >/= 13 yo

74
Q

fertility preservation options in girls

A

○ Oocyte and embryo cryopreservation
Prepubertal girls scarcity of evidence for ovarian tissue cryopreservation

75
Q

what effects gonads in males in oncology tx?

A

**Chemotherapy impacts spermatogenesis

**Radiotherapy impacts testosterone production

76
Q

how to assess spermatogenesis in males?

A

Semen analysis = gold standard primary surveillance

also
Testicular volumes + FSH + inhibin B

77
Q

how is ant pit formed

A

Invagination of Rathke’s Pouch (ectoderm)

78
Q

what is pars intermedia

A

boundary between anterior & posterior – remnant of Rathke’s Pouch

79
Q

what ant pit hormones do not bind to protein coupled receptors

A

what ant pit hormones DO NOT bind to Protein coupled receptor

80
Q

what kind of hormones are TRH, CRH, GHRH, GnRH

A

peptides

81
Q

what kind of hormones are the following hormones:

ACTH:

LH, FSH, TSH:

GH, PRL:

A

ACTH: Peptide

LH, FSH, TSH: Glycoproteins

GH, PRL: Protein

82
Q

in GPCR what does Gqα do

A

ACTH: Peptide

LH, FSH, TSH: Glycoproteins

GH, PRL: Protein

83
Q

in GPCR what does Gsα do

A

stimulates AC, makes PKA

Adenyl cyclase

Protein kinase A

84
Q

what hormones bind to Gsα

A

CRH
ACTH
TSH
GHRH
LH,FSH
CaSR
PTH

85
Q

what hormones bind to Gqα

A

TRH
GnRH
GHS-R
AVP (1b)
Oxy

86
Q

in GPCR what does Giα do

A

inhibits Adenyl cyclase

87
Q

what stimulates GH

A

Hormones:
GHRH
Ghrelin
Thyroid hormone
Estrogen
Dopamine (L-Dopa)
Glucocorticoids

Nutrition
Fasting
Hypoglycemia
- Glucagon
- Insulin
Protein/amino acids
- Arginine
Malnourished

Other:
Galanin
Alpha agonists (Clonidine)
Beta antagonists (Propranolol)
Exercise
Stress
Trauma
Sepsis

88
Q

What inhibits GH secretion

A

Hormones:
SRIF
IGF-1
Hypothyroidism
Hyperthyroidism
Glucocorticoids
Chronic admin
Deficiency

Nutrition:
Glucose
FFA

Other:
Depression
Emotional deprivation
β-adrenergy

89
Q

what hormones share a common Alpha unit and have a specific beta unit

A

TSH
LH
FSH
HCG

CαSβ
Common Alpha
Specific Beta

Rock the Casbah

90
Q

How does TSH work at receptor

A

Binds GPCR (Gsα) - PKA

This increases:
- Iodide influx into cell, efflux into colloid
- Synthesis of
—NADPH
—Hydrogen Peroxide
—Thyroglobulin (TG)
—TPO
-Uptake of TG into cell, release into plasma

91
Q

PRL role

A

Important in pregnancy
-Mammary
- Lactation if suckling
- No milk during pregnancy

Not primary for milk ejection
Oxytocin

Inhibits LH, FSH
(Secondary amenorrhea while breast feed)
- Inhibit Kisspeptin

92
Q

pathologic cause of high PRL

A

Prolactinoma (> 1000ug/dl)
Stalk Compression/dissection
Hypothyroidism
Surgery
Seizure
Head Trauma
Renal Failure
Hypothalamic mass
Prolactin receptor mutation

93
Q

physiologic causes of hyperPRL

A

Pregnancy
Lactation
Stress
Coitus
Nipple stimulation
Sleep
Exercise

94
Q

what drugs can cause high prolactin

A

Dopamine antagonists (Parkinson meds)
Antipsychotics: Risperidone
Estrogen
Ranitidine
Anti epileptics: Phenytoin
Opiates
Anti depression: SSRIs, TCAs

95
Q

What syndrome to think of w PRLoma

A

MEN1

96
Q

most common presentation of PRLoma

A

hypogonadism

97
Q

w/u for hyperPRL

A

TFTs
Macroprolactin (less bioactive)

98
Q

most common tumours affecting pituitary

A

1) craniopharyngioma
2) pituitary adenoma

germinoma

99
Q

craniopharyngioma
- what is it
- benign /maglinant

A
  • remnant of Rathke pouch
  • sellar tumour
  • benign tissue but mass affect causes a lot of problems

most common type: Adamantinomatous

100
Q

Pituitary adenoma - most common pit abn

A

PRL
ACTH

101
Q

germinoma - most common assoc

A

DI because of stalk

DI most common, followed by growth, puberty (may be precocious)

102
Q

Hypopituitarism following cranial XRT
Less than what is def unlikely?
Above what is def very likely?

what are other cutoffs?

A

<10 Gy
>50 Gy

≥22? Gy: GH, LH, FSH

≥30 Gy: TSH, ACTH

103
Q

infiltrative causes of hypo pit

A

Sarcoidosis
LCH

104
Q

inflammatory causes hypopit

A

Lymphocytic hypophysitis (autoimmune)

105
Q

What will unmask central AI

A

T4
GH

106
Q

what will unmask Central DI

A

cortisol
T4

107
Q

Anorexia nervosa - H-P effects

A

● Gonadal axis – low energy state resulting in hypothalamic amenorrhea (low LH/FSH)
○ Also have low androgen as well as estrogen
● Adrenal axis – chronically stimulated
○ hypercortisolemia
● Thyroid axis – nonthyroidal illness syndrome
○ Low total T3, high rT3 (due to increased peripheral deiodination of T4 to reverse T3)
○ Level of fT4 vary from normal to low-normal
○ TSH varies from normal to low-normal
● Growth – GH resistance due to chronic nutritional deprivation
○ GH high, Low IGF-1

i) Decreased BMD
ii) Hypoglycemia and hyperinsulin
- decreased leptin

108
Q

pituitary adenoma - post op PRL goes up - what kind of tumour?

A

prolactinoma!!

b) What explains the pre-op and post-op findings?
Hook effect
c) What would you do to confirm the diagnosis?
Serial dilution

109
Q

adv/dis for carbergoline
s/e

A

● Advantages: only administered once or twice a week, higher rates of success suppressing prolactin
● Disadvantage: risk of valvular heart disease, only at high doses used in Parkinson’s

-nausea
-vomiting
-heartburn
-dizziness
-dysmenorrhea
-fatigue
-constipation
-orthostatic hypotension
-fibrotic valvulopathy
-psychiatric disturbances (esp impulse control disorders)

110
Q

adv/dis for bromocryptine
s/e

A

● Advantage: reduces adenoma size effectively
● Disadvantage: nausea (++), no as effective at lowering prolactin levels as cabergoline, given twice daily

-nausea
-orthostatic hypotension
-headache
-diarrhea
-abdominal pain
-anorexia
-fibrotic valvulopathy
-psychiatric disturbances (esp impulse control disorders)

111
Q

reasons to consider transphenoidal surgery in adenoma

A

-Resistant to treatment (ie prolactin not coming down)
-macroprolactinomas with no tumour shrinkage with treatment and/or cannot tolerate dopamine agonist therapy consider pre-pregnancy resection
-Cannot tolerate medications (++ side effects)
-compressive symptoms

112
Q

When considering stopping dopaminergic therapy what factors to consider?

A

○ Prolactin - needs to be normal
○ Duration of therapy - 2 years min
○ MRI finding - no evidence of adenoma
○ Initial prolactin level - the higher the PRL, the lower the chance of remission
○ Size of adenoma
○ Persistently symptomatic
○ Previously failed wean of therapy
○ (Menopause)

113
Q

what is most common deficiency with holoprosencephaly

A

DI - 70% of individuals with holoprosencephaly have DI

Anterior pituitary deficiencies are less common

114
Q

after cranio tx, what is most likely H def, and how does it present?

A

growth hormone deficiency

normally presents with normal growth velocity and excess weight gain

The treatment of GH deficiency does not cause improved final height, since growth velocity is normal, but can help with weight loss and improving lean muscle mass.

115
Q

liver finding in hypopit

A

giant cell hepatitis

116
Q

where is the Steroid receptor located

A

in the cytoplasm bound to heat shock proteins;

when steroid ligand binds, HSP dissociates and nuclear translocation signal is exposed and initiates transport into nucleus where it will bind with the hormone response element, initiating transcription etc.

117
Q

antenatal u/s signs of hypopit

A

Cleft Lip/palate
Abnormal midline brain malformation - Absence/dysgenesis of corpus callosum, absence/dysgenesis of septum pellucidum, holoprosencephaly
Craniofacial abnormalities
Umbilical hernia (TSH)
Bradycardia (TSH)
Micropenis (GH, LH/FSH)

Cryptorchidism (LH/FSH) - but won’t see this on US
***not IUGR - usually normal BW, then have poor weight gain

RC Peds Endo 2023 (17 decks)

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