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STEP 1 > 02a: Endocrinology > Flashcards

02a: Endocrinology Flashcards

1
Q

Thyroid tissue arises from (ecto/meso/endo)-derm. And the parafollicular cells, which produce (X), arise from (ecto/meso/endo)-derm.

A

endoderm
Parafollicular (C) cells produce
X = calcitonin
Neural crest

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2
Q

Adrenal cortex arises from (ecto/meso/endo)-derm. And the adrenal medulla, arises from (ecto/meso/endo)-derm.

A

Mesoderm;

Neural crest

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3
Q

Normal remnant of thyroglossal duct is:

A

Foramen cecum

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4
Q

Adenohypophysis derived from (ecto/meso/endo)-derm.

A 
(Anterior pituitary)
Oral ectoderm (Rathke pouch)
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5
Q

Which four hormones have the same alpha subunit but different beta subunits?

A

LH, FSH, TSH, beta-hCG

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6
Q

Proopiomelanocortin (POMC) derivatives:

A

ACTH, MSH

and beta-endorphin (endogenous opioid)

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7
Q

Which anterior pituitary hormones are basophils?

A

“B-FLAT”

Basophils - FSH, LH, ACTH, TSH

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8
Q

Which anterior pituitary hormones are acidophils?

A

Prolactin, GH

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9
Q

Neurohypophysis derived from (ecto/meso/endo)-derm. Where exactly are the hormones made?

A

Neural ectoderm

Supraoptic (ADH) and paraventricular (oxytocin) nuclei of hypothalamus

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10
Q

Post pituitary: hypothalamic axons terminate on (X) and hormones eventually secreted into (Y).

A 
X = Herring bodies (storage sites)
Y = hypophysial vein (and then systemic circulation)
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11
Q

Some cases of inherited (AD) (X) disease are due to mutation in (ant/post) pituitary neurophysins. What’s the mechanism?

A

X = DI; post pit
Neurophysins carry hormones to post pit from hypothalamus but mutation causes misfolding and removal of proteins from ER (along with hormones)

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12
Q

Insulinoma v. exogenous insulin use v. sulfonylurea use. Which will cause concomitant increase in (X) peptide?

A

X = C

Insulinoma and sulfonylurea (endogenous insulin being made/secreted)

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13
Q

T/F: Insulin crosses placenta.

A

False

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14
Q

GLUT-4 on (X) tissues is insulin (dependent/independent).

A

X = striated muscle and adipose
Dependent (actions of insulin include releasing GLUT4 vesicles for these tissuses; but exercise can also increase GLUT4 expression)

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15
Q

Why might a patient with (Grave’s/Hashimoto’s) present with galactorrhea?

A

Hashimoto’s (high TRH)

TRH stimulates secretion of TSH and prolactin

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16
Q

Prolactin is structurally homologous to (X). What hormones stimulate/inhibit its release?

A

X = GH

Stim: TRH
Inhibit: DA

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17
Q

Post-partem “contraception” by breast-feeding occurs due to the action of (X).

A

X = prolactin

Inhibits GnRH synthesis/release (thus inhibiting ovulation in F and spermatogenesis in M)

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18
Q

T/F: High blood glucose levels will increase secretion of GH.

A

False - hypoglycemia will (GH is a diabetogenic that increases insulin resistance); negative feedback by glucose

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19
Q

Ghrelin produced by (X) and stimulates (Y)

A 
X = Stomach
Y = hunger (orexigenic) AND GH release
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20
Q

Name a genetic disorder with increased ghrelin production

A

Prader willi

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21
Q

Leptin produced by:

A

adipose tissue

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22
Q

What symptom would you expect to see in all congenital adrenal enzyme deficiencies?

A

Skin hyperpigmentation (due to high ACTH stimulation); also both adrenal glands will be enlarged (hence “CAH”)

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23
Q

Male with 17a-hydroxylase deficiency. What would you expect to find on physical exam?

A

Female outward appearance but blind vagina/lack of internal F genitalia (undescended testes)

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24
Q

Rate limiting step in adrenal steroid synthesis

A

Cholesterol entry via StAR

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25
Key actions of cortisol
Cortisol is "A BIG FIB" 1. increase Appetite 2. increase Blood pressure 3. increase Insulin resistance 4. increase Gluconeogenesis, lipolysis, proteolysis 5. decrease Fibroblast activity (poor wound healing) 6. decrease Inflammatory/Immune responses 7. decrease Bone formation
26
Why does (acidosis/alkalosis) cause cramps, paresthesias, and carpopedal spasm?
Alkalosis | High pH increases negative charge on albumin, allowing higher affinity for and increased binding to Ca (hypocalcemia)
27
Which vitamins typically need to be supplemented in purely breastfed infants?
Vit D and K
28
Vit D deficiency results in decreased absorption of:
Ca and PO4 from gut
29
Pt on diuretic has increased PTH levels. A few weeks later, his PTH is now low. What serum ion is likely responsible for this?
Mg; when low, PTH increases but when extremely low (diarrhea, aminoglycosides, diuretics, EtOH abuse), PTH declines
30
Main T3 hormone functions
4 B's for the T3s 1. Bone growth 2. BMR (increased; increase Na/K pump and increase breakdown glycogen, fat and increase gluconeogenesis) 3. Beta-adrenergic effects 4. Brain maturation
31
Pregnant patients are most commonly (hypo/hyper/eu)-thyroid despite (increase/decease/no change) in T3/T4 synthesis. Why?
Euthyroid; Increase (and increase T3/T4 pools) Estrogen also increases TBG production (which binds most T3/T4 in blood anyway)
32
Thyroid hormone synthesis: (X) ion enters thyroid follicle via (Y) and then undergoes:
``` X = I- Y = Na/I symporter ``` Oxidization into I2 (before organification with thyroglobulin)
33
Thyroglobulin is synthesized from:
Tyrosine
34
List the endocrine hormones that work via cAMP pathway
"FLAT ChAMP" 1. FSH 2. LH 3. ACTH 4. TSH 5. CRH 6. hCG 7. ADH at V2-R 8. MSH 9. PTH
35
List the endocrine hormones that work via IP3 pathway
"GOAT HAG" 1. GnRH 2. Oxytocin 3. ADH (at V1-R) 4. TRH 5. His (H1-R) 6. A-II 7. Gastrin
36
Which other pituitary hormone, aside from GH, works via (X) signaling pathway?
X = non-R tyrosine kinase | Prolactin
37
Dexamethasone stimulation test used to diagnose/evaluate:
Cushing's syndrome cause (is it ectopic or pituitary?)
38
CRH stimulation test used to diagnose/evaluate:
Cushing's syndrome cause (is it ectopic or pituitary?)
39
Metyrapone stimulation test used to diagnose/evaluate:
Adrenal insufficiency
40
Metyrapone stimulation test: metyrapone (stimulates/inhibits) (X) so the test would show which changes in normal patient?
Inhibits X = 11-beta-hydroxylase (last step in cortisol synthesis) Decrease cortisol; increase ACTH and 11-deoxycortisol (aka 17 hydroxycorticosteroids after liver metabolism)
41
Metyrapone stimulation test in primary adrenal insufficiency
Increase ACTH but 11-deoxycortisol (aka 17 hydroxycorticosteroids after liver metabolism) remains low
42
Metyrapone stimulation test in secondary/tertiary adrenal insufficiency
ACTH and 11-deoxycortisol remain low
43
Explain the metabolic (acidosis/alkalosis) in primary adrenal insufficiency
Non-gap acidosis; less H+ secretion (low aldosterone) results in low serum HCO3 (binding acid) and compensatory increase in Cl-
44
Most common cause of chronic primary adrenal sufficiency in the developing world
TB (in Western world, it's autoimmune)
45
Tertiary adrenal insufficiency commonly caused by (X). Which parts of HPA axis are (atrophied/hypertrophied)?
X = chronic exogenous steroid use (experience insufficiency if stop abruptly) Entire HPA axis is atrophied!
46
Aldosterone escape mechanism ensures (X) finding in (Y) disease.
``` X = normal serum Na (no hypernatremia) Y = hyperaldosteronism ```
47
3 yo patient with abdominal distension and firm, irregular mass that crosses midline.
Neuroblastoma (v. Wilms tumor is smooth, unilateral)
48
Homer-Wright rosettes are characteristic of:
Neuroblastoma and medulloblastoma
49
Neuroblastoma associated with which mutation?
N-myc (oncogene)
50
Patient presents with lump on posterior calf that rises after the muscle is percussed with reflex hammer. This phenomenon is called (X) and patient likely has:
X = myoedema | Hypothyroidism
51
Key difference between hypo and hyper-thyroid myopathy
Both present with proximal muscle weakness but hypothyroidism will have high CK (normal in hyperthyroidism)
52
(Hypo/hyper)-thyroidism presents with myxedema.
Both; hypo is facial/periorbital and hyper is pretibial/periorbital
53
High TSH, normal T3, low T4: findings in which disease?
Hypothyroidism (T3 levels fluctuate and may be normal until later stages of disease)
54
T/F: Hyper and hypothyroid states affect LDL receptor.
True - increased expression in hyper (hypocholesterolemia), decreased in hypo (hypercholesterolemia)
55
Key antibodies in Hashimoto's
Anti-TPO and anti-thyroglobulin
56
Hashimoto's: increased risk of which cancer?
NHL (esp of Bcell origin)
57
Congenital hypothyroidism, aka Cretinism, presents at (X) age and can be the result of:
X = 2 months (maternal T4 until then) Maternal hypothyroidism, thyroid agenesis/dysgenesis, iodine deficiency
58
Thyroid histology in de Quervain thyroiditis
Granulomatous inflammation with infiltrating macrophages and multi-nucleated giant cells
59
Pt with fixed, hard, painless goiter. Thyroid shows fibrosis and inflammatory infiltrate on biopsy. Most likely diagnosis is (X) and Sx are likely those of (hyper/hypo)-thyroidism
X = Riedel thyroiditis | Hypothyroid
60
Thyroid-stimulating Ig in (X) disease is an Ig(Y) and the reaction is Type (1/2/3/4) HS
X = Graves Y = G 2
61
Pretibial myxedema is the result of (X) stimulation
X = dermal fibroblasts (stimulated by TSI; increased GAG secretion, osmotic muscle swelling/inflammation)
62
Rx for exophthalmos of Graves is:
Glucocorticoids
63
List some specific Sx of Graves not present in other causes of hyperthyroid
1. Pretibial myxedema 2. Exophthalmos/periorbital edema 3. Eye movement limitations
64
Thyroid storm should be treated with:
4Ps against the Ts 1. Propranolol (beta blockers) 2. PTU 3. Prednisolone (corticosteroids) 4. Potassium iodide
65
Most common thyroid cancer, (X), also has (good/bad) prognosis.
X = papillary carcinoma | Excellent
66
(X) thyroid cancer arises from C cells
X = medullary carcinoma
67
Thyroid cancer: Annie Orphan eyes with (X) bodies and associated with (Y) mutations
Papillary carcinoma X = psammoma Y = RET and BRAF
68
Thyroid cancer: stains with Congo red, spindle-shaped cells on amorphous background, and associated with (X) mutations
Medullary carcinoma | X = RET (MEN 2A, 2B)
69
Pseudohypoparathyroidism is due to:
Kidney unresponsive to PTH (so high PTH but hypocalcemia)
70
Pseudopseudohypoparathyroidism differs from Pseudohypoparathyroidism in which ways?
Same physical exam features, but no end-organ PTH resistance (normal PTH); defect inherited from dad instead of mom
71
Patient femur on xray shows cystic bone spaces filled with brown fibrous tissue. This condition is referred to as (X) and is often associated with (Y).
``` X = osteitis fibrosa cystica ("brown tumor" of osteoclasts and deposited hemosiderin) Y = primary (sometimes secondary) hyper-PTH ```
72
Which GI and urinary complications are seen in primary hyper-PTH?
Constipation and peptic ulcer disease; | Polyuria and kidney stones (hypercalciuria)
73
What serum level would make you almost certain that the secondary hyper-PTH is due to chronic renal disease?
Hyperphosphatemia (most other cases have low phosphate)
74
Defect in G-coupled Ca sensing receptors results in which disease? PTH levels are (low/high).
Familial hypocalciuric hypercalcemia Normal or high PTH
75
Failure to suppress (X) secretion following (Y) administration indicates acromegaly
``` X = GH Y = oral glucose ```
76
First choice of therapy for acromegaly due to adenoma is (X). If not cured, what are second-choice options?
X = Pituitary adenoma resection Octreotide (somatostatin analog) or Pegvisomant (GH-R antagonist) or Cabergoline (DA agonist)
77
Diabetes Insipidus: (increase/decrease) osmolality and (increase/decrease) volume in (ECF/ICF).
Hypotonic volume loss; | Increase osm in both compartments; decrease V in both compartments (hyperosmotic volume contraction)
78
Central DI Rx:
Hydration and desmopressin
79
Nephrogenic DI Rx:
Hydration and salt restriction; hydrochlorothiazide/indomethacin/amiloride
80
SIADH patient is (hyper/eu/hypo)-volemic due to:
Euvolemic Transient hypervolemia/water retention inhibits RAAS, so Na excretion increases
81
SIADH Rx:
1. Fluid restriction and salt tablets/IV hypertonic saline (correct slowly to avoid osmotic demyelination syndrome) 2. Diuretics 3. Vasopressin antagonist (conivaptan, tolvaptan)
82
Patient presents to ER due to sudden-onset severe headache. You're nearly certain it's a SAH, but then he complains of concurrent loss of peripheral vision. What's at the top of your differential?
Pituitary apoplexy (sudden hemorrhage of pituitary)
83
Pituitary apoplexy Rx:
Timely administration of glucocorticoids (to prevent life-threatening hypotension)
84
Which type of nephropathy seen in DM?
Nodular glomerulosclerosis (with KW nodules) leading to proteinuria and arteriosclerosis
85
DM: osmotic damage occurs in organs with (X) enzyme or low/absent (Y) enzymes due to accumulation of which sugar alcohol?
``` X = aldolase Y = sorbitol dehydrogenase ``` Sorbitol (ex: cataracts)
86
Islet Insulitis seen in DM (I/II) and amyloid deposits in DM (I/II)
I; II
87
Mechanisms of diabetic neuropathy:
1. Hyalinization and arteriosclerosis leads to ischemic nerve damage 2. Osmotic nerve damage (due to sorbitol accumulation) in axons and Schwann cells
88
Carcinoid syndrome: most common malignancy in (X) and tumor secretes (Y)
``` X = small intestine (metastatic) Y = serotonin ```
89
Which GI (benign/metastatic) tumor is associated with pellagra and R sided valvular heart disease?
``` Carcinoid syndrome (tumor secreting high SA levels) Metastatic ```
90
Dermatitis, diabetes, DVT, and depression. Which GI tumor?
Glucagonoma
91
ZES is diagnosed via (X) administration test if (Y) levels stay elevated
``` X = secretin Y = gastrin ```

STEP 1 (21 decks)

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