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DEMS > Exam 4 Week 2 > Flashcards

Exam 4 Week 2 Flashcards

1
Q

Cortisol physiology

A

10% free in blood, 90% bound (CBG, albumin)
Receptor is cytosolic (HSP-90)
Delayed onset, longer response

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2
Q

Metabolic effects of cortisol

A

Counter-regulatory hormone:

  1. Liver gluconeogenesis
  2. Fatty acid oxidation (centripedal obesity)
  3. Protein breakdown (increased AA)
  4. Permissive epi: increased glycogenolysis and HSL activity)
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3
Q

Circulatory effects of cortisol

A
  1. Increased RBC production (polycythemia, anemia)

2. Permissive epi: enhance ß-adrenergic activity (CV tone)

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4
Q

Bone effects of cortisol

A
  1. Increased cortisol: decreased fibroblast proliferation (decreased collagen synthesis)= thin skin, striae
  2. Cortisol = vit D antagonist
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5
Q

Anti-inflammatory and immunosuppression effects of cortisol

A

Inhibits phospholipase A2 (PLC?) to prohibit arachidonic acid formation (affects COX and LOX downstream)
Decreased T cell activation and proliferation (decreased IL-2)
Decreases WBC, but increases neutrophils
Inhibits release of histamine

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6
Q

ACTH derived from

A

POMC gene

Also includes MSH genes (including on ACTH)

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7
Q

Hypocortisolemia and labs

A

1˚: Addison’s (destruction)
Cort down, ACTH up, aldo down
2˚: Pituitary or hypothalamus
Cort down, ACTH down, nml aldo (RAAS)

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8
Q

Stress response overview

A

Two physiologic areas:

  1. Locus ceruleus: increased NE, arousal
  2. Hypothalamus: CRH, ACTH, cortisol
  3. Hypothalamus: Splanchnic nerve, epi
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9
Q

Effects of epi

A 
Increase of blood glucose
Increase FFA (via HSL)
Decreased insulin (alpha-2 stimulation)
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10
Q

Layers of adrenal gland and production

A

Glomerulosa: mineralcorticoids (salt)
Fasciculata: glucocorticoids (sugar)
Reticularis: weak androgens, DHEA/androstenedione (sex)
Medulla: epi (and some NE)

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11
Q

Adrenal medulla origin and cell type

A

Neural crest origin

Chromaffin cells secrete epi and NE

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12
Q

Dopamine/NE pathway
Transporter in/out of vesicle
Enzymes

A

Tyrosine - L DOPA - Dopamine - NE - Epi
VMAT-1
Tyrosine hydroxylase, Decarboxylase, Dopamine ß-hydroxylase, PNMT

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13
Q

Aldosterone release, effects

A

Stimulated by ATII and ACTH
Principal cell: K+ out, Na+ in
alpha intercalated cell: H+ out

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14
Q

Hyperaldosteronism

A

HTN, hypokalemia, metabolic alkalosis (basic pH)
Primary: often bilateral adrenal hypoplasia (low renin)
Secondary: chronic activation of RAAS (high renin)
Ex: CAD, HF, cirrhosis

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15
Q

Types of congenital adrenal hyperplasia

A

21-OH deficiency: low cort, low aldo, high sex
11-OH deficiency: low cort, nml aldo, high sex
17-OH deficiency: low cort, low sex, high aldo

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16
Q

Pheochromocytoma triad presentation

A

Intermittent:
Headache
Palpitations
Diaphoresis

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17
Q

Pheo: origin and associated syndromes

A 
Adults
Adrenal medulla
Chromaffin cells (from neural crest)
NF-1, VHL, MEN1/2 (RET)
SDHB and SDHD (B=bad, D=dad)
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18
Q

Rule of 10’s for pheo

A 
Malignant
Bilateral
Extra-adrenal (bladder)
Calcify
Kids
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19
Q

Pheo dx, imaging, and tx

A

Urine/plasma metanephrines/catecholamines
Clonidine suppression tet
CT, MRI, I-123 (localize)
Surgical resection after irreversible a-blockers and ß-blockers (phenoxybenzamine)
Genetics follow up!

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20
Q

Paraganglioma

A

Neuroendocrine derived tumor
Chromaffin negative
Sympathetic

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21
Q

MEN gene associations

A

MEN2A: Pheo, thyroid carcinoma, hyperparathyroidism
MEN2B: Pheo, thyroid carcinoma, mucosal neuro tumor
2B - often marfanoid habitus

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22
Q

DDx for pheo

A

Exogenous drug
Hyperthyroidism
Carcinoid tumor
GAD with HTN

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23
Q

Primary hyperaldosteronism (Conn’s)

A

High aldo, low renin
1/3= adenoma
2/3= bilateral adrenal hypertrophy
rare= carcinoid tumor

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24
Q

Mechanism of glucocorticoid-remediable aldosteronism and treatment

A

Autosomal dominant
Crossing over between genes for 11-OH and aldose synthase leading to ACTH activated (and overactivated) aldose synthase
= Hyperaldosteronism
Tx: GC’s to suppress ACTH

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25
Q

2 main clinical features of hyperaldosteronism

A

Difficult to control HTN

Hypokalemia

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26
Q

Aldosteronism lab eval

A

Correct K and measure plasma renin and aldo
Aldo/renin >20 = primary hyperaldo
Saline suppression test (aldo>10)
CT to localize (>35 with >1cm mass also AVS)
No mass or <1cm = AVS
Bilateral enlargement = genetic testing GRA

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27
Q

Adrenal insufficiency causes

A

Primary (high ACTH, pigmentation):
Autoimmune, infections (TB, HIV), hemorrhagic, CA, ketoconazole (block cortisol receptor)

Secondary (low ACTH, nml pigmentation and MC):
Exogenous GC drug, hypopituitarism, hypothalmic dysfxn

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28
Q

Lab findings in primary vs. secondary adrenal insufficency

A

Primary: ACTH high, MSH high, hyperkalemia
Secondary: ACTH low, no hyperkalemia
Both: Hypoglycemia, eosinophilia

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29
Q

Waterhouse-Friderichsen syndrome

A

Acute primary adrenal insufficency due to hemorrhage

Associated with sepsis in N. men, DIC, and endotoxic shock

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30
Q

Neuroblastoma

A

Most common adrenal medullary tumor in children

Crosses midline, occurs anywhere in sympathetic chain (from neural crest cells)

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31
Q

Licorice induced hyperaldosteronsim

A

Licorice inhibits breakdown of cortisol in kideny
Cortisol has greater affinity for MC receptor
Build up of cortisol activates MC receptor

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32
Q

Hyperaldo treatment

A

Unilateral: surgery
Bilateral: MC antagonist (K+ sparing)

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33
Q

Adrenal incidentalomas - benign

A 
Majority are non-fxnal adenoma
HU<10 on noncon CT = benign nodule
Dropout on MRI = benign nodule
<4cm, homogenous, smooth
Rapid washout (>50%)
Observation and follow up
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34
Q

Adrenal incidentalomas - malignant

A 
Central necrosis
HU>10 on part without necrosis
HU>30 likely adrenocortical carcinoma
HU>20 likely pheo
HU>10 likely mets
Low washout
Surgery - removal
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35
Q

TPO functions

A

Oxidation of I- to I2 at apical surface (colloid surface)
Organification (TG+I2) in colloid
Coupling rxn: production of T3/T4 from TG/DIT/MIT

36
Q

TG pathway

A 
TG synthesized in rER
Tyrosine to tyrosyl residues then iodinated
MIT+DIT (T3)
DIT+DIT (T4) added
LARGE TG concentration in colloid
37
Q

Functions of thyroid hormone

A
  1. Regulate BMR (Na/K ATPase)
  2. Development, especially brain
  3. Permissive effects on ß-adrenergic receptors
  4. Brain effects even as adult (depression)
38
Q

TSH regulation

A
  1. Growth and number of follicular cells
  2. Transporters/enzyme regulation (TPO, TG)
  3. Increase iodine uptake (NIS- Na/I symporter)
39
Q

Deiodinase types

A

Type 1/2 lead to active T3

Type 3 leads to inactive T3 (rT3)

40
Q

Physiologic and drug states driving rT3 synthesis (via type 3 deiodinase)

A

Starvation, stress, neonatal period

GC’s, Propanolol, amiodarone, radiocontrast

41
Q

Thyroid hormone in blood

A

Most bound to TBG, TBPA (T4 only), Albumin
Increased binding proteins lead to increased free (after lag)
Stimulated by OCP’s, E2

42
Q

4 causes of hypothyroidism

A

Hashimoto’s
Low iodine in diet
Ablation/post-op nodule removal
Pituitary dz (Sheehan’s)

43
Q

Thyroid hormone affects on reproductive hormones in women

A

Increased T4: increased SHBG, decreased E2, light bleeding/amenorrhea
Decreased T4: decreased SHBG, increased E2, heavy bleeding
Pregnancy also increases TBG

44
Q

Factitious disorder

A

Iatrogenic, levothyroxine supplementation
T4, T3, TSH, RAIU
No goiter, decreased thyroid size with chronic

45
Q

Hot nodule and TMNG

A

T4, T3, TSH, RAIU
Palpable nodule on exam
TMNG often TSH receptor mutation (TSH independent)
I-131 ablation or surgery if CI

46
Q 
Subacute granulomatous thyroiditis (DeQ.)
Silent thyroiditis (postpartum)
A 
DeQ= tender thyroid
Silent= non tender
T4, T3, TSH, RAIU
Observation, GC's if severe
NSAIDs in DeQ.
47
Q

Graves’ disease

A

T4, T3, TSH, RAIU
Goiter, eye disease, pretibial myxedema
Thyroid stimulating Ig’s (TSI)
Scalloped colloid

48
Q

Thyroid storm treatment

A

Propranolol
PTU
Prednisolone (GC’s)
Potassium iodide (Lugol iodine)

49
Q

Hashimoto thyroiditis

A

HLA-DR5
Increased risk of Bcell lymphoma with chronic
Hurthle cells, lymphoid aggregates w/ germinal centers
Enlarged, non-tender thyroid

50
Q

Riedel thyroiditis

A

Hard as wood thyroid
Fibrous tissue with inflammatory infiltrate
Extended to local structures (like anaplastic carcinoma, but more likely in younger patients)

51
Q

Struma ovarii

A

Ectopic T3/T4 secreting tumor in ovary
Radio-iodide uptake over pelvis
Surgery

52
Q

Jod-Basedow

A

Excess iodide
Found in iodine deficient areas and TMNG
Opposite of Wolff-Chaikoff where excess iodine temporarily inhibits TPO

53
Q

Types of malignant thyroid cancer

A 
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
B cell lymphoma
54
Q

Types of benign thyroid cancer

A

Follicular adenoma
Intact capsule
Can’t differentiate from carcinoma on FNA

55
Q

Papillary carcinoma

A 
Good prognosis, even with LN spread
Most common, well defined
Orphan Anne eyes
Nuclear grooves and inclusions
Low mito (well differentiated)
Psammoma bodies (calcification)
56
Q

Follicular carcinoma

A

Invaded capsule

Hematologic spread - mets

57
Q

Medullary carcinoma

A

MEN2A and MEN2B - RET gene
Neuroendocrine tumor (derived from C cells)
IHC for calcitonin, negative for TG
Amyloid deposits and psammoma bodies

58
Q

Anaplastic carcinoma

A

Poor prognosis, aggressive
Dysplastic, necrosis, hemorrhage
Local effects (similar to Riedel but older patients)

59
Q

Physical signs of thyroid malignancy

A

Increased size
Hard
Fixation
Lymphadenopathy

60
Q

Evaluation of thyroid masses

A
  1. TSH
  2. Ultrasound
  3. FNA (US guided)
    Iodine uptake study (cold 10% chance malignancy)
61
Q

Worrisome height definition

A

<2 STD for age + gender
OR
<3.5in of midparental target height

62
Q

Midparental target height calculation

A

Female: (DAD-5in + MOM)/2
Male: (MOM+5in + DAD)/2

63
Q

Worrisome velocity definition

A

Decrease of >/= 2 centiles (crosses two lines)

64
Q

Rule of 5’s in velocity

A

Birth to 1yr to 4 yr to 8yr to 12yr

25cm, 10cm, 5cm, 5cm

65
Q

Skeletal maturation diagnostic test

A

Left wrist xray

66
Q

Familial short stature: definition

A

Velocity/height WNL for parents

67
Q

Constitutional growth delay

A 
Fall off before age 2-3
Delayed bone age/pubertal onset
Fall off at average puberty age
Catch up in their puberty
"Late bloomers"
68
Q

Failure to thrive

A

Only applies to children <2yrs
2 or more centiles crossed
Poor nutrition/physcosocial factors

69
Q

Nutritional growth retardation
Causes
Growth chart

A

“Neglect”
Malabsorptive disorder (TTG/IgA, ESR, CF test)
Weight leads drop off

70
Q

Cushing’s syndrome on growth chart

A

Weight spike

Height levels

71
Q

Hormonal causes of worrisome growth

Growth chart findings

A

Hypothyroidism
GH deficiency
Look similar on growth chart
Often co-morbid (MRI for tumor)

72
Q

Eval of worrisome growth

A 
Bone age
TSH, T4 levels
GH, IGF-1, IGF BP-3 levels
Karyotype
TTG/IgA, ESR, Met panel with phos, CBC
73
Q

Turner syndrome: genes
Growth chart
S/S
Tx

A

Haplo SHOX
Start short, fall off more at puberty
Web neck, coarc, bicuspid aorta, horseshoe, otitis media
Early ID and GH therapy

74
Q

Side effects of GH thearpy

Gain of GH in non-deficient patients

A

Wallet deficiency
SCFE, HTN, pseudotumor cerebri
?Long term efficacy
0-3in

75
Q

Does hypo or hypercalcemia present with neuro symptoms?

A

Both

76
Q

Does hypo or hyperthyroidism present with anxiety and depression

A

Both

77
Q

Psych symptoms can be worsened by what thyroid condition?

A

Subclinical hypothyroidism

Replacement may improve outcomes

78
Q

Timeline for thyroid migration and activation

A

Begins around 10-12 weeks
TSH detectable around 12 weeks
TSH/T4 rise to term

79
Q

Thyroid levels after birth

A

TSH: spike=30min (60-80) fall in 24 hours
T4: spike=24hr (10-15) fall in week

80
Q

Fetal brain development with thyroid hormone

A

T4 crosses placenta

Fetal brain increases expression of type 2 deiodinase (forming T3)

81
Q

Causes of congenital hypothyroidism

A 
Thyroid dysgenesis
Thyroid dyshormonogenesis
TSH resistance
Central deficiency (pituitary or hypothalamus)
Transient
82
Q

Thyroid dysgenesis

A

Aplasia, ectopic (migratory issue)
PAX8: AD - renal dysgenesis
TITF1: associated with lung, forebrain, pituitary deficit
Homo= respiratory distress
TITF2: associated with cleft, hair follicles (Bamforth Lazarus Syn)
Homo= cleft palate, spiky hair

83
Q

Thyroid dyshormonogenesis

A

Pendred Syndrome AR
SLC25A4: pendrid I transport protein (follicular cell into colloid)
Goiter, deafness (semicircular canal dilation)

84
Q

TSH resistance

A

Receptor mutation
Hetero: increased TSH
Homo: decreased T4, hypoplastic gland
Many maternal transient causes

85
Q

Central hypothyroidism

A

Pituitary/hypothalamus issue

Almost alway presents with GH deficiency

86
Q

Signs of untreated congenital hypothyroidism

A

Big tounge, unbilical hernia, hoarse cry

Usually screened at 2/3 days after TSH drops

87
Q

Neonatal labs and T3 uptake

A

Neonatal labs often confused by TBG
T3 uptake/T4 same direction: thyroid dz
T3 uptake/T4 different direction: TBG deficiency

DEMS (10 decks)

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