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Endocrinology > Nate extra endocrine > Flashcards

Nate extra endocrine Flashcards

1
Q

What is the function of prolactin? What regulates prolactin?

A

Prolactin stimulates milk production and inhibits GnRH, thereby inhibiting ovulation in females after giving birth (**this is also why excess prolactin from a prolactinoma will also cause amenorrhea).

Dopamine from the arcuate nucleus of the hypothalamus inhibits prolactin release. Dopamine agonists (bromocriptine) and estrogens (OCPs) also inhibit prolactin release. TRH increases prolactin release.

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2
Q

What happens to the adrenals in all congenital enzyme deficiencies?

A

Bilateral adrenal hyperplasia (enlargement) due to incr ACTH.

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3
Q

What is the function of cortisol?

A

BIG FIB

  • Blood pressure -> upreg. of alpha 1 receptors
  • Inflammation (anti) -> inhibits PLA2 which decreases leukotrienes and prostaglandins, decr leukocyte adhesion (neutrophilia), blocks histamine release and eosinophils, blocks IL-2 production
  • Gluconeogenesis, lipolysis, proteolysis increase
  • Fibroblast inhibited (striae, tx Keloid)
  • Insulin resistance- increased
  • Bone formation decreased
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4
Q

What cells make calcitonin? What embryologic tissue are they derived from? Neoplastic proliferation of these calcitonin producing cells causes what cancer?

A

Parafollicular cells of the thyroid. Neural crest derived. Medullary thyroid cancer.

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5
Q

What hormones signal using cAMP?

A

FLAT ChAMP Calc-ulates GrowthRelease and Glucagon

FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH, Calcitonin, GHRH, Glucagon

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6
Q

What hormones signal using cGMP?

A

Vasodilators

ANP, NO

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7
Q

What hormones signal using IP3?

A

GRowing GOAT Gonads H-Ang II

GHRH, Gastrin, Oxytocin, ADH (V1), TRH, GnRH, Histamine (H1), Ang II

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8
Q

What hormones signal using steroid receptor?

A

VETTT CAP

Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

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9
Q

What hormones signal via intrinsic tyrosine kinase?

A

Think insulin and growth factors

Insulin, IGF-1, PDGF, FGF, EGF

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10
Q

What hormones signal via a tyrosine receptor kinase?

A

PIG

Prolactin, Immunomodulators, GH

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11
Q

What are the functions of T3?

A

4 B’s
Brain maturation (cretinism w/o)
Bone growth (cretinism w/o)
Beta adrenergic effects (incr beta 1 receptors)
Basal metabolic rate incr (incr Na+/K+ activity)

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12
Q

What are the function of thyroid peroxidase?

A

1) oxidation of iodine
2) organification
3) coupling

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13
Q

What is the Wolff-Chaikoff effect?

A

Giving excess iodine temporarily inhibits thyroid peroxidase and decreases T4 production (T4 converted to T3 by peripheral 5’ deiodinase)

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14
Q

What are the most common causes of Cushings syndrome and Addisons disease?

A

Cushings- Exogenous steroids -> decr ACTH

Addison’s- Acute withdrawal from exogenous steroids

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15
Q

What are the most common endogenous causes of cushing syndrome?

A

ACTH producing adenoma w/ moderate ACTH increas-(bilateral enlarged adrenals) -> 70%

Ectopic ACTH production w/ CRAZY increased ACTH (bilateral enlarged adrenals) -> 15%

Adrenal adenoma, carcinoma or hyperplasia- incr cortisol production and decr ACTH (one large adrenal) -> 15%

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16
Q

What is dexamethasone? What is it used for?

A

A glucocorticoid. Functions like cortisol so it is used as the dexamethasone suppression test to determine what is causing Cushings syndrome. Small dose of dexamethasone will suppress cortisol in a normal person. Large dose will suppress cortisol in a person with an ACTH producing adenoma. Large dose will not drop cortisol in ectopic ACTH producing malignancy or in an adrenal cortisol producing tumor. In ectopic ACTH production there should be bilateral involvement of the adrenals, whereas in the cortisol secreting tumor only 1 adrenal should be enlarged.

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17
Q

What is the difference between primary and secondary hyperaldosteronism (Conn syndrome)?

A

Primary is incr aldo d/t adrenal adenoma > hyperplasia > carcinoma. **LOW plasma renin

Secondary is incr aldo d/t a perceived low volume (renal artery stenosis, CKD, cirrhosis, nephrotic syndrome) **INCREASED plasma renin

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18
Q

What is the clinical presentation of hyperaldosteronism?

A

Increased Aldo
Na+ reabsorption -> HTN
K+ excretion -> hypokalemia
H+ excretion -> metabolic alkalosis

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19
Q

Besides autoimmune, what are other causes of adrenal insufficiency?

A

TB (developing countries) and metastases (boards love this -> esp lung cancer)

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20
Q

What are the presenting symptoms in adrenal insufficiency? How can you distinguish primary from secondary?

A

Adrenal insufficiency will cause decr cortisol and aldosterone. This will cause an opposite effect as hyperaldosteronism. You will see hypotension, hyperkalemia and metabolic acidosis. Other symptoms: weakness, weight loss, fatigue, anorexia.

Primary will have high ACTH trying to stimulate non-working adrenals. Secondary will have low ACTH b/c that is the problem. Also, primary will have skin hyperpigmentation due to the increased POMC transcription.

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21
Q

What is Waterhouse Friderichsen syndrome? What is it associated with? What is the common picture shown in question stem?

A

This is acute primary adrenal insufficiency d/t adrenal hemorrhage/ necrosis.

A/w Neisseria meningitidis septicemia, DIC, endotoxic shock.

Classic image = sack of blood adrenal glands

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22
Q

What cells comprise the adrenal medulla and what is their origin?

A

Chromaffin cells, neural crest

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23
Q

What do pheochromocytomas secrete and therefore, what are the breakdown products seen in serum and urine of this tumor.

A

Dopamine -> HVA
Epinephrine -> metanephrines —MOA–> VMA
NE -> normetanephrines —MOA–> VMA

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24
Q

What are pheochromocytomas a/w?

A

Neurofibromatosis type 1, MEN2a/b, VHL disease

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25
Q

What is the treatment for pheochromocytoma?

A

ORDER IS VERY IMPORTANT:

  1. Alpha blockade (phenoxybenzamine- irreversible alpha1/2)
  2. Beta blockade
  3. Surgery
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26
Q

What are the 5P’s of Pheochromocytoma?

A 
Episodic....
Pressure (incr BP)
Palpations
Pain (headache)
Perspiration
Pallor
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27
Q

Metastatic pheochromocytomas will show elevated levels of what?

A

only dopamine and Epinephrine (SAM and adrenal enzymes needed to make NE)

28
Q

What is the rule of 10’s with pheochromocytomas?

A 
10%.....
Metastasize
Bilateral
Familial
Malignant
Calcify
Kids
29
Q

What is a common location of pheochromocytoma metastasis and what would it present like?

A

Mets to bladder, adrenergic symptoms while urinating.

30
Q

What can pheochromocytomas do related to the blood?

A

Incr EPO -> polycythemia

31
Q 
Adrenal neuroblastoma is....
Most common in?
A/w elevated \_\_\_\_\_\_\_\_?
Likely to cause HTN?
A/w overexpression of \_\_\_\_\_\_\_\_\_\_?
Tumor marker = \_\_\_\_\_\_\_\_\_\_?
IHC stain = \_\_\_\_\_\_\_\_\_?
Histology: \_\_\_\_\_\_\_\_\_\_
A 
Most common in children
A/w elevated HVA (dopamine breakdown)
Likely to cause HTN? No
A/w overexpression of N-myc oncogene
Tumor marker = bombesin
IHC stain = neurofilament stain
Histology: Homer wright pseudorosettes (tumor cells around tangled fibril)
32
Q

Myxedema can be seen in both hypo and hyper thyroidism. What locations distinguish the two?

A

Hyper (Graves): pretibial and retro-orbital

hypo: facial -> esp tongue and larynx (deep voice)

33
Q

Most things are revved up in hyperthyroidism -> whats toned down?

Most things are toned down in hypothyroidism -> whats revved up?

A

Hypocholesterolemia in hyperthyroidism

Hypercholesterolemia in hypothyoridism

34
Q

What MHC gene is associated with Hashimoto’s thyroiditis?

A

HLA-DR5

35
Q

What is the most common cause of hypothyroidism where iodine is sufficient?

A

Autoimmune (anti thyroglobulin ab, anti- thyroid peroxidase ab)

36
Q

What are the histological findings in hashimotos thyroiditis?

A

Hurthle cells (stain pink) and lymphocyte infiltration with germinal centers

37
Q

A 50 year old patient with longstanding hashimoto’s thyroiditis presents with a rapidly enlarging thyroid. What is your diagnosis?

A

B-cell lymphoma (hashimotos increases risk for this)

38
Q

What is the thyroid gland like in hashimotos?

A

Enlarged, non tender

39
Q

What does a large thyroid (goiter) tell you about thyroid hormone levels?

A

NOTHING!!!

40
Q

What are the 5P’s of Cretinism?

A 
A child that is.....
Pot-bellied
Pale
Puffy faced
Protruding umbilicus
Protuberant tongue

Cretinism also has mental retardation, short stature/ skeletal defects.

41
Q

One week after a flu-like illness, a man presents with a elevated ESR, jaw pain and a tender thyroid. Diagnosis?

A

De Quervains, subacute, granulomatous thyroiditis

42
Q

What are the important features of Riedels thyroiditis?

A

Riedels is Rockhard ->hypothyroid or euthyroid
Young females break riedel wine glasses -> broken glass can extend into local structures (ie airway)
PAINLESS. IgG4 disease
Macropages and eosinophils > lymphocytes

43
Q

What type of hypersensitivity is graves disease? What antibody?

A

Type 2 hypersensitivity. IgG

44
Q

What is the Jod Basedow phenomenon?

A

Iodine deficient goiter patient is given sufficient iodine leading to thyrotoxicosis

45
Q

Is graves disease a hyperplasia or hypertrophy of the thyroid?

A

BOTH!

46
Q

What causes the myxedema in graves?

A

It is not the increased levels of thyroid hormone. There is increases deposition of connective tissue (glycosaminoglycans) b/c fibroblasts have a receptor for TSH that is now being stimulated by the TSI antibodies.

47
Q

What is the histology seen with graves disease?

A

scalloping of the colloid and irregular colloid shape (no longer round)

48
Q

What are treatments for Graves disease:

A

Beta blocker (propranolol)
Thioamide, PTU, methimazole
Radioactive iodine ablation

49
Q

Important features of papillary thyroid carcinoma

A
  • Most common (75%)
  • Orphan annie nuclei (perinuclear halo)
  • BRAF mutation (serine/ threonine kinase)
  • Activation of receptor tyrosine kinase
  • Psammoma bodies
  • Childhood radiation exposure
  • Excellent prognosis
50
Q

Important features of Follicular thyroid carcinoma

A
  • Second most common (10%)
  • Hematogenous spread
  • a/w RAS mutation or PAX8-PPAR1 gamma rearrangement
  • follicles extend thru fibrous capsule
  • good prognosis
51
Q

Important features of medullary thyroid carcinoma

A
  • Parafollicular C cells- secrete calcitonin
  • Sheets of cells in “amyloid stroma”
  • possible hypocalcemia, but more commonly causes amyloid deposition
  • a/w MEN2a/b
  • RET oncogene mutation (prophylactic thyroidectomy warranted)
  • NTRK-1 mutation
52
Q

Important features of undifferentiated/ anaplastic thyroid carcinoma

A

Older patients, very poor prognosis, local invasion (dysphagia or respiratory compromise) -> similar to Riedels but age of patient very important

53
Q

What type of biopsies are done with the thyroid?

A

Fine needle aspirations (FNA) only -> thyroid is very bloody.

54
Q

Can an FNA distinguish b/w a Follicular carcinoma or follicular carcinoma?

A

No

55
Q

What 4 carcinomas break the rule of spreading to lymph nodes, by spreading hematogenously?

A

1) RCC-> renal v
2) HCC -> hepatic v
3) Follicular carcinoma
4) Choriocarcinoma

56
Q

What are the alk phos levels in both primary and secondary hyperPTH?

A

Actually increased, because osteoblasts are activated by PTH before osteoclasts start bone resorption

57
Q

What is the first line treatment for prolactinoma?

A

ALWAYS use cabergoline or bromocriptine first (dopamine agonists). NEVER surgery first. These do a very good job at shrinking tumors by inhibiting prolactin production/ release.

58
Q

What are the clinical features of Acromegaly

A

large tongue -> gap teeth, large hands/ feet, coarse facial features, glucose intolerance (GH inhibits glucose uptake into cells)

59
Q

How is acromegaly diagnosed?

A

increased serum IGF-1 (b/c it has more consistent levels than GH which is secreted in a pulsatile fashion, failure of glucose to suppress GH

60
Q

Acromegally tx?

A

Surgery is first line, followed with octreotide if needed.

61
Q

What would you expect to see in diabetes insipidus

A

Polyuria, polydipsia, low urine osmolality, high serum osmolality

62
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test -> inability to concentrate urine due ADH lack. Desmopressin or DDAVP administration distinguishes between central or nephrogenic DI. If administration increases urine osmolality it is central, if not = nephrogenic.

63
Q

What are secondary causes of nephrogenic DI?

A

Hypercalcemia, demeclocycline (ADH antagonist), tetracyclines, lithium

64
Q

What is the treatment for nephrogenic DI?

A

hydrochlorothiazide, indomethacin, amiloride (must be added when lithium is the cause)

65
Q

What is the happens in SIADH?

A

Too much ADH causes very highly concentrated urine and excess fluid retention with low sodium (hyponatremia). Body responds with lowering aldosterone to keep a near normal volume status. Hyponatremia can lead to seizures.

66
Q

What is the treatment for SIDAH?

A

fluid restriction, IV saline, conivaptan, tolvaptan, demeclocycline (ADH antagonist helps block the affects of ADH)

67
Q

What are the SE’s of glucocorticoids?

A

Moon face, buffalo hump, truncal obesity, thin extremities due to muscle wasting, thin skin, purple striae (decr collagen synthesis), thin skin, easy bruising, osteoporosis, peptic ulcers (cortisol stimulates gastrin), diabetes, insomnia, glaucoma, acne, psychosis

Endocrinology (3 decks)

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