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Endocrinology > MTB and important from FA > Flashcards

MTB and important from FA Flashcards

1
Q

increased sex hormone-binding globulin in MEN –>

A

lowers free testostosterone –> gynecomastia

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2
Q

decreased sex hormone-binding globulin in WOMEN –>

A

raises free testosteron –> hirsutism

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3
Q

causes of increased sex hormone-binding globulin

A

OCP

PREGANCY

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4
Q

increased sex hormone-binding globulin - estrogen levels

A

unchanged

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5
Q

MC ectopic thyroid tissue site is the

A

tongue (lingual thyroid)

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6
Q

α subunit is common to (hormones)

WHAT DETERMINES THEIR SPECIFICITY

A
  1. TSH 2. LH 3. FSH 4. hCG

β subunit determines their hormone specificity

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7
Q

vasopressin and oxytocin production and secretion (where and transportation)

A

made in hypothalamus (supraoptic and paraventricular nuclei) and transported to posterior pituitary via neurophysins

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8
Q

insulin release regulators (and how)

A
  1. glucose (increases)
  2. GH (increases)
  3. β2 agonists (increase)
  4. cortisol (increase)
  5. α2 agonists –> decrease insulin release
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9
Q

Dopamine function (hypothalamic pituitary)

A

decreases prolactin and TSH secretion

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10
Q

GHRH analog?

used for

A

tesamorelin

used to tread HIV lipodystrophy

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11
Q

TRH funtion

A
  1. increases TSH secretion

2. increases prolactin secretion

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12
Q

prolactin secretion is regulated by

A
  1. TRH (positively)
  2. dopamine (negatively)
  3. prolactin (negatively by increasing dopamine secretion)
  4. estrogen and progesterone (positively, in pregnany)
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13
Q

somatostatin function (on hypothalamic pituitary axon)

A

decreases secretion of

  1. GH
  2. TSH
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14
Q

TSH is regulated by

A
  1. T3/T4 (negatively, decrease sensitivity of TRH)

4. dopamine (negatively)

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15
Q

GH secretion is regulated by

A
  1. glucose (negatively)
  2. somatostatin (negatively, release via negative feedaback by somatomedin)
  3. GHRH (positively)
  4. Ghrelin (positively, via GH secretagog receptor)
  5. somatomedin C (negatively, via somatostatin)
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16
Q

TBG - increased (situations)

A

estrogen (pregnancy or OCP use)

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17
Q

TBG - decreased (situations)

A
  1. hepatic failure

2. steroids

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18
Q

etiology of endogenous hepercortisolism (and percentages)

A
  1. Cushing disease (Pituitary production) - 70%
  2. Adrenals - 15%
  3. Unknown source of ACTH - 5%
  4. ecropic ACTH (cancer or carcinoid) - 10%
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19
Q

adrenal disorders - diagnostic algorithm - genarally

A
  1. establish the presence of hyperctortisolism

2. establish the cause of hypercotisolism

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20
Q

establish the presence of hyperctortisolism - best initial test

A

24h urine cortisol
if this is not in the choices: answer 1 mg overnight dexamethasone suppression test or late night salivary cortisol levels (normal exclude)

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21
Q

establish the presence of hyperctortisolism - 1 mg overnight dexamethasone suppression test

A

1 mg should normally suppress the morning cortisol level –> if this suppression occurs, hypercortisolism can be ecxluded
THERE ARE FP

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22
Q

establish the presence of hyperctortisolism - 24 urine vs 1 mg dexamethasone

A

24h urine cortisol test is a more specific –> if 24h urine cortisol is elevated -> confirm

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23
Q

causes of FP in 1mg overnight suppresson testing

A
  1. Depression
  2. alcoholism
  3. obesity
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24
Q

establish the cause of hypercortisolism - best initial test

A

ACTH testing is the best initial test determine the cause (source) or location of hypercrtisolism

  • low –> adrenal source or exogenous
  • elevated –> pituitary, ectopic production (carcinoid, lung cancer)
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25
Q

enstablish the cause of an high-ACTH hypercortisolism

A

suppresses with high doses dexamethasone –> pituitary

not suppresses –> ectopic production (carcinoid, lung cancer)

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26
Q

hypercortisolism with low ACTH - next step

A

means ACTH independence cushing syndrome

–> CT ADRENALS (adrenal mass?)

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27
Q

cushuing with high ACTH that not suppresses on high dose dexamethasone - next step

A

(ectopic ACTH secreting tumor?)

CHEST CT

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28
Q

cushuing with high ACTH that suppresses on high dose dexamethasone - next step

A

(pituitary mass)
head MRI –> if not seen any mass (some lsions are to small to be detected on MRI) –> petrosal sinus sampling from ACTH (possibly after CRH stimulation)
–> if not detected –> check for ectopic

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29
Q

cushing - head MRI from the begining

A

(pituitary mass)
head MRI –> if not seen any mass (some lsions are to small to be detected on MRI) –> petrosal sinus sampling from ACTH (possibly after CRH stimulation)
–> if not detected –> check for ectopic

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30
Q

evaluation of adrenal incidentaloma - steps

A

4% of the population has. Do not start with a scan or you will remove the wrong organ. STEPS

  1. metanephrines in blood and urine to exclude (pheo)
  2. renin + ald levels to exclude hyperaldosteronism
  3. 1 mg overnight dexamthasone suppression test
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31
Q

the most specific test for adrenal function

A
  • cosyntropin stimulation test (Synthetic ACTH)
  • you measure the cortisol level before and after the administration
  • in a patient whose health is otherwise normal, there should be rise in corstisol level after giving the drug
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32
Q

all forms of 2ry hypertension are more likely in those whose onset:

A
  1. is under age 30 or above age 60
  2. is not controlled by 2 antihypertensive medications
  3. has a characteristic finding on the history, physical or labs
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33
Q

hyperaldosteronism - DI

A

nephrogenic DI due to hypokalemia

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34
Q

primary hyperaldosteronism - best initial test

A

measure the ratio of plasma aldosterone to plasma renin –> an elevated plasma renin excludes 1ry hyperaldosteronism

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35
Q

primary hyperaldosteronism - the most accurate to confirm test the presence of unilateral adenoma

A

a sample of the cenous blood draining adrenal –> iw will show a high aldosterone level

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36
Q

primary hyperaldosteronism - CT

A

should only done after biochemical testing confirms:

  1. low K+
  2. High aldosterone despite a high salt diet
  3. low plasma renin level
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37
Q

primary hyperaldosteronism - treatment

A
  1. unilateral adenoma is resected by laparoscopy

2. bilateral hyperplasia is treated with eplerone or spironolactone

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38
Q

pheochromocytoma - best initial test

A

level of metanephrines in plasma

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39
Q

pheochromocytoma - confirmation

A

with 24h urine collection for metanephrines

more sensitive that vanillymandelic acid level

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40
Q

pheochromocytoma - imaging

A
  • imaging of the adrenal glands with CT or MRI is done ONLY after biochemical testing
  • MIBG: nuclear isotope scan that detects the location of pheochromocytoma that originates outside the adrenal gland
41
Q

high TSH - when to treat

A
  • when TSH is very high (more than double upper limit of normal) with normal T4 –> replace hormone
  • when TSH is less than double the normal (kai nmz normal T4) –> get antirhyroid peroxidase/antithyroglobulin antibodies –> if positive –> replace with thyroid hormone
42
Q

thyroid disorder - diagnostic tests

A

all thyroid disorders are best tested first with a TSH
if it is suppressed, measure free T4 levels
TSH levels are markedly elevated if the gland has failed

43
Q

Hyperthyroidism - etiology

A
  1. Graves
  2. subacute thyroiditis
  3. painless silent thyroiditis
  4. exogenous thyroid hormone use
  5. pituitary adenoma
44
Q

hyperthiroidism - Graves - unique feature

A

eye (proptosis (20-40% and skin (5%) findings

45
Q

Painless silent thyroiditis is aka

A
  • subacute lymphocytic thyroiditis
  • lymphocytic thyroiditis with spontaneously resolving hyperthyroidism
  • may follow pregnancy
  • self-limited / b-blockers for symptoms
46
Q

graves treatment

A
  1. thionamides (methimazole is preferred over PTU)
  2. radioablation or subtotal thyroidectomy for definitive
  3. atenolol for symptomatic
  4. steroids is the best initial therapy for opthalmopathy – . if refractory radiation –> surgery (very rare)
47
Q

treatment of acute hypothyoridism and thyroid storm

A
  1. propranolol: blocks target organ effect, inhibit peripheral conversion of T4 to T3
  2. Thiourea drugs (methimazole + propylthiouracil)
  3. Iodinated contrast material: iopanoic acid and ipodate: block peripheral conversion of T4, also blocks the release of existing hormone
  4. steroids: hydrocortisone
  5. radioactve iodine: ablates the gland for a permanent cure
  6. prophylaxis with thiourea drgs
    METHIMAZOL IS BETTER
48
Q

subacute thyroiditis - treatment

A

self-limited, NSAID or aspirin and β-blockers to treat symptoms
thyroid replacement if hypothyroidism

49
Q

Job-Basedow phenomenon - definition

A

thyroitoxicosis if a patient with iodine deficiency and partially autonomous thyroid tissue (eg. autonomous nodule) is made iodine replete

50
Q

Hashimoto thyroiditis - pathophysiology / HLA

A

autoimmune disease disorder
antibodies: 1. thyroid peroxidase (antimicrosomal)
2. antithyroglobulin
HLA-DR5

51
Q

Wolf-Chaikoff effect

A

thyroid gland downregulation in response to increased iodine

52
Q

Thyrotoxic vs hypothyroid myopathy

A

both proximal muscle weakness
thyrotoxic –> normal CK
hypothyroid –> increased CK

53
Q

hypercalcemia - bone lesions

A

osteoporosis

54
Q

hypercalcemia - renal

A
  1. nephrolithiasias
  2. diabetes insibitus (nephrogenic)
  3. renal insuficiency
55
Q

acute hypercalcemia - treatment

A
  1. saline hydration at high volume
  2. bisphosphonates: pamidronate, zolendronic acid
  3. if not respond after saline and biphosponates
    - -> calcitonin (rapid action)
  4. in renal failure –> dialysis
  5. prednisone –> if sarcoidosis or granoulomatous
56
Q

1ry hyperparathyroidism - treatment

A
  • surgical resection of single adenoma
  • for 4 gland hyperplasia –> all glands removed, and a portion of 1 gland is implanted in the muscle of forearm
  • if surgery non possible –> cinacalcet
  • preoperativ imaging of the neck with sonography or nuclear is helpful in determining the surgical approach
57
Q

Primary hyperparathyroidism - diagnostic tests

A
  1. high calcium and PTH levels
  2. low P
  3. EKG with short QT
  4. sometimes elevated BUN and CR
  5. ALP from PTH on bone
  6. bone x-ray is not good test –> dexa is better
58
Q

hypocalcemia - Mg

A
  1. Mg is necessary for PTH to be released from the gland

2. low Mg levels also lead to increased urinary loss of calcium

59
Q

hypocalcemia - diagnostic tests

A
  1. EKG –> prolonged QT –> arrhythmia

2. slit lamp exam –> EARLY CATARACTHS

60
Q

hypocalcemia - treatment

A

replace calcium and vit D –> orally if symptoms are mild or absent and IV is severe
orally if symptoms are mild or absent and IV is severe

61
Q

Pseudohypoparathyroidism - def / treatment

A

aka ALbright hereditary osteodystrophy (short stature, seizures, poor mental)
- treatment: Ca and VIT D

62
Q

Ca2+ - QT

A

hypo –> long GT

hyper –> short QT

63
Q

pseudopseudohypoparathyroidism - mechanism / presentation

A

physical exam features of Albright hereditary osteodystrophy (1. short stature 2. shortened 4th/5th digits) but without end-organ PTH resistance –> occurs when the defective Gs protein α-subunit is inherited from father

64
Q

thyroid cancer - types (MC?)

A
  1. papillary carcinoma (MC)
  2. follicular carcinoma
  3. medullary carcinoma
  4. anaplatic/undifferentiated carcinoma
  5. lymphoma
65
Q

Papillary carcinoma - histology

A
  1. nuclear grooves
  2. psammoma bodies
  3. Orphan Annie eyes
  4. Lymphatic invasion (common)
66
Q

thyroidectomy - complications

A
  1. hoarseness
  2. hypocalcemia
  3. transection of recurrent and superior laryngeal nerve
  4. compressing hematoma
67
Q

thyroid cancer with BRAF mutation

A

papillary

68
Q

thyroid cancer - childhood irradiation

A

papillary

69
Q

multiple endocrine neoplasia (MEN) - mode of inheritance

A

ALL AD

70
Q

MEN 1 - manifestations

A

3Ps

  1. Parathyroid tymors
  2. Pituitary tumors (prolactin or GH)
  3. Pancreatic endocrine tumors
71
Q

MEN 1 - pancreatic endocrine tumors

A
  1. Zollinger Ellison syndrome
  2. insulinomas
  3. VIPomas
  4. Glucagonomas
72
Q

MEN 2A - manifestations

A
  1. Parathyroid hyperplasia
  2. Pheochromocytoma
  3. Medullary thryroid carcinoma
73
Q

MEN 2B - manifestations

A
  1. Pheochromocytoma
  2. Medullary thryroid carcinoma
  3. Oral/intestinal ganglioneuromatosis (mucosal neuromas)
  4. Marfanoid habitus
74
Q

glucagonoma symptoms

A

5 Ds

  1. Dermatitis (necrolytic migratory erythema)
  2. Diabetes (hyperglycemia)
  3. DVT
  4. Depression
  5. declining weight
75
Q

Zolinger-Ellison syndrome - area of tumor / causes / manifestation

A
  1. pancreas 2. duodenum
    acid hypersecretion –> recurrent ulcers in duodenum and jejunum
    manifestation: 1. abdominal pain (peptic ulcer disease, distal ulcers)
  2. diarrhea (malabsorption)
76
Q

Zollinger -Ellison synsdrome - diagnostic test

A

secretin stimulation test

positive –> gastrin levels remain elevated after administration of secretin

77
Q

Carcinoid syndrome - rarely can cause (why)

A 
pellagra 
niacnin deficiency (increased tryptophan metabolism)
78
Q

pellagra symptoms p

A
  1. Diarrhea
  2. Dementia
  3. Dermatitis
79
Q

somatostatinoma may present with

A
  1. diabetes/glucose intolerance
  2. statorrhea
  3. gallstones
80
Q

somatostatinoma - treatment

A 
surgical resection 
somatostain anglogs (eg. octreotide) for symptom
81
Q
  • T3 vs T4

- TBG leves are influenced by

A
  • T3 more potent but shorter HT
  • pregnancy + OCP increase TBG –> normal fT4
  • nephrotic syndrome + androgen decrease TBG –> normal fT4
82
Q

hyperprolactinemia - etiology

A
  1. cosecretion with GH (acromegaly)
  2. hypothyroidism (because high TRH)
  3. physiologic causes
  4. drugs
  5. prolactinoma
83
Q

hyperprolactinemia - etiology - physiologic causes

A
  1. pregnancy
  2. intense exercise
  3. renal insufficiency
  4. increased chest wall stimulation
  5. also cutting the pituitary gland eliminates dopamine delivery to the anterior pituitary
  6. cirrhosis
84
Q

hyperprolactinemia - drugs

A
  1. antipsychotic medications
  2. methyldopa
  3. metoclopramide
  4. opioids
  5. tryciclic antidepressants
  6. verapamil (the only Calcium channel blocker)
  7. OCPs
85
Q

hyperprolactinemia - diagnostic tests after prolactin is found to be high

A
  1. thyroid function tests
  2. pregnancy test (always exclude pregnancy first)
  3. BUN/creatinine (kidney diseases elevates prolactin)
  4. liver function tests (cirrhosis elevates prolactin)
  5. MRI (AFTER)
86
Q

hyperprolactinemia - MRI - when

A
  1. confirmed high prolactin levels
  2. 2ry causes like medication are excluded
  3. patient is not pregnant
87
Q

hyperprolactinemia - treamtent (generally)

A
  1. medication (cabergolide is better tolerated than bromocriptine)
  2. transphenoidal surgery (if no response to meds)
  3. radiation rarely)
88
Q

acromegaly - etiology

A
  1. almost always by adenoma (i can be associated with one of MEN when it is combined with parathyroid and pancreatic disorders
  2. rarely is caused by ectopic GH or GHRH production from lymphoma or bronchial carcinoid
  3. abuse of GH
89
Q

Acromegaly enlarges soft tissue like cartilage + bone resulting in

A
  1. increased hat, ring, and shoe size
  2. carpal tunnel syndrome and obstructive sleep apnea (from soft tissue enlarging)
  3. body odor from sweat gland hypertrophy
  4. coarsening facial features and teeth widening from jaw growth
  5. deep voice + macroglossia (big tongue)
  6. colonic polyps and skin tags
  7. arthralgias from joint growing out of alignment
  8. hypertension for unclear reasons in 50%
  9. cardiomegaly + CHF
  10. erectile dysfunction from increased prolactin cosecreted with pituitary adenoma
90
Q

acromegaly - diagnostic tests

A
  1. glucose intolerance and hyperlipidemia (contribute to cardiac dysfunction)
  2. best initial test: IGF-1
  3. most accurate: glucose suppression test
  4. MRI: only after lab identification of acromegaly
  5. prolactin levels (cosecretion)
  6. increased GH 1 to 2 hr following 100 g glucose load (decreases in normal cases
91
Q

acromegaly - complications

A

HF, DM (insulin resistance - in 10%), spinal cord compressionm vision loss 2ry to pressure of tumor optic on nerve

92
Q

acromegaly - medication

A
  1. cabergoline: dopamine will inhibit GH release
  2. octreotide or lanreotide: somatostatin inhibtis GH release
  3. Pegvisomant: GH receptr antagonists –> inhibit IFG release from liver
93
Q

GH is an antinsulin - why does it make insulinelike growth factor

A

only the effect on proteins + aminoacids is inslulinlike

94
Q

Prolactin deficinecy - presentation in men /women

A

never symptoms in men

in women: inhibits lactation after childbirth –> cannot lactate normally

95
Q

GH deficiency - presentation in children vs adults

A

children: short stature and dwarfism
adults: few symptoms (several other hormones act: catecholamines, glucagon, cortisol), central obesity, reduce muscle mass, increased LDL and ch levels

96
Q

clinical symptom that distinguish DKA from nonketotic hyperglycemia

A

Kussmaul breathing

97
Q

psychiatric disease associated with psychogenic polydipsia

A

schizophrenia (NOT DEPRESSION)

98
Q

metastatic tumor that causes CDI

A

very rare

Breast ca by far the MC

Endocrinology (5 decks)

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