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DEMS 4 > Endocrine extras > Flashcards

Endocrine extras Flashcards

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
Q

Post pit derived from?

A

neuroectoderm (its an extension of the brain) - still attached to neurons - an evagination of the diencepalon (3rd ventrilce)

26
Q

2 parts of Post Pit & functions?

A

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
Q

Blood supply and flow

A

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
Q

Rule of 10 for Pheochromocytoma

A

Familial, Extra-adrenal, malignant, bilateral

29
Q

Pheochromocytoma screen?

A

Metanephrines >1300 in urine, urine catecholamine (2 fold increase)
LOTS OF POSSIBLE FALSE POSITIVES

30
Q

Treat pheochromoctyoma

A
  1. a-blockers first
  2. then B-blockers
    OR CCBs by themselves
    THEN adrenalectomy surgery
31
Q

High Lipid-Low Hounsfeld?

Low Lipid-High Hounsfeld?

A

Benign
Malignant
FOR adrenal incidentalomas (REMOVE if >4.5, growing, secreting hormone, if not MONITOR)

32
Q

Most common mutation in thyroid cancer?

A

BRAF

33
Q

What deiodinase is in the fetal brain?

And where are the others?

A

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
Q

Spiky hair kid?

A

Bamforth Lazarus, TITF2, congenital, also has cleft palate

35
Q

Pendred’s syndrome?

A

Deafness and goiter, PEDNRIN mutation, SCL26A4

36
Q

PAX8 mutation?

A

RENAL AGENESIS

37
Q

Low T3 uptake and low T4 (same direction)

A

hypothyroidism

38
Q

Hi T3 uptake and low T4 (opposite direction)

A

TBG defic

39
Q

Eval of worrisome growth

A

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
Q

MEN2A

A

Pheo, Medullary Thyroid carcinoma, HYPERPARATHYROIDISM

41
Q

MEN2B

A

Pheo, Medullary Thyroid carcinoma, MUCOSAL NEUROMAS

42
Q

Receptor involved in Germline MEN mutations?

A

RET receptor

43
Q

Most common malignant thryoid nodule?

A

Papillary Carcinoma BUT GOOD PROGNOSIS
Large pale nuclei ORPHAN ANNIE (looks like curly hair)
Diagnx by Nuclear Features

44
Q

Effect of Rathke Cleft Cyst?

A

Diabetes Insipidus

45
Q

Brown Crooke cells indicate?

A

Elevated cortisol from ACTH producing adenoma

46
Q

Craniopharyngoma

A

KIDS, beta-catenin mutations, squish everything

47
Q

Basophilic pit tumors produce?

A

ACTH

DEMS 4 (4 decks)

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