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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
2 main clinical features of hyperaldosteronism
Difficult to control HTN | Hypokalemia
26
Aldosteronism lab eval
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
27
Adrenal insufficiency causes
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
28
Lab findings in primary vs. secondary adrenal insufficency
Primary: ACTH high, MSH high, hyperkalemia Secondary: ACTH low, no hyperkalemia Both: Hypoglycemia, eosinophilia
29
Waterhouse-Friderichsen syndrome
Acute primary adrenal insufficency due to hemorrhage | Associated with sepsis in N. men, DIC, and endotoxic shock
30
Neuroblastoma
Most common adrenal medullary tumor in children | Crosses midline, occurs anywhere in sympathetic chain (from neural crest cells)
31
Licorice induced hyperaldosteronsim
Licorice inhibits breakdown of cortisol in kideny Cortisol has greater affinity for MC receptor Build up of cortisol activates MC receptor
32
Hyperaldo treatment
Unilateral: surgery Bilateral: MC antagonist (K+ sparing)
33
Adrenal incidentalomas - benign
``` 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 ```
34
Adrenal incidentalomas - malignant
``` 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 ```
35
TPO functions
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
TG pathway
``` TG synthesized in rER Tyrosine to tyrosyl residues then iodinated MIT+DIT (T3) DIT+DIT (T4) added LARGE TG concentration in colloid ```
37
Functions of thyroid hormone
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
TSH regulation
1. Growth and number of follicular cells 2. Transporters/enzyme regulation (TPO, TG) 3. Increase iodine uptake (NIS- Na/I symporter)
39
Deiodinase types
Type 1/2 lead to active T3 | Type 3 leads to inactive T3 (rT3)
40
Physiologic and drug states driving rT3 synthesis (via type 3 deiodinase)
Starvation, stress, neonatal period | GC's, Propanolol, amiodarone, radiocontrast
41
Thyroid hormone in blood
Most bound to TBG, TBPA (T4 only), Albumin Increased binding proteins lead to increased free (after lag) Stimulated by OCP's, E2
42
4 causes of hypothyroidism
Hashimoto's Low iodine in diet Ablation/post-op nodule removal Pituitary dz (Sheehan's)
43
Thyroid hormone affects on reproductive hormones in women
Increased T4: increased SHBG, decreased E2, light bleeding/amenorrhea Decreased T4: decreased SHBG, increased E2, heavy bleeding Pregnancy also increases TBG
44
Factitious disorder
Iatrogenic, levothyroxine supplementation T4, T3, TSH, RAIU No goiter, decreased thyroid size with chronic
45
Hot nodule and TMNG
T4, T3, TSH, RAIU Palpable nodule on exam TMNG often TSH receptor mutation (TSH independent) I-131 ablation or surgery if CI
46
``` Subacute granulomatous thyroiditis (DeQ.) Silent thyroiditis (postpartum) ```
``` DeQ= tender thyroid Silent= non tender T4, T3, TSH, RAIU Observation, GC's if severe NSAIDs in DeQ. ```
47
Graves' disease
T4, T3, TSH, RAIU Goiter, eye disease, pretibial myxedema Thyroid stimulating Ig's (TSI) Scalloped colloid
48
Thyroid storm treatment
Propranolol PTU Prednisolone (GC's) Potassium iodide (Lugol iodine)
49
Hashimoto thyroiditis
HLA-DR5 Increased risk of Bcell lymphoma with chronic Hurthle cells, lymphoid aggregates w/ germinal centers Enlarged, non-tender thyroid
50
Riedel thyroiditis
Hard as wood thyroid Fibrous tissue with inflammatory infiltrate Extended to local structures (like anaplastic carcinoma, but more likely in younger patients)
51
Struma ovarii
Ectopic T3/T4 secreting tumor in ovary Radio-iodide uptake over pelvis Surgery
52
Jod-Basedow
Excess iodide Found in iodine deficient areas and TMNG Opposite of Wolff-Chaikoff where excess iodine temporarily inhibits TPO
53
Types of malignant thyroid cancer
``` Papillary carcinoma Follicular carcinoma Medullary carcinoma Anaplastic carcinoma B cell lymphoma ```
54
Types of benign thyroid cancer
Follicular adenoma Intact capsule Can't differentiate from carcinoma on FNA
55
Papillary carcinoma
``` 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
Follicular carcinoma
Invaded capsule | Hematologic spread - mets
57
Medullary carcinoma
MEN2A and MEN2B - RET gene Neuroendocrine tumor (derived from C cells) IHC for calcitonin, negative for TG Amyloid deposits and psammoma bodies
58
Anaplastic carcinoma
Poor prognosis, aggressive Dysplastic, necrosis, hemorrhage Local effects (similar to Riedel but older patients)
59
Physical signs of thyroid malignancy
Increased size Hard Fixation Lymphadenopathy
60
Evaluation of thyroid masses
1. TSH 2. Ultrasound 3. FNA (US guided) Iodine uptake study (cold 10% chance malignancy)
61
Worrisome height definition
<2 STD for age + gender OR <3.5in of midparental target height
62
Midparental target height calculation
Female: (DAD-5in + MOM)/2 Male: (MOM+5in + DAD)/2
63
Worrisome velocity definition
Decrease of >/= 2 centiles (crosses two lines)
64
Rule of 5's in velocity
Birth to 1yr to 4 yr to 8yr to 12yr | 25cm, 10cm, 5cm, 5cm
65
Skeletal maturation diagnostic test
Left wrist xray
66
Familial short stature: definition
Velocity/height WNL for parents
67
Constitutional growth delay
``` 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
Failure to thrive
Only applies to children <2yrs 2 or more centiles crossed Poor nutrition/physcosocial factors
69
Nutritional growth retardation Causes Growth chart
"Neglect" Malabsorptive disorder (TTG/IgA, ESR, CF test) Weight leads drop off
70
Cushing's syndrome on growth chart
Weight spike | Height levels
71
Hormonal causes of worrisome growth | Growth chart findings
Hypothyroidism GH deficiency Look similar on growth chart Often co-morbid (MRI for tumor)
72
Eval of worrisome growth
``` Bone age TSH, T4 levels GH, IGF-1, IGF BP-3 levels Karyotype TTG/IgA, ESR, Met panel with phos, CBC ```
73
Turner syndrome: genes Growth chart S/S Tx
Haplo SHOX Start short, fall off more at puberty Web neck, coarc, bicuspid aorta, horseshoe, otitis media Early ID and GH therapy
74
Side effects of GH thearpy | Gain of GH in non-deficient patients
Wallet deficiency SCFE, HTN, pseudotumor cerebri ?Long term efficacy 0-3in
75
Does hypo or hypercalcemia present with neuro symptoms?
Both
76
Does hypo or hyperthyroidism present with anxiety and depression
Both
77
Psych symptoms can be worsened by what thyroid condition?
Subclinical hypothyroidism | Replacement may improve outcomes
78
Timeline for thyroid migration and activation
Begins around 10-12 weeks TSH detectable around 12 weeks TSH/T4 rise to term
79
Thyroid levels after birth
TSH: spike=30min (60-80) fall in 24 hours T4: spike=24hr (10-15) fall in week
80
Fetal brain development with thyroid hormone
T4 crosses placenta | Fetal brain increases expression of type 2 deiodinase (forming T3)
81
Causes of congenital hypothyroidism
``` Thyroid dysgenesis Thyroid dyshormonogenesis TSH resistance Central deficiency (pituitary or hypothalamus) Transient ```
82
Thyroid dysgenesis
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
Thyroid dyshormonogenesis
Pendred Syndrome AR SLC25A4: pendrid I transport protein (follicular cell into colloid) Goiter, deafness (semicircular canal dilation)
84
TSH resistance
Receptor mutation Hetero: increased TSH Homo: decreased T4, hypoplastic gland Many maternal transient causes
85
Central hypothyroidism
Pituitary/hypothalamus issue | Almost alway presents with GH deficiency
86
Signs of untreated congenital hypothyroidism
Big tounge, unbilical hernia, hoarse cry | Usually screened at 2/3 days after TSH drops
87
Neonatal labs and T3 uptake
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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