Endocrine extras Flashcards

(47 cards)

1
Q
Hormone classes (by chem nature)
Tyrosine derived?
Peptide?
Proteins?
Steroids?
A

Tyr - NE, epi, DA
Peptides - Hypothalamic, also Growth Hormone
Protein - Insulin, (GH?), PRL
Steroids - Gluco, Mineralo, Sex Steroids (HAVE LONGER HALF LIVES IN BLOOD, BUT NOT STORED IN CELL)

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2
Q

G protein mechs, and the Hypothalamic peptides that use them:

A

Gs –> incr cAMP (TRH, CRH, GHRH)
Gi –> drops AC so drops cAMP and activates K+ channels (SST, PIH (DA))
Gq –> PKC –> IP3, DAG (GnRH GHRH)

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3
Q
Receptors for hormone classes
For steroids?
Who binds GPCR?
Who binds cytokine?
WHo binds EGF?
A

Steroids: enter nucleus and bind HRE –> gene transcription
Surface GPCR: Hypothalamic peptides (so not DA!)
Surface Cytokine: GH, prolactin (JAK/STAT - activation transcription)
Surface EGF family: insulin (binds and activates protein kinase)

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4
Q

Posterior and Anterior pituitary (anatomical relation to hypothalamus?)

A

PP is continuation of Hypo

AP is epithelial in original (from pharyngeal epithelium - Rathke’s pouch)

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5
Q

Effect of GH on insulin?

A

Counters action of insulin - i.e. it gets everything ready for growth rather than storage - increases availability of glucose ready for growth
BUT for GH to release IGF-1 you NEED NORMAL INSULIN LEVELS

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6
Q

Laron’s dwarfism vs African pygmies

A

Laron’s normal GH but bad receptors

Pygmies: normal GH but bad IGF-1 receptors

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7
Q

Tertiary, Secondary, Primary

A

Tertiary is Hypo, Secondary is Pit (BOTH CENTRAL)

Primary is target organ (PERIPHERAL)

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8
Q

Scant pubic hair?

A

Central adrenal insuff!

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9
Q

Order for loss of pit hormones

A

1) GH and LH/FSH
2) TSH/ACTH
3) finally PRL
reflects importance of each (except PRL)

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10
Q

ADH defic common in which tumors?

A

Common in metastatic tumors but NOT in pituitary adenomas

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11
Q

Made in adrenal cortex?

A

steroids! (gluco-, mineralo-, sex-)

has 3 zonas

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12
Q

Zona glomerulosa

A
outermost adrenal cortex
makes aldosterone (a mineralo)
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13
Q

Zona fasciculata

A
middle of adrenal cortes
makes cortisol (a gluco)
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14
Q

Zona reticularis

A

inner adrenal cortex

makes adrenal androgens

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15
Q

Made in adrenal medulla?

A

Epi and NE (both tyrosine derived) - the catecholamines

Made from chromaffin cells

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16
Q

Epi works on what adrenergic receptors?

A

a1 –> Gq –> IP3/DAG
a2 –> Gi/o –> decr AC and thus dec cAMP, & open K+
B1-3 –> incr cAMP

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17
Q

Permissive affect of cortisol …

A

Incr epi release and incr B-adrenergic activity (by producing and inserting B-receptors)

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18
Q

Sx unique to primary adrenal defic

A

vitiligo, pigmentation, HYPERkalemia

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19
Q

APS-1

A

autoimmune polyglandular syndrome
INVOLVING AUTOIMMUNE REGULATOR GENE
hypoPARATHYROIDism and mucocutaneous candida
both have adrenal defic (Addi.) and T1DM

20
Q

ADPS-1

A

autoimmune polyglandular syndrome
HLA ASSOCIATED
hypoTHYROIDism (Hashimoto)
both have adrenal defic (Addi.) and T1DM

21
Q

Cortisol levels for Adrenal insuff?

A

100 = primary (small adrenal glands on CT for autoimmune or metabolic, large on all others)
ACTH LOW or nl = Secondary (with path on pit MRI)

22
Q

Primary aldosteronism (two types and who to screen)

A

1) Aldosterone producing ademoma (APA) 34% - SURG poss (likely if age 160/100 (severe) or RESISTANT (2 drugs), HTN under 20 y/o, adrenal incidentaloma, IF UNDER 40, HYPOkalemic) give aldost antagonists
2) Idiopathic hyperaldosteronism (IHA) 66% - give aldost antagonists WITH BP meds, IF OVER 40

23
Q

3 parts of Ant Pit & functions?

A

1) pars distalis (makes and secretes hormone)
2) pars tuberalis (round the infundibulum)
3) pars intermedia (between distalis and pars nervosa of post pit) FOLLICLES HERE

24
Q

Ant pit derived from?

A

RATHKE’S POUNCH oral/pharyngeal ectoderm (completely separates and wraps around stalk)

25
Post pit derived from?
neuroectoderm (its an extension of the brain) - still attached to neurons - an evagination of the diencepalon (3rd ventrilce)
26
2 parts of Post Pit & functions?
1) pars nervosa (releases ADH/vaso and oxytocin) HUGE AXON BUNDLE from hypothalamus (herring's bodies) 2) median eminence and infundibulum (has portal veins connecting to AP par distalis - nerves here regulate hormone secreting cells of AP's pars dsitalis
27
Blood supply and flow
Superior hypophyseal arteries: supply blood to (top part) median eminence, pars, tuberalis, and infundibulum. Inferior hyphophyseal arteries: blood to pars nervosa (bottom part). Pars distalis gets it blood form the hypophyseal portal veins that get it form the superior hypophyseal artery Then LEAVES through hypophyseal veins
28
Rule of 10 for Pheochromocytoma
Familial, Extra-adrenal, malignant, bilateral
29
Pheochromocytoma screen?
Metanephrines >1300 in urine, urine catecholamine (2 fold increase) LOTS OF POSSIBLE FALSE POSITIVES
30
Treat pheochromoctyoma
1. a-blockers first 2. then B-blockers OR CCBs by themselves THEN adrenalectomy surgery
31
High Lipid-Low Hounsfeld? | Low Lipid-High Hounsfeld?
Benign Malignant FOR adrenal incidentalomas (REMOVE if >4.5, growing, secreting hormone, if not MONITOR)
32
Most common mutation in thyroid cancer?
BRAF
33
What deiodinase is in the fetal brain? | And where are the others?
TYPE 2 in the fetal brain (large rise in TSH 30 min after birth so by 24 hours after birth increase in T3 and T4) Type 1 is in liver and kidney Type 3 is in the placenta and brain
34
Spiky hair kid?
Bamforth Lazarus, TITF2, congenital, also has cleft palate
35
Pendred's syndrome?
Deafness and goiter, PEDNRIN mutation, SCL26A4
36
PAX8 mutation?
RENAL AGENESIS
37
Low T3 uptake and low T4 (same direction)
hypothyroidism
38
Hi T3 uptake and low T4 (opposite direction)
TBG defic
39
Eval of worrisome growth
Check bone age with XRay and book (L hand and wrist) Labs: BMP, CBC (anemia in chronic dz and skeletal dysplasia) UA, karytope (for Turner's) TSH and T4 (hypothyroid) IGF-1 Nutritional: ESR (IBD), TTG & IgA (celiac),
40
MEN2A
Pheo, Medullary Thyroid carcinoma, HYPERPARATHYROIDISM
41
MEN2B
Pheo, Medullary Thyroid carcinoma, MUCOSAL NEUROMAS
42
Receptor involved in Germline MEN mutations?
RET receptor
43
Most common malignant thryoid nodule?
Papillary Carcinoma BUT GOOD PROGNOSIS Large pale nuclei ORPHAN ANNIE (looks like curly hair) Diagnx by Nuclear Features
44
Effect of Rathke Cleft Cyst?
Diabetes Insipidus
45
Brown Crooke cells indicate?
Elevated cortisol from ACTH producing adenoma
46
Craniopharyngoma
KIDS, beta-catenin mutations, squish everything
47
Basophilic pit tumors produce?
ACTH