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USMLE STEP 1 > Hypothalamic-Pituitary Axis > Flashcards

Hypothalamic-Pituitary Axis Flashcards

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USMLE® Step 1 flashcards
1
Q

Which type of cells are rarely clinically functional in an adenoma?

A

Gonadotrophs

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2
Q

From where is IGF-1 secreted? What triggers this?

A

Liver, along with other somatomedins in response to growth hormone

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3
Q

Rate limiting step of cholesterol biosynthesis

A

Cholesterol side chain cleavage enzyme (P450scc/CYP11A1/desmolase) cleaves off 6-carbon side chain to yield pregnenolone

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4
Q

First step of cholesterol biosynthesis

A

Cholesterol side chain cleavage enzyme (P450scc/CYP11A1/desmolase) cleaves off 6-carbon side chain to yield pregnenolone

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5
Q

21-alpha-hydroxylase deficiency- presentation

A
  • Decreased cortisol
  • Increased androgens causes virilization of female (shunting)
  • Decreased aldosterone leads to salt wasting
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6
Q

Where does vitamin D regulate intestinal calcium absorption?

A

Duodenum

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7
Q

Graves’ disease- ultrasound findings

A

Diffuse enlargement with high vascularity

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8
Q

Sheehan’s syndrome- presentation

A

Postpartum hypopituitarism. Acute presentation may include failure to lactate and hypotension/tachycardia (even after correction for blood loss and hypoglycemia). Presentation may also be chronic/late.

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9
Q

What is familial hypocalciuric hypercalcemia?

A

A rare disease caused by an inactivating mutation of CaSR. Chief cells do not sense high free calcium, so they keep secreting PTH. Kidneys keep reabsorbing calcium.

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10
Q

What is cushinoid syndrome?

A

Iatrogenic cause due to oral corticosteroids for immune suppression

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11
Q

Hypothyroidism- symptoms

A

Weakness, lethargy, somnolence, slow speech, cold intolerance, memory impairment, constipation, weight gain, dyspnea, menorrhagia, hair loss, myxedematous edema

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12
Q

123-iodine scintigraphy- toxic multinodular goiter findings

A

Non-uniform uptake with hot and cold areas. Uptake in upper normal or mildly elevated range

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13
Q

Conn syndrome- causes

A

adrenal adenomas, adrenal hyperplasia, aldosterone-producing adrenocortical carcinoma, familial hyperaldosteronism, ectopic aldosterone-producing tumors

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14
Q

What is hypercalcemia of malignancy?

A

Malignant tumor secretes PTHrP, excess calcitriol production, or osteolytic bone metastases

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15
Q

Acromegaly- diagnosis

A

Serum IGF-1 level or lack of GH suppression during oral glucose tolerance test; MRI to confirm

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16
Q

What is sacrificed in a radical lateral dissection of the neck?

A

sternocleidomastoid, CN-XI, internal jugular vein

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17
Q

What do acidophiles in the pituitary gland secrete?

A

Prolactin and growth hormone

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18
Q

Pheochromocytoma- classic triad

A

1) Sustained or paroxysmal HTN
2) Headache
3) Generalized sweating

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19
Q

M1CR ligand and function

A

MSH and ACTH are ligands; simulates melanin production

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20
Q

Adrenal cortical adenoma pathophysiology

A

Well defined, may be encapsulated, yellow to black color, rarely foci of necrosis. Neoplastic cells resemble normal cells. Clear, lipid-filled cells in sheets/nests. Uninvolved gland shows lipid-depleted, compact cells.

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21
Q

Pheochromocytoma cell type

A

Tumor of catecholamine-producing chromaffin cells

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22
Q

Enzyme that changes steroid from glucocorticoid path to androgen path

A

17,20-desmolase

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23
Q

Most common cause of primary hyperparathyroidism

A

Solitary single adenoma

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24
Q

Anaplastic/undifferentiated thyroid carcinoma- presentation

A

Very poor prognosis. Highly aggressive tumor in the elderly. Often kills by direct airway invasion.

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25
Q

Diabetes insipidus- presentation

A

Polyuria, polydipsia, hypernatremia, high plasma and low urine osmolality

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26
Q

11-beta-hydroxylase deficiency

A
  • Decreased cortisol
  • Increased mineralocorticoid activity (non-aldosterone mineralocorticoids with loss of negative feedback by aldosterone; elevated DOC [protein S])
  • Increased androgens in utero
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27
Q

Blood supply to adrenal glands

A

Superior (from aorta), middle (from renal), and inferior (from renal) adrenal arteries

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28
Q

Inheritance pattern of congenital adrenal hyperplasias

A

Autosomal recessive

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29
Q

Neuroblastoma- presentation

A
  • Infant/child
  • abdominal mass
  • fever
  • weight loss
  • opsoclonus myoclonus syndrome (OMS)
  • Secretion of vasoactive intestinal peptide (VIP)
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30
Q

Factors regulating prolactin secretion

A

Releasing factors:
Oxytocin (need milk), TRH, others

Inhibiting factors:
Parvocellular dopamine, prolactin negative feedback on lactotrophs and activation of arcuate nucleus for DA secretion

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31
Q

PTH function

A

1) Increase DCT reabsorption of calcium (TRPV5)
2) Inducer of 1-alpha-hydroxylase to catalyze final step of calcitriol synthesis from calcidiol
3) Stimulates clearance of renal phosphate
4) Stimulates activity of osteoclasts by inducing RANKL expression in osteoblasts

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32
Q

Thyroid surgery complication causing breathy hoarseness

A

Unilateral recurrent laryngeal nerve injury

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33
Q

Pre-biosynthetic step of steroid hormones that is a rate-limiting factor

A

Transport of free cholesterol across outer mitochondrial membrane by steroidogenic acute regulatory protein (StAR)

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34
Q

How do the parathyroid glands sense calcium?

A

Calcium-sensing receptor (CaSR) on chief cells

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35
Q

What do you think when you see 2 or more parathyroid adenomas?

A

MEN1

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36
Q

MEN2 genetics

A

Autosomal dominant pattern. Gain-of-function RET mutation (chromosome 10). RET is a receptor tyrosine kinase. Activates MAPkinase cascade. Mutation causes constitutive growth signal in absence of GDNF (ligand).

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37
Q

Prolactinoma treatment

A

Dopamine agonists are first line.

  • Cabergoline
  • Bromocriptine
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38
Q

LH/FSH deficiency- presentation in women

A

Amenorrhea/oligomenorrhea, infertility, breast atrophy, vaginal dryness; note- no change in pubic and axillary hair (only source of androgens is adrenal gland, which is unaffected)

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39
Q

Common cause of gigantism

A

Growth hormone excess (often a GH/PRL adenoma) prior to epiphyseal plate closure

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40
Q

Where does RANKL bind?

A

Pre-osteoclasts, causing them to mature

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41
Q

Hashimoto’s thyroiditis- pathology

A
  • Glandular enlargement (diffuse goiter)
  • Lymphocytic infiltrate with germinal centers
  • Atrophic follicles
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42
Q

What is the pyramidal lobe?

A

Most caudal remnant of the thyroglossal tract, present in 1/3 of normal subjects

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43
Q

What is pseudohypoparathyroidism?

A

Receptor mutation causes PTH resistance

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44
Q

Hypophysitis- pathophysiology

A

Lymphocytic or granulomatous (TB/sarcoid)

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45
Q

What is MEN2A ?(Sipple syndrome)

A

Medullary-thyroid carcinoma (amyloid-producing) with pheochromocytoma and hyperparathyroidism

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46
Q

Graves’ disease presentation

A

Nervousness, fatigue, weakness, sweating, heat intolerance, tremor, hyperactivity, palpitations, appetite decrease, weight loss, menstrual disturbance, Graves’ opthalmopathy (variant of lid lag sign of thyrotoxicosis), Graves’-associated dermopathy (pretibial myxedema)

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47
Q

Lipoid congenital adrenal hyperplasia

A

Rare; accumulation of fatty deposits in the adrenal gland on biopsy due to accumulation of cholesterol. Genetic defects in StAR or cholesterol desmolase.

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48
Q

What metabolite is used to determine vitamin D deficiency?

A

Calcidiol (25-hydroxycholecalciferol, made in the liver from vitamin D3)

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49
Q

Central compartent of neck- level and boundaries

A

Level VI; hyoid bone (superiorly), carotid arteries (laterally), innominate artery (inferiorly)

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50
Q

Remnants of the thyroglossal duct that do not degenerate

A

Thyroglossal duct cysts, ectopic thyroid gland

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51
Q

Cushing syndrome- pathophysiology

A

Systemic disease due to chronic glucocorticoid excess

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52
Q

Thyroid hormone synthesis

A

Iodide is taken up from serum by the sodium-iodide transporter (NIS). Thryoglobulin is synthsized and exocytosed into the follicular lumen (colloid). Free iodide is transported into the follicle by pendrin, and it is oxidized to iodine by thyroid peroxidase (TPO). Iodination of thyroglobin tyrosine residues generates monoiodothyronine (MIT) or diiodothyronine (DIT). Conjugation of two of these products generates T3 or T4. If the MIT is the inner tyrosine, then it is inactive reverse T3. Iodinated is endocytosed, fusing with the lysosome to form the lysoendosome. Proteolysis liberates T3, T4, and RT3.

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53
Q

What non-IGF-1 receptor does IGF-1 bind?

A

Insulin receptor (insulin-like effects)

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54
Q

Where is calcium reabsorption hormonally controlled? What is the name of the channel?

A

In the distal convoluted tubule via TRPV5 (upregulated by PTH)

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55
Q

Pituitary apoplexy- pathophysiology

A

Sudden hemorrhage, often secondary to adenoma as it lays down new, leaky vessels

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56
Q

Fludrocortisone use

A

Low aldosterone activity (high affinity for mineralocorticoid receptor)

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57
Q

Effect of growth hormone on blood glucose

A

Diabetogenic: decreases glucose uptake by muscle and adipose, increases lipolysis

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58
Q

123-iodine scintigraphy- Toxic adenoma/nodule findings

A

Single hot nodule, suppression of the rest of the thyroid gland, uptake generally in normal range

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59
Q

What/where are the magnocellular neurons?

A

They originate in the paraventricular and supraoptic nuclei of the hypothalamus and go through the infundibulum to the neurohypophysis. They synthesize and secrete ADH and oxytocin

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60
Q

Aromatase actions

A

1) Androstenedione to estrone

2) Testosterone to estradiol

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61
Q

What blocks Levothyroxine absorption?

A

Calcium, soy, iron (CSI)

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62
Q

Metabolic effects of cortisol

A
  • diabetogenic, mobilizing glucose
  • mobilizes amino acids and glycerol backbones for gluconeogenesis
  • “planning for stress”
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63
Q

Embryological origin of the neurohypophysis

A

Diencephalon; evagination termed the infandibulum

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64
Q

Medullary thyroid carcinoma- pathology

A

Organoid appearance with nests and cords. Immunostain for calcitonin.

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65
Q

Factors that regulate growth hormone release

A

Stimulatory: GHRH, ghrelin, low glucose, low FFAs, fasting, puberty, hormones, exercise

Inhibitory: somatostatin, GH and IGF-1 (negative feedback), high glucose, high FFAs, obesity, pregnancy

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66
Q

Medications for acromegaly

A

Octreotide and lanreotide (somatostatin analogs), pegvisomant (mutated GH receptor), cabergoline (only on STEP)

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67
Q

123-iodine scintigraphy- procedure

A

Give oral dose of iodine, then scan in 24 hours. Measure 24-hour uptake in thyroid.

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68
Q

Pituitary macroadenoma- presentation

A

1) Hormone excess/deficiency
2) Bitemporal hemianopsia
3) Headache (dura stretching)
4) Hydrocephalus (compression of CSF system)
5) Diplopia (CN-III) or other cranial nerve palsies if there is lateral extension

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69
Q

Pheochromocytoma- lab findings

A
  • Elevated plasma metanephrines
  • Elevated 24-hour urinary catecholamines and metanephrines
  • Homovanillic acid and vanillylmandelic acid
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70
Q

What medications increase levothyroxine requirements?

A

Estrogen, antidepressants, anti-seizure meds, reflex meds

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71
Q

Congenital defect associated with hypoparathyroidism

A

DiGeorge syndrome

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72
Q

Hyperparathyroidism- presentation

A

Hypercalcemia symptoms, fractures, osteitis fibrosa cystica, GI symptoms, neuropsych, HTN, shortened QT, nephrolithiasis, band kerotopathy

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73
Q

Adrenal cortical carcinoma- hereditary syndromes

A

Li-Fraumeni, Beckwith-Wiedemann, MEN1

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74
Q

Hypoaldosteronism- diagnosis

A

History, plasma renin activity, serum aldosterone, serum cortisol

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75
Q

Hashitoxicosis- presentation

A

Similar to Graves’ at first (may even have antibodies) but then patients become hypothyroid due to changes in the immune reaction

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76
Q

What happens when the Rathke’s pouch fails to regress?

A

Pharyngeal hyopphysis, Rathke cyst, craniopharyngioma (benign)

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77
Q

Conn syndrome- treatment

A

Surgery is ideal if unilateral. Medications include mineralocorticoid antagonists (spironolactone, epleronone) and potassium-sparing diuretics (amiloride, triamterene)

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78
Q

Mineralocorticoid zone

A

Zona glomerulosa

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79
Q

Sources of cholecalciferol (vitamin D3)

A

1) de novo from cholesterol

2) dietary (fish, eggs, fortified milk)

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80
Q

Hypoaldosteronism- causes

A
  • Hyporeninemic hypoaldosteronism, associated with diabetic nephropathy and chronic nephritis
  • Medications, such as NSAIDs and ACE inhibitors
  • Addison’s disease
  • Inherited disorders (e.g. aldosterone synthase deficiency)
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81
Q

Pathway activated by growth hormone

A

JAK-STAT; mutations in this pathway can cause GH insensitivity/dwarfism

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82
Q

Inferior parathyroid glands embryological origin

A

Third pharyngeal pouch

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83
Q

Hypocalcemia treatment

A

IV calcium, oral calcitriol in acute cases. Oral calcium and cholecalciferol for maintenance.

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84
Q

Lid-lag sign of thyrotoxicosis

A

Result of hyperadrenergic effects. Sympathetic stimulation of Muellers muscle (superior tarsal plate).

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85
Q

For which type of pituitary adenoma is surgery NOT the primary treatment?

A

Prolactinoma

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86
Q

Drugs that interfere with thyroid function

A

Tyrosine kinase inhibitors, lithium, amiodarone, interferon-alpha

87
Q

Iodine for treatment and particle(s)

A

Iodine-131 (gamma and high-energy beta)

88
Q

Common cause of mortality in acromegaly

A

Cardiovascular disease (HTN, LVH, cardiomyopathy)

89
Q

Portion of adrenal cortex that appears to be “tubular”

A

Zona fasciculata

90
Q

Hyperthyroidism- treatment

A

Thionamides, (Methimazole, Propothiouracil) block oxidation of iodine by TPO. Propothiouracil also blocks conversion of T4 to T3. Radioiodine (I-131) can be used to ablate the thyroid.

91
Q

Other name for toxic multinodular goiter

A

Plummer’s disease

92
Q

Three forms of calcium

A

1) free (majority)
2) protein-bound (albumin)
3) complexed to anions (least)

93
Q

What happens to pregnenelone in the zona glomerulosa?

A

Converted to progesterone by 3-beta-hydroxysteroid dehydrogenase

94
Q

Most common RET mutation in MEN2B

A

Methionine switched for threonine (M918T) at codon 918

95
Q

Most important regulator of TSH levels

A

Free T4. Remember, most T4 is bound to thyroid-binding globulin, TBG.

96
Q

Hashimoto’s thyroiditis- ultrasound

A

Hypoechoic appearance

97
Q

Follicular thyroid carinoma- presentation

A

Good prognosis. More common in women 40-60. Produces thyroglobulin. Hematologic spread more common, especially to bone. Requires histology for diagnosis.

98
Q

Imaging agent taken up by any cells expressing catecholamine intake

A

Metaiodobenzylguanidine (MIBG)

99
Q

Neuroblastoma cell type

A

Neuroblast cells (primitive sympathetic ganglion)

100
Q

Embryological origin of the adenohypophysis

A

Evagination of oral ectoderm (Rathke’s pouch), which regresses

101
Q

Iodine for imaging and particle(s)

A

Iodine-123 (gamma)

102
Q

Which adrenal vein is more difficult to cannulate in adrenal vein sampling?

A

Right side. Enters IVC directly at an acute angle.

103
Q

Graves’ disease- pathology

A

Follicular cells become columnar in shape. Active resorption of thyroglobulin. Infolding of epithelium. May progress to lymphocytic infiltrate and destruction of follicles, resulting in hypothyroidism.

104
Q

What is the normal function of PTHrP

A

Secreted by mammary gland in lactation, mobilizing calcium for milk production.

105
Q

How does iodine cause HYPOthyroidism?

A

Inadequate synthesis of T4. Compensatory TSH causes hyperplasia, resulting in a diffuse goiter.

106
Q

Most common hormone-secreting pituitary adenoma

A

Prolactinoma

107
Q

Sheehan’s syndrome- pathophysiology

A

The adenohypophysis is enlarged during pregnancy with no additional blood supply. A superimposed peripartum hemorrhage can cause an infarction due to hypovolemic shock.

108
Q

Mitotane

A

Breaks down entire adrenal cortex

109
Q

Cortisol-cortisone shunt- mechanism

A

Kidneys (and colon, sweat glands, salivary glands) express 11-beta-hydroxysteroid dehydrogenase 2, which converts cortisol to cortisone (cannot activate receptor). The liver recycles cortisone back to cortisol via 11-beta-hydroxysteroid dehydrogenase 1.

110
Q

Full name and other name for IGF-1

A

Insulin-like growth factor 1; somatomedin C

111
Q

Medullary thyroid carcinoma- presentation

A

Neuroendocrine carcinoma of C cells. Produces calcitonin. Most are sporadic. Hereditary associated with MEN2/FMTC.

112
Q

Follicular thyroid carcinoma- genes

A

Gain of function mutations that activate RAS or PI-3K/AKT arm of receptor tyrosine kinase signaling pathway. PTEN loss of function (tumor suppressor) may also occur.

113
Q

What type of receptor is the thyroid hormone receptor (TR)? What does it do?

A

Nuclear receptor. When bound, it acts as a transcription factor. Increases BMR, heat production, and O2 consumption. Increases sodium-potassium pumps, which consume ATP.

114
Q

Under what pH conditions is ionized calcium increased?

A

Acidosis

115
Q

Androgen zone (adrenal)

A

Zona reticularis

116
Q

What is desmopressin?

A

Synthetic ADH (vasopressin) with modifications to reduce the effect on vasculature and increase half-life

117
Q

Growth hormone insensitivity treatment

A

Mecasermin, a recombinant IGF-1

118
Q

What is MEN2B? (Wagemann-Froboese)

A

Medullary thyroid carcinoma with pheochromocytoma, mucosal neuromas, ganglioneuromas, marfanoid habitus

119
Q

Thyroid surgery complication causing airway obstruction (inspiratory stridor)

A

Bilateral recurrent laryngeal nerve injury

120
Q

Action of 5/3 monodeiodinase

A

Clips inner iodine molecule to make reverse T3 (inactive)

121
Q

How do you catch a pituitary microadenoma that is not appearing on MRI?

A

Inferior petrosal sinus sampling

122
Q

Thyroid surgery complication causing loss of high pitch voice/projection

A

Superior laryngeal nerve injury

123
Q

Where does cortisol have negative feedback?

A

It has negative feedback on corticotrophs and the hypothalamus.

124
Q

What is ergocalciferol and where do you get it?

A

Vitamin D2; vegetables

125
Q

Where is RANKL synthesized?

A

Osteoblasts

126
Q

M2CR ligand and function

A

ACTH is the ligand; stimulates glucocorticoid production

127
Q

How does iodine cause HYPERthyroidism?

A

TSH increases to compensate for inadequate T4. If there is just enough iodine to “get by,” it may cause some follicles to proliferate more than others to form a nodular goiter. Some nodules may become autonomous and secrete more thyroid hormone. This is a toxic multinodular goiter.

128
Q

Blood supply to the thyroid

A

Superior thyroid artery (from external carotid), inferior thyroid artery (from thyrocervical trunk), thyroid ima artery (from brachiocephalic, found in 5-10% of individuals)

129
Q

Differential diagnosis for painful and tender thyroiditis

A

Subacute (de Quervain’s/granulomatous) thyroiditis, infections thyroiditis, radiation-induced thyroiditis, trauma-induced thyroiditis

130
Q

What is MEN1? (Werner’s syndrome)

A

Hyperparathyroidism (first), islet cell tumor, pituitary tumors. Caused by Menin on chromosome 11 (tumor suppressor). Autosomal dominant inheritance pattern; recessive mechanism (two-hit).

131
Q

How do chronic granulomatous disorders cause hypercalcemia?

A

Activation of 1-alpha-hydroxylase

132
Q

Neuroblastoma- median age

A

18 months

133
Q

Anaplastic/undifferentiated thyroid carcinoma- genes

A

loss of p53 function

134
Q

LH/FSH deficiency- presentation in men

A

Impotence, infertility, small testis, decreased muscle mass, reduced facial/body hair, thinning of skin (finely wrinkled)

135
Q

What is the main function of IGF-1?

A

Promote organ and linear growth

136
Q

What/where are the parvocellular neurons?

A

They originate in the paraventricular and arcuate nuclei of the hypothalamus and terminate in the median eminence. They secrete releasing hormones into the hypothalamic-hypophyseal portal vessels to act on the adenohypophysis.

137
Q

Why isn’t T3 helpful in hypothyroid diagnosis?

A

5’/3’ deiodinase is upregulated to maitain T3 levels as normal

138
Q

Pheochromocytoma- Rule of Tens

A
  • 10% outside adrenal gland (e.g. organ of Zuckercandl)
  • 10% of sporadic cases are bilateral
  • 10% are malignant
  • 10% do not present with HTN
139
Q

Conn syndrome- diagnosis

A

Plasma aldosterone concentration (PAC), plasma renin activity(PRA);
PAC/PRA ratio of >20

May confirm with suppression tests (IV normal saline loading, fludrocortisone)

CT is good for masses. Bad for discerning unilateral vs. bilateral.

Adrenal vein sampling to determine side..

140
Q

Superior parathyroid glands embryological origin

A

Fourth pharyngeal pouch

141
Q

Compressive symptoms of goiter

A

Dyspnea (especially lying down), compression of recurrent laryngeal nerve, Horner’s syndrome, jugular vein compression

142
Q

Assays to diagnose growth hormone deficiency

A

IGF-1 and IGFBP-3 (both decreased); GH is pulsatile and not as useful clinically

143
Q

Embryological origin of the thyroid (follicular cells)

A

foramen cecum of the tongue (ventral diverticulum during 4th week of gestation)

144
Q

Hashimoto’s thyroiditis antibody

A

Anti-TPO (diagnostic with symptoms but found in 20% of normal women). Anti-thyroglobulin may also be seen.

145
Q

Non-metabolic effects of cortisol

A

Lymphocyte apoptosis, anti-inflammatory, bone health, BP regulation, CNS effects

146
Q

17-alpha-hydroxylase is the same protein as what enzyme?

A

17,20-desmolase

147
Q

Action of 5’/3’ monodeiodinase

A

Converts T4 to more active T3

148
Q

Name for primary hyperaldosteronism

A

Conn syndrome

149
Q

What is a sestamibi scan?

A

Technetium is a tracer that collects in overactive parathyroid tissue

150
Q

Waterhouse-Friderichsen syndrome

A

Hemorrhagic adrenalitis caused by bacteremia (e.g. Neisseria meningitidis)

151
Q

Normal prolactin level

A

2-20 ng/mL

152
Q

Pheochromocytoma- treatment

A
  • Alpha and beta adrenergic blockade

- Resection if possible

153
Q

Conn syndrome- presentation

A

HTN, hypokalemia (1/3; may cause mild metabolic alkalosis and cramps/weakness), mild hypernatremia, higher CV mortality

154
Q

Hyperprolactinemia- presentation

A

Hypogoadotropic hypogonadism, galactorrhea, infertility, amenorrhea/oligomenorrhea, impotence

155
Q

Goiter hereditary association

A

MEN2A

156
Q

ACTH rhythm and half-life (generally)

A

Circadian and pulsatile; highest in the morning and causes cortisol spike; short half-life

157
Q

Papillary thyroid carcinoma- genes

A

Gain-of-function in growth factor receptor pathway, resulting in MAPkinase/ERK activation. RET, NTRK1 are receptor tyrosine kinases. BRAF is a serine-threonine kinase.

158
Q

Usual order of hypopituitarism

A

Gonadotrophs (hypogonadotropic hypogonadism), then somatotrophs (dwarfism in children), then thyrotrophs (central hypothyroidism), and finally corticotrophs (secondary adrenal insufficiency)

159
Q

Pituitary apoplexy- presentation

A

Acute onset of headache, diplopia, and hypopituitarism

160
Q

Presentation, diagnosis, and treatment of follicular thyroid adenoma

A

Benign neoplasms that are usually nonfunctional but may produce thyroid hormone and cause thyrotoxicosis. Gain-of-function at TSH receptor. Suspected adenomas are removed for diagnostic lobectomy (fine needle aspiration is not useful).

161
Q

Describe the embryological basis of the inferior parathyroid glands

A

Derived from third pharyngeal pouch. Descend with thymus. Reside anterior to the recurrent laryngeal nerve.

162
Q

123-iodine scintigraphy- Graves’ findings

A

Darker appearance, elevated uptake (50-80%), ballooning lobes, prominent isthmus, pyramidal lobe seen

163
Q

Propothiouracil side effects

A

Agranulocytosis, aplastic anemia, vasculitis, hepatitis (these side effects are rare)

164
Q

What is familial medullary thyroid carcinoma (FMTC)?

A

Variant of MEN2 with thyroid tumor only.Must be four or more cases in a pedigree with absece of other MEN2-associated tumors.

165
Q

Primary sources of cholesterol (3)

A

1) LDL molecules via LDL-R
2) Made from acetyl-CoA
3) Esterified cholesterol stored in lipid droplets

166
Q

SIADH- presentation

A

Hyponatremia with low plasma osmolality, normal/high urine osmolality, absence of hypotension or hypovolemia

167
Q

Prolactin level with greatest concern for prolactinoma

A

200 ng/mL

168
Q

Hereditary conditions associated with pheochromocytoma

A
  • MEN2

- von Hippel-Lindau

169
Q

Growth hormone excess after epiphyseal plate closure

A

Acromegaly

170
Q

Struma ovarii

A

Ovarian teratoma with mature thyroid tissue that secretes hormone

171
Q

Normal calcium level

A

8.5-10.5 mg/dL

172
Q

Darkest/most basophilic part of adrenal cortex on histology

A

Zona reticularis

173
Q

Hypoaldosteronism- presentation

A

Metabolic acidosis with normal anion gap; typically not associated with sodium wasting. AKA type IV renal tubular acidosis.

174
Q

Where are most craniopharyngiomas found?

A

Most from the pituitary stalk, with a minority found in the intrasellar space.

175
Q

Embryological origin of parafollicular (C) cells

A

Ultimobranchial body (part of fourth pharyngeal pouch)

176
Q

Papillary thyroid carcinoma- pathology

A

Psammoma bodies are microcalcifications (visible on ultrasound). Orphan-Annie nuclei have a ground glass apearance. Intranuclear grooves.

177
Q

Follicular thyroid carcinoma- pathology

A

Tightly packed, small follicles with scant colloid. Occasional cells with abundant granular eosinophilic cytoplasm (Hurthle cell variant).

178
Q

Hypoaldosteronism- treatment

A

Fludrocortisone

179
Q

Some somatotrophs are also what type of cell?

A

Lactotrophs

180
Q

Cushing syndrome presentation

A

moonface, dorsocervical fat bad, central obesity, etc.

181
Q

Cretinism- cause

A

Hypothyroidism during fetal development. Supplementation may improve stature but not mental deficits.

182
Q

Calcitonin function

A

Inhibits bone resorption of bone in times of stress on skeleton. May inhibit renal calcium absorption. In normal adults, little effect on serum calcium. Strong effect when bone turnover is increased (thyrotoxicosis, Paget’s)

183
Q

Graves’ disease- antibody

A

TSH receptor antibody (TRAB), which agonizes receptor and does not let go

184
Q

Enzyme that converts testosterone to DHT

A

5-alpha-reductase

185
Q

Cortisol-cortisone shunt- purpose

A

Prevents large volume of cortisol from activating mineralocorticoid receptor

186
Q

Time course of thyroiditis and treatment

A

Initially, leakage of stored thyroid hormone from colloid causes a 3-8 thyrotoxic phase, with a euthyroid phase as levels decline. The hypothyroid phase is usually asymptomatic. Recovery usually happens at 5-6 months. Beta-blockers for symptom relief.

187
Q

SIADH- treatment

A

Fluid restriction, high solute intake/IV saline

188
Q

Ghrelin promotes the secretion of which pituitary hormone?

A

Growth Hormone (synergistic with GHRH)

189
Q

Papillary thyroid carcinoma- presentation

A

Best prognosis. Usually in individuals age 25-50, often with exposure to ionizing radiation. Produces thyroglobulin. Commonly spreads to lymphatics/nodes. Hypoechoic on ultrasound, and may show calcifications.

190
Q

Enzyme that changes steroid from mineralocorticoid path to glucocorticoid path

A

17-alpha-hydroxylase

191
Q

Central diabetes insipidus- treatment

A

Desmopressin

192
Q

In what disease is a RET loss-of-function mutation observed?

A

Hirschsprung disease

193
Q

Adrenal insufficiency- presentation

A

Weakness, fatigue, muscle/joint pain, hhponatremia, hypoglycemia, hyperpigmentation (sun exposed areas, due to increased ACTH and aMSH)

194
Q

Craniopharyngioma- presentation

A

Headache, visual impairment, hormonal deficiency (growth failure)

195
Q

Number of carbons in cholesterol

A

27

196
Q

Pro-opiomelanocortin (POMC) cleavage products

A

ACTH and alpha-melanocyte stimulatinghormone (aMSH)

197
Q

Treatment of hypercalcemia

A

Bisphosphonates (antiresorptive), cinacalcet (calimimetic). AVOID thiazides, lithium. In severe cases, saline loading, denosumab (RANKL inhibitor)

198
Q

Name for hypersecretion of vasopressin

A

Syndrome of Inappropriate ADH (SIADH)

199
Q

Cushing syndrome diagnosis

A

Overnight dexamethasone suppression test (fail to suppress cortisol), high midnight salivary cortisol, 24-hour urinary free cortisol, metyrapone test, ACTH levels

200
Q

What is Laron Dwarfism?

A

Growth hormone insensitivity due to a mutation in the GH receptor

201
Q

Empty sella (primary)- pathophysiology

A

Defect in the diaphragma sella allows CSF through, compressing the pituitary gland and enlarging the sella over time. Usually an asymptomatic, incidental finding.

202
Q

Chief cell function in parathyroid glands

A

Synthesize, store, and secreate PTH

203
Q

What are clinical tests for hypocalcemia?

A

Chvostek’s sign, Trousseau’s sign

204
Q

Neuroblastoma- diagnosis

A

Elevated urine levels of catecholamines, metanephrines, homovanillic acid, VMA

205
Q

Cortisol rhythm and half-life

A

Highest in the morning; long half-life

206
Q

Order of enzyme actions in the zona glomerulosa

A

1) Cholesterol => prenenolone by cholesterol desmolase
2) Pregnenolone => progesterone by 3-beta-hydroxysteroid dehydrogenase
3) Progesterone => 11-deoxycortisone by 21-hydroxylase
4) 11-deoxycortisone-corticosterone by 11-beta-hydroxylase
5) Corticosterone => aldosterone by aldosterone synthase

207
Q

Role of M3CR and M4CR

A

Appetite suppression; M4CR suppressed by agouti-related peptide (ghrelin pathway)

208
Q

Oxyphil cell function in parathyroid glands

A

Who knows?

209
Q

123-iodine scintigraphy- subacute/silent thyroiditis findings

A

Diffusely suppressed, may be patchy, uptake is very low

210
Q

Causes of hyperprolactinemia

A
  • Pregnancy
  • Nipple stimulation
  • Physical activity/stress
  • Pituitary adenoma
  • Hypothyroidism
  • Exogenous estrogens
  • Interfering with dopamine inhibition of lactotrophs
211
Q

Where are calcium and magnesium passively reabsorbed between cells?

A

Thick ascending limb of the loop of Henle

212
Q

Adrenal cortical adenoma- pathophysiology

A

Benign neoplasm of adenocortical cells that can secrete steroids independently of ACTH or RAS pathway

213
Q

Glucocorticoid zone

A

Zona fasciculata

USMLE STEP 1 (24 decks)

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