Exam 4 Week 1 Flashcards

1
Q

Basic endocrine secretion

A

Basolateral side of cell
No ducts
Secretion into blood via fenestrated endothelium

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2
Q

Anterior pituitary blood/hormone flow

A

Superior hypophysial a
Trabecullar a
Hypothalamic capillary beds (pick up releasing hormones)
Portal system
Pituitary capillary beds (act on pituitary cell bodies to release hormones)
Hormones release into blood and go to target organs

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3
Q

Posterior pituitary hormones and origin

A

ADH/vasopressin (supraoptic nucleus - hypothalamus)

Oxytocin (paraventricular nucleus - hypothalamus)

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4
Q

Adrenal zones and hormones (superficial to deep)

A

Zona glomerulosa: aldosterone (RAAS)
Zona fasiculata: cortisol (ACTH, CRH)
Zona reticularis: sex hormones (ACTH, CRH)
Medulla: NE, epi, enkephalins

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5
Q

Thyroglobulin get iodinated in the _________

A

Colloid

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6
Q

Main difference between parathyroid and thyroid on path? Parathyroid cell types

A
  1. Adipocytes
  2. Oxyphil cells (rich in mitochondria)
  3. Chief cells (secrete PTH)
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7
Q

Actions of parathyroid hormone

A

Overall: increase serum Ca2+, decreased serum PO4

  1. Osteoclast activation (RANK)
  2. Increased enterocyte uptake of dietary Ca2+
  3. Increased Ca2+ reabsorption in DCT
  4. Decreased PO4 in PCT
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8
Q

Actions of calcitonin

A

Overall: decrease serum Ca2+

1. Decreased osteoclast activity

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9
Q

Pituitary origin tissues

A

Anterior pit: oral ectoderm (Rathke’s pouch)
Posterior pit: diencephalon (neuroectoderm)
Vessels: mesoderm

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10
Q

Adrendal origin tissues

A
Medulla: chromaffin cells (from sympathogonia, neural crest)
Cortex: mesoderm
First wave: reicularis
Second wave: fasciularis
Inside out development
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11
Q

Thyroid origin

A

Derived from endoderm

Thyroid diverticulum between 1st and 2nd pharyngeal pouches

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12
Q

Parafollicular cell/parathyroid origin

A

Ex: C cells
Neural crest cells
Ultimobronchial body
Between 3/4 (superior) and below 4 (inferior) pharyngeal pouches

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13
Q

What percent of patients don’t report IHM medications?

A

72%

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14
Q

DSHEA Regulations

A

1994 regulations (previous were grandfathered)
Manufacturer responsible for safety and truthfullness
FDA acts only after on market and proved dangerous
Must be different shelf from OTCs

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15
Q

Higher quality supplements labeling

A

MUST have FDA disclaimer
OPTIONAL to have structure/function claim
May contain seal

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16
Q

Dyslipidemia supplements

A

Fish oil
Fiber
Niacin
Plant sterols/stanols

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17
Q
Fish oil:
Safety in pregnancy
Indications
Mercury CI
TC, LDL, TG effects
DHA/EPA?
A
Pregnancy limit of 12oz/wk
Avoid shark,swordfish,tilefish due to mercury
Option for CI/non-tolerance of niacin
No effect on total cholesterol or LDL
More DHA/EPA = better
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18
Q

Plant sterols/stanols:
Timeline
Side effects
DDIs

A

Equally effective
2/3wks to work
GI side effects
DDI w/ ezitimibe

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19
Q

Bitter orange

A

GRAS, but no evidence is safer than Ephedra

Often contains caffeine

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20
Q

Weight loss supplements

A

Ephedra
Bitter orange
Alli
Ca2+ (inferior to low fat dietary intake)

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21
Q

Alli:
Mech
BMI indications
SE

A

Inhibits gastric and pancreatic lipase (take with fatty meal)
FDA approved, BMI>27 seen improvements
Risk of liver injury

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22
Q

Diabetes supplements

A

Chromium

Vanadium

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23
Q

Chromium

A

Type III in food/supplements
Decreases oxidative stress
Loss of DDI, renal elimination

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24
Q

Vanadium

A

Increases insulin sensitivity -> T2DM
Adverse rxn: green tongue
DDI with G herbs (coag risk)

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25
Q

HTN supplements

A

Garlic
Co Q-10 (additive effect, not on own)
Flavonoids (straw/blueberries, dark chock)

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26
Q

Garlic

A

Allicin is active ingredient (and stinky part)

DDI with G herbs

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27
Q

G herbs

A

Garlic
Ginger
Ginseng
Ginkgo

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28
Q

Tyrosine derivative hormones

A

NE
Epi
Thyroid hormone
Dopamine

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29
Q

Peptide hormones

A
Oxytocin
ADH
Angiotensin
TRH
GnRH
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30
Q

Protein hormones

A
Insulin
Glucagon
GH
PRL
ACTH
TSH
31
Q

Steroid hormones

A

Sex hormones
Cortisol
Aldosterone
Vitamin D

32
Q

Water soluble hormones characteristics
Storage
Half life
Receptors

A

Stored in vesicles (Ca2+ release)
Shorter half life in blood (unbound)
Receptors membrane bound: GPCR, Cyto, EGFR

33
Q

3 classes of water soluble hormone receptors and ligands

A

GPCR: hypothalamic hormones
Cytokine: GH, PRL
EGFR: Insulin, IGF-1

34
Q
Steroid hormones characteristics
Storage
Half life
Receptors
Regulation
A

Bound in blood (95%)
Longer half life
Free is active and regulated
Intracellular receptors (then bind HRE, affect transcription)

35
Q

Measuring hormone levels

A

Bioassays: exogenous system measurement, longer, more complex
Immunoassays: Ab binding, RIA/ELISA, need normal hormone, faster

36
Q

3 methods of hormone control

A
  1. Pulsatile hormone release
  2. Circadian control
  3. Receptor regulation
37
Q

2 pituitary end hormones

A

Growth hormone

Prolactin

38
Q

GPCR receptor types and ligands

A

Gs: CRH, GHRH, ADHV2
Gi: SST, Dopamine
Gq: ADHV1, GnRH, TRH

39
Q

Cytokine receptor ligands and mech

A

GH, PRL

JAK-STAT pathway

40
Q

Milk feedback from PRL, E, Progesterone, Dopamine
Mammogenesis
Lactogenesis
Galactopoiesis

A

Mammogenesis (+)= PRL, E, Progesterone (-)= D
Lactogenesis (+)=PRL (-)= D, E, Progesterone
Galactopoiesis (+)=PRL (-)= D, E, Progesterone

41
Q

Prolactinoma s/s

A

Galactorrhea
Amenorrhea
Loss of libido (via GnRH)

42
Q

Hypopituitarism

A

Nonfunctional pituitary adenoma
Sheehan syndrome: postpartum infarct following complicated delivery (failure to lactate, cold intolerance)
Empty sella syndrome (common in obese women)
Pituitary apoplexy
Trauma
Radiation
Tx: HRT

43
Q

Growth hormone direct actions

A
Counter regulatory (diabetogeneic in excess)
Increased gluconeogenesis
Increase FA oxidation via HSL
Increased AA uptake into muscle
Increased water and salt retention
44
Q

Growth hormone indirect actions (mediated by IGF)

A

Increased long bone growth

Increased muscle growth

45
Q

Metabolic states regulating IGF

A

High glucose, AA, insulin, GH -> IGF release by liver

IGF activated by combo of GH and insulin

46
Q

Growth hormone dysfxn: hyper

A

Diabetogeneic
Gigantism
Acromegaly (after plates have fused, puberty)
Cardiac hypertrophy

47
Q

Growth hormone dysfxn: hypo

A

Dwarfism (decreased GH)
Laron’s dwarfism (decreased GH receptor)
African pygmies (decreased IGF response)

48
Q

POMC products

A

MSH

ACTH

49
Q

Elevated prolactin:
2 physiologic
3 pathologic
2 pharmacologic

A

Physio: pregnancy, lactation/suckling
Path: prolactinoma, stalk compression, hypothyroidism
Pharm: estrogen, antipsychotic meds

50
Q

Chronology of anterior pituitary hormone deficiency

A
  1. GH
  2. FSH/LH (gonadotropins)
  3. ACTH
  4. TSH
  5. PRL
    Good Felines Always Trash Pants
51
Q

Prolactin lab values in excess

A

Normal <150
Stalk issues >150, <250
Macroadenoma >250

52
Q

Treatment for pituitary adenoma

A

Prolactinoma: dopamine agonist (regardless of size), surgery if unresponsive
Surgery: transnasal (trans sphenoidal) approach

53
Q

DI findings and difference in central vs. nephrogeneic

A
Low urine specific gravity (<1.006)
High serum osm
Hyperosmotic volume contraction
Central: Low ADH
Nephro: Normal or high ADH
54
Q

Water deprivation test central vs nephro DI

A

With hold water for 2-3 hours
Administer ADH analog
>50% increase in urine osm = central
No change = nephrogenic

55
Q

Treatment of DI

A

Central: ADH, hydration
Nephro: Water restriction, HCTZ, amiloride, indomethacin

56
Q

Acromegaly s/s

A
Acral and facial changes
Teeth spacing
Hyperhydrosis
HA
Oligo/amenorrhea
CV complications - HTN, valve dz, hypertrophy
57
Q

Acromegaly diagnostic tests

A

Clinical features
Elevated IGF-1 (gender, age matched - decreases with age)
OGTT, GH levels

58
Q

GH Deficiency tests

A

Insulin induced hypoglycemia (<40 with GH > 3-5)

Arg, glucagon test performed now

59
Q

ACTH dysfunction tests

A
  1. 24 hour urine cortisol
  2. 12am salivary cortisol
  3. 1mg dex suppression w/ 8am serum cortisol (<1.8)
60
Q

ACTH hyper vs. hypo

A

Hyperactivity: cushingings
Hypoactivity: adrenal insufficiency

61
Q

SIADH Labs

A

Low serum Na
Low serum osm
Inappropriately high urine osm

62
Q

SIADH treatment

A
Water restriction
V2 antagonist
Hypertonic saline (CAREFUL: central pontine myelinolysis)
63
Q

Pituitary image gold standard

A

MRI

CT if contraindication

64
Q

MRI types and indications

A

T1: Anatomy
T2: Pathology and anatomy

65
Q

Relax rate with T1 and T2

A

T1: protons align with magnetic field
T2: loss of magnitization

66
Q

Pituitary masses: overview

A

Generally WHO type I (excision)
Hyperfunctional, mass effect, visual disturbances
Generally present middle aged adults

67
Q

Rare types of pituitary tumor that present similar to adenoma

A

Pituicytoma (derived from posterior gland)
Spindle cell onocytoma
Rathke’s cyst (common, only removed if HA)
Hypophysitis

68
Q

Consequences of mass effect

A

HA
Visual disturbances
Invasion of cavernous sinus (3,4,6): diplopia, ptosis
DON’T invade blood vessels

69
Q

Craniopharyngeoma

A
Bimodal age distribution
Develops from Rathke's pouch epithelium
Calcification is common
Papillary = adult (BRAF)
Adam = kids (WNT/ßcatenin)
70
Q

Pituitary masses and transcription factors and IHC

A

SF-1: FSH/LH (gonadotrophs, nonfxnal)
Pit-1: TSH, PRL, GH (somatotrophs, fxnal) acidophils
T-pit: ACTH (corticotrophs)
TTF-1: posterior gland
Reticulin: nml anterior gland, disruption = pathologic

71
Q

Familial pituitary tumor syndromes and 1 example

A

95% are sporadic, only 5% familial
Multi tumor, FHx, and early onset provide clues
DICER1: ACTH secreting tumor (pituitary blastoma)

72
Q

Nonfunctional pit tumors

A
Present with mass effect
Often gonadotrophs (SF-1 positive)
73
Q

Functional pit tumors

A

GH secreting (dense vs. sparse keratin stain)
Mixed GH/PRL (don’t respond well to D2 agonist)
Prolactinoma
ACTH secreting

74
Q

Mets to the pituitary

A

very rare, usually breast cancer (estrogen receptor positive)