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Endocrine Final > Clinical > Flashcards

Clinical Flashcards

1
Q

most widely used test to determine whether thyroid dysfunction exists:

A

TSH measurement

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2
Q

Increased T3 is useful in:

A

thyrotoxicosis

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3
Q

best method to differentiate benign from malignant and diffuse goiters:

A

thyroid biopsy – fine needle aspiration

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4
Q

Anti-TPO Abs:

A

Hashimoto’s thyroiditis

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5
Q

TSI (thyroid stimulating immunoglobulin):

A

Graves disease

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6
Q

TQ

  • symptoms of faintness, facial congestion
  • external jugular venous obstruction
  • when arms are raised above head, thyroid is drawn into thoracic inlet
A

Pemberton’s sign

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7
Q

hoarseness may due to compression of:

A

recurrent laryngeal nerve

think malignancy.

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8
Q
  • focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor
  • increased release of T3 and T4
  • often elderly, atrial fib
  • tremors, weight loss
  • hot nodules are rarely malignant
A

toxic multinodular goiter

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9
Q

TQ
tumors of parathyroid, pancreas, pituitary
think…

A

MEN 1

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10
Q

TQ
medullary CA of thyroid, pheo, hyperparathyroidism
think…

A

MEN 2A

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11
Q

TQ
mucosal neuromas, medullary CA of thyroid, pheo, possibly marfanoid habitus
think…

A

MEN2B

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12
Q

cold nodule on thyroid scan

think…

A

cancer

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13
Q

psammomatous calcifications

think…

A

papillary CA

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14
Q
  • RET mutations
  • produce excessive amounts of calcitonin
  • mets to lung, liver, bone
  • cold nodule on thyroid scan
  • tx: total thyroidectomy with T4 supplementation later
A

medullary CA

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15
Q
  • menstrual irregularities
  • weight gain, constipation, fatigue
  • goiter
  • bradycardia
  • HTN
  • DTRs “hung up”
A

hypothyroidism

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16
Q
  • autoimmune disorder (anti-TPO, anti-microsomal, anti-thyroglobulin Abs)
  • increased risk of non-Hodkin lymphoma
  • Hurthle cells, lymphocytic infiltration with germinal centers
  • moderately enlarged, nontender thyroid
  • reduced SV, increased PVR (why they’re cold), increased BP
A

Hashimoto’s (autoimmune) thyroiditis

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17
Q

TQ

meds that cause hypothyroidism: (4)

A
  • amiodarone (iodine content&raquo_space; negative feedback to decrease conversion of total T4 to total T3)
  • lithium carbonate
  • IFNa
  • IL-2
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18
Q

greatest complication of hypothyroid (mortality > 50%):

A

myxedema coma

  • older women
  • winter season
  • hypothermic, hypoventilation
  • hypoglycemia
  • hyponatremia
  • shock/death
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19
Q
  • MC cause of hyperthyroidism
  • auto-Abs (IgG) stimulate TSH receptors (thyroid stimulating immunoglobulin)
  • exophthalmos: proptosis, extraocular muscle swelling
  • dermal fibroblasts (pretibial myxedema)
  • often presents during stress (e.g., childbirth)
A

Graves disease

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20
Q

-usually benign follicular adenoma; hot nodule on one side with decreased uptake on other side

A

Toxic adenoma causing hyperthyroidism

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21
Q

amiodarone may cause thyrotoxicosis

Rx?

A

Rx: ß-blocker and prednisone

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22
Q
  • hyperactive, irritable
  • palpitations
  • weight loss with increased appetite
  • polyuria
  • tachycardia, atrial fib* in elderly; angina, CHF
  • goiter (firm), tremor
  • exophthalmos
  • dermopathy (pretibial myxedema)
A

thyrotoxicosis

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23
Q

-elderly, atrial fib, fatigue, weight loss – mistaken for depression

A

apathetic hyperthyroidism

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24
Q

tx for hyperthyroidism:

A
  • antithyroid drugs (PTU, methimazole)
  • ß-blockers
  • RAI – I131
  • thyroidectomy
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25
Q
  • stress-induced catecholamine surge seen as a serious complication of thyrotoxicosis due to dz and other hyperthyroid disorders
  • presents with agitation, delirium, fever, diarrhea, coma, and tachyarrhythmia (a-fib, cause of death)
  • fever out of proportion to other findings
  • may see increased ALP due to increased bone turnover
  • tx with 3 P’s: ß-blocker (Propranolol), Propylthiouracil, corticosteroids (Prednisolone)
A

thyroid storm

thyrotoxic crisis

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26
Q
  • TSH – mutations
  • palpable nodule
  • thyrotoxicosis is usually mid; absence of Graves dz features
  • increased uptake in hyperfunctioning nodule and decreased uptake in remainder of tissue
  • Rx: RAI ablation
A

hyperfunctioning solitary nodule – toxic adenoma

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27
Q

Clinical features:

  • hypogonadism
  • amenorrhea, oligomenorrhea
  • infertility
  • decreased libido
  • impotence
  • hirsutism, acne
  • headache
A

prolactinoma

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28
Q

mass-effect symptoms assoc with pituitary tumors (e.g., prolactinoma):

A
  • visual loss – bitemporal hemianopsia
  • hypopituitarism
  • headache
  • CSF rhinorrhea
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29
Q
  • pregnancy, postpartum, nursing, nipple stimulation, surgery, resection of pituitary stalk, seizure
  • primary hypothyroidism – TRH stimulates prolactin secretion
  • renal failure
  • cirrhosis

All cause:

A

hyperprolactinemia

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30
Q
  • phenothiazines
  • tricyclics
  • methyldopa
  • verapamil
  • cimetidine IV
  • estrogens
  • licorice
  • MAO inhibitors

all cause:

A

hyperprolactinemia

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31
Q

neurogenic:

  • chest wall lesions
  • herpes zoster; trauma
  • spinal cord lesions
  • breast stimulation

sella masses:

  • prolactinomas
  • cysts
  • infiltrative lesions

all cause:

A

hyperprolactinemia

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32
Q

what imaging modality is more sensitive in the diagnosis of a pituitary tumor?

A

MRI

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33
Q

prolactinoma typically has prolactin levels > ?

A

prolactinoma: prolactin > 200ng/ml

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34
Q

therapy for macroadenoma prolactinoma:

A

medical therapy first in order to shrink mass (> 2cm)

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35
Q

therapy for microadenoma prolactinoma:

A
  • cabergoline (or bromocriptine) to shrink mass – restores gonadal function and fertility
  • transsphenoidal surgery (TSS)
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36
Q

TQ

Rx for prolactinomas:

A

cabergoline (D2 agonist) – more effective, longer acting, fewer side effects

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37
Q

TQ

cardiovascular-related causes of death in acromegaly: (4)

A
  • HTN
  • ischemic heart disease
  • ventricular hypertrophy
  • cardiomyopathy
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38
Q
  • excess GH in adults
  • typically caused by pituitary adenoma
  • assoc with increased morbidity and mortality due to cardiovascular, malignant, and respiratory events
A

acromegaly

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39
Q 
clinical features:
proliferation of bone, cartilage, and soft tissues
-coarse facial features
-large hands and feet
-macroglossia
-prognathism
-excessive sweating, oily skin
-insulin resistance, DM
-increased risk of colorectal polyps and cancer
A

acromegaly

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40
Q
  • elevated serum IGF-1 and GH on 2 occasions (IGF-1 levels reflect GH activity)
  • GH level failing to drop below 1 ng/ml after an hour following oral glucose load ***
A

acromegaly

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41
Q

treatment of choice for pituitary tumor causing acromegaly?

A

transsphenoidal surgery

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42
Q

Rx for acromegaly:

A

somatostatin analogs:

  • octreotide
  • lanreotide

GH receptor antagonist:
-pegvisomant

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43
Q

side effects of octreotide:

A

nausea, diarrhea, steatorrhea, gallstones*

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44
Q

TQ

  • high cortisol levels due to ACTH-secreting pituitary adenoma
  • age 20-40, mostly young women
  • increased 24 hour urine cortisol
  • tx: TSS
A

Cushing disease

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45
Q

TQ
increased cortisol caused by pituitary adenomas, adrenal adenomas, adrenal CA, ectopic ACTH production, or exogenous steroids (see decreased ACTH due to negative feedback and bilateral adrenal atrophy due to lack of use)

A

Cushing syndrome

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46
Q
  • rarest of all pituitary tumor subtypes
  • elevated T4, normal or elevated TSH ***
  • symptoms of hyperthyroidism, goiter
  • tx: TSS if lesion is found
  • Rx: octreotide (somatostatin analog)
A

TSH-secreting tumor

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47
Q
  • present with sx of mass effect, visual field abnormality, or headache
  • may produce LH or FSH
  • sellar mass
  • > 1cm refer to neurosurgery
A

non-functioning pituitary tumor

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48
Q
  • asymptomatic sellar masses

- screening for hormone excess: IGF-1, prolactin/testosterone, urine free cortisol, free T4

A

sellar incidentaloma

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49
Q

TQ

  • hemorrhage or infarct of pituitary gland, often in the presence of an existing pituitary adenoma
  • headache, visual field defects, altered mental status, ophthalmoplegia
  • tx: control and neurological decompression
A

pituitary apoplexy

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50
Q
  • very rare
  • macroadenoma – mass effect
  • secretes ACTH and PRL
A

pituitary CA

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51
Q

28 y/o Caucasian male presents to ER with complaints of R. Flank pain that radiates to groin. Associated with nausea and mild hematuria.
• PMHX: Gerd/ PUD.
• Sx: None
• Meds: Protonix 40mg bid, tums prn.
• ROS: is pertinent for moderate constipation requiring laxatives 2‐3 times per week. In addition pt complains of polydipsia and polyuria.

Dx?

A

Kidney stone, hypercalcemia

Primary hyperparathyroidism at 28 yo and male (normally 50-56 yo female)?

!!Must be MEN1!!

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52
Q

TQ

What are the 3 P’s in MEN1?

A
  • Parathyroid
  • Entero- pancreatic endocrine
  • Pituitary tumors
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53
Q

TQ

What is the diagnosing criteria for MEN1?

A

-2 of the 3 main MEN1 tumors
OR
-One tumor in a pt with family members diagnosed with MEN1

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54
Q

TQ

What kind of gene is the MEN1 gene? What does it produce?

A

-Tumor suppressor gene

MENIN protein, a regulatory protein in endocrine glands.

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55
Q

TQ

What is the most common manifestation of MEN1, displaying almost 100 percent penetrance by age 40 to 50 years?

A

Multiple parathyroid adenomas causing hyperparathyroidism

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56
Q

TQ

What is the initial manifestation of MEN1?

A

Hyperparathyroidism

Up to 18% of patients with primary hyperparathyroidism will have MEN1!!!!!!

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57
Q

Dx?

  • Age: 20‐40
  • Sex: 1:1 F/M, AD
  • Multiple parathyroid adenomas (almost universal).
  • Reoccurance: > 50% by 12 years in one study.
  • Treatment: Subtotal parathyroidectomy (3.5 glands plus thymectomy as well) vs total parathyroidectomy with 0.5 gland transplanted to forearm
A

MEN1

TQ MULTIPLE adenomas vs just one (sporadic hyperparathyroidism)

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58
Q
  • Age: 50‐60
  • Sex: 2‐3:1 F/M
  • Single parathyroid adenoma 85%
  • Reoccurance: not likely.
  • Treatment: excision of the abnormal gland.
A

sporadic hyperparathyroidism

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59
Q

TQ
T/F:
Multiple pituitary tumors are very rare in MEN1

A

TRUE

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60
Q

TQ

  • Pituitary macroadenoma: 85%
  • Treatment normalized hypersecretion of hormones: 42% :(
  • Tumors tend to be much larger and much more aggressive!!!
A

MEN1

Mostly prolactinomas

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61
Q

TQ

  • Pituitary macroadenoma: 42%
  • Treatment normalized hypersecretion of hormones: 90% :) ..basically cures
A

Sporadic pituitary tumor

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62
Q

What is the MOST fatal Manifestation of MEN1?

A

Entero‐pancreatic tumors

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63
Q

TQ
Functioning pancreatic islet cell or gastrointestinal endocrine cell tumors are clinically apparent in approximately _______ of patients with MEN1

A

one-third

60% of patients with MEN1 have either the Zollinger- Ellison syndrome or asymptomatic elevation in serum gastrin concentrations.

20-60% of Z-E pt’s have MEN1.

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64
Q 
Penetrance of entero‐pancreatic and foregut tumors in MEN1:
#1: \_\_\_\_\_\_\_\_\_\_\_\_\_30-40%
#2: Non-functioning tumor 30-40%
#3: Insulinoma 10%
A

Gastrinoma (ZE)

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65
Q

TQ

What is the primary life-threatening manifestation of MEN1?

A

The malignant potential of pancreatic endocrine tumors (PETs)

Like hormonally active enteropancreatic tumors in MEN1, clinically “nonfunctioning” PETs may be malignant and capable of causing liver metastases.

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66
Q
  • Gastrinoma is Multifocal and small.
  • Occurs in duodenum and/or pancreas
  • Low risk of death
  • Surgical tx: Pancreato‐ duodenectomy (symptomatic tx).
A

MEN1

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67
Q

-Gastrinoma tends to be single
-Occurs in duodenum and/or
pancreas
-Risk of death
-Surgical tx: Tumor resection

A

Sporadic gastrinoma

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68
Q

ZES was the initial presenting symptom of MEN1 in 40% of Pt’s

Why is it important to screen for calcium levels in MEN1 pts?

A

Hypercalcemia from hyperparathyroidism may severely exacerbate acid secretion, and thus ulcer formation in ZES pt’s. Thus it needs to be screened for and treated.

PTH–>Incr Ca–>Incr H+ :(

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69
Q

What are some other associated tumors of MEN1?

A 
Angiofriboma
Collagenoma
Meningioma
Thymic Carcinoid
Lipomas
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70
Q

MEN1 Diagnosis?

A
  • The occurrence of TWO or more primary MEN1 tumor types (parathyroid gland, anterior pituitary, and pancreatic islet cells).
  • In family members of a patient with a clinical diagnosis of MEN1, the occurrence of ONE of the MEN1 associated tumors is consistent with familial MEN1
    note: recommend offering MEN1 mutational analysis to any index patient with clinical MEN1, and to individuals with suspicious or atypical MEN1.
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71
Q

Hypercalcemia, nephrolithiasis, amenorrhea, galactorrhea, erectile dysfunction, peptic ulcer disease, diarrhea, and neuroglycopenic or sympathoadrenal symptoms from hypoglycemia.

A

Annually screen for MEN1

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72
Q

2 factors which promote 1,25(OH)2–D production:

A
  • High PTH

- Low P

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73
Q

4 factors which decrease 1,25(OH)2–D production:

A
  • High Ca
  • High P
  • FGF-23
  • Decreased kidney tissue (chronic kidney dz)
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74
Q

PTH secretion is stimulated by: (2)

A
  • Low serum Ca

- High P

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75
Q

High Ca, high 1,25(OH)2–D, and very low Mg (stimulate/suppress) PTH secretion.

A
  • High Ca
  • High 1,25(OH)2–D
  • Very low Mg

All suppress PTH secretion.

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76
Q

T/F: Small changes in Ca result in significant changes in PTH.

A

TRUE

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77
Q

Excess PTH may cause: (3)

A
  • Bone dz
  • Urolithiasis
  • Kidney damage
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78
Q

Parathyroids (and kidneys) read serum Ca (and Mg) through the:

A

Ca-sensing receptors (CaSR)

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79
Q

TQ

When the CaSR is inactive – low serum Ca (or Mg) – what happens to the vesicles of PTH?

A

When the CaSR is inactive (low serum Ca/Mg), vesicles move into the cell membrane and release their stores of PTH.

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80
Q

TQ

When the CaSR is activated by high serum Ca (or Mg), what happens to the release of PTH?

A

When the CaSR is activated by high serum Ca (or Mg), the release of PTH is inhibited.

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81
Q

Where are CaSR located in the kidney?

A

Thick ascending limb of the loop of Henle

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82
Q

High serum Ca will activate the CaSR in the kidney causing:

A

Increased Ca excretion (increased Ca in urine)

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83
Q

Tetany is possible when:

  • Total serum Ca is less than:
  • Ionized Ca is less than:
  • Mg is less than:
A

Tetany when:

  • Total serum Ca < 7.0 (almost always when serum Ca < 5.0)
  • Ionized Ca < 3.0 (almost always when ionized Ca < 2.5)
  • Mg < 1.0 (nl 1.5 - 2.6)
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84
Q
  • Chvostek sign
  • Trousseau sign
  • Erb sign
  • Prolonged QT interval

All signal:

A

Hypocalcemia, latent tetany

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85
Q

In a hypocalcemic state, it is important to check levels of:

A

PTH

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86
Q

Neonatal hypocalcemia–

Early hypocalcemia would show:

A

Early hypocalcemia would show calcitonin/PTH imbalance.

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87
Q

Neonatal hypocalcemia–

Delayed post-feeding hypocalcemia would show:

A

Delayed post-feeding hypocalcemia would show transient hypoparathyroidism.

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88
Q

Congenital hypoparathyroidism: (3)

A
  • Aplasia or hypoplasia of the parathyroids
  • DiGeorge syndrome (parathyroid and thymic aplasia, CHD)
  • CaSR abnormalities (gain of function)
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89
Q

Acquired hypoparathyroidism: (3)

A
  • Idiopathic hypoparathyroidism
  • Genetic autoimmune hypoparathyroidism
  • Surgical hypoparathyroidism
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90
Q

Hypocalcemic states–

Inadequate responsiveness of target tissue to PTH: (4)

A
  • vitamin D deficiency or a block in vitamin D metabolic cycle resulting in deficiency of the active vitamin D metabolite
  • Pseudohypoparathyroidism types I and II
  • Magnesium deficiency
  • Acute and chronic renal failure
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91
Q

Tx of hypocalcemia: (4)

A
  • IV calcium (avoid extravasation)
  • Oral calcium
  • Vitamin D metabolites
  • Check serum Mg
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92
Q

Tx of hypercalcemia: (5)

A
  • Fluids (hypercalcemia is always assoc with dehydration)
  • Furosemide (blocking Ca reabsorption)
  • Steroids?
  • Calcitonin (physiologically appropriate)
  • Bisphosphonates
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93
Q

Tx of hypercalcemia due to malignancy: (3)

A

Fluids
Furosemide
Bisphosphonates

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94
Q

MC cause of kidney stones in children after insufficient fluid intake:

A

Hypercalciuria

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95
Q

Child presents with hematuria, dysuria, frequency, wetting accidents, abdominal and back pain.
Think…

A

Hypercalciuria

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96
Q

(Low/high) Na/K ratio is protective of and decreases the frequency of kidney stones.

A

LOW Na/K ratio (less than 2.5) is protective of and decreases the frequency of kidney stones.

97
Q

Preferred pharmacologic tx of hypercalciuria in children:

A

K-citrate

98
Q

Pharmacologic tx of hypercalciuria in general population:

A

Thiazides (increase Ca reabsorption), may consider adding amiloride (K-sparing diuretic)

99
Q

“In essence, whereas cartilage growth continues it does not become mineralized bone.”

This describes:

A

Rickets

100
Q

TQ

Rickets is the result of:

A

Hypophosphatemia

101
Q

TQ

MC the hypophosphatemia is 2º to elevated PTH due to:

A

Vitamin D deficiency, causing hypocalcemia

102
Q

The bone-specific alkaline phosphatase is located at the plasma membrane of:
What is the job of these cells? What do they cleave?
Therefore, the activity of which enzyme is elevated in phosphate deficiency?

A

Osteoblasts – their job is to supplement phosphate to the cells by cleaving the precursor beta-glycerol phosphate.

Phosphate deficiency causes increased activity of beta-glycerol phosphate.

103
Q
  • Lack of exposure to sunlight AND dietary intake of vit D
  • Results in bowed legs, a large soft cranium, and other skeletal abnormalities
  • Hallmark = low serum 25(OH)D
  • Other findings: low P, high ALP, high PTH, normal Ca
  • Tx: vitamin D and in some cases Ca supplementation

Dx?

A

Vitamin D-deficiency rickets

104
Q
  • Decreased secretion of bile salts, causing decreased absorption of fat-soluble vitamins
  • Decreased production of 25(OH)D
  • Increased degradation of 25(OH)D

What do these values point to?
Tx?

A

Liver dz and anti-seizure meds

Tx: 25(OH)D

105
Q
  • Results from a genetic absence/defect in renal 1a-hydroxylase, which converts 25(OH)D to 1,25(OH)2–D
  • Pts present with rickets, tetany
  • Normal 25(OH)D, low 1,25(OH)2–D
  • Tx: calcitriol
A

Vitamin D-dependent rickets

106
Q
  • Results from a defect in vitD receptor in tissues (end-organ resistance)
  • Infants/children present with tetany
  • Low serum Ca and P, high PTH and 1,25(OH)2–D
  • Tx: high doses of calcium (IV and oral) (and blockage of PTH release by calcimimetics)
A

Vitamin D-resistant rickets

107
Q
  • Boys more severely affected
  • Bowed legs, short stature, waddling gait, bone pain, dental abscesses
  • Xrays = rickets
  • Low serum P
  • High ALP
  • Normal Ca, PTH, 25(OH)D, 1,25(OH)2–D
  • Urine – loss of P, normal Ca
A

X-linked dominant hypophosphatemic rickets (XLH)

108
Q

“Hormone” secreted from bone cells in response to dietary phosphate load:

A

FGF-23

109
Q

FGF-23 levels are (high/low) in XLH.

A

FGF-23 levels are HIGH in XLH.

110
Q

Actions of FGF-23 in the PCT: (2)

A
  • Block phosphate reabsorption
  • Block 1a-hydroxylase activity

This leads to hypophosphatemia and decreased 1,25(OH)2–D levels.

111
Q

Tx of XLH:

A

Phosphate and calcitriol

112
Q
  • An isolated defect in tubular P reabsorption (actual problem in PCT of kidney), resulting in low serum P
  • Presents as rickets and urolithiasis
  • Elevated 1,25(OH)2–D (in contrast to XLH) and pt has hypercalciuria
  • Tx: phosphate
A

Familial hypophosphatemic rickets with calciuria

113
Q 
Renal bone dz–
Diminished kidney tissue results in:
-(Incr/decr) production of 1,25(OH)2–D
-(Incr/decr) clearance of phosphate
-Due to (high/low) levels of FGF-23 further contributing to decreased production of 1,25(OH)2–D
A 
Renal bone dz–
Diminished kidney tissue results in:
-DECREASED production of 1,25(OH)2–D
-DECREASED clearance of phosphate
-Due to HIGH levels of FGF-23 further contributing to decreased production of 1,25(OH)2–D
114
Q
  • Insufficient 1,25(OH)2–D
  • Decreased Ca reabsorption from the gut
  • High serum P

All contribute to:

A

2º hyperparathyroidism

115
Q

The first indication of abnormal mineral metabolism is elevated serum:
What is second to elevated?

A

1st: FGF-23
2nd: PTH (while Ca and P are still normal)

116
Q

Tx for renal bone dz: (5)

A
  • Dietary P restriction (no proteins)
  • P-binders
  • Ca supplementation
  • 1,25(OH)2–D
  • Cinacalcet (calcimimetic)
117
Q

It’s possible that FGF-23, besides being a marker of abnormal mineral metabolism, may have a direct adverse effect on the:

A

Heart

118
Q

Calcimimetics are low MW organic molecules, which cause selective activation of:

How do they work?

A

CaSR

They “bluff” the parathyroid gland to believe that serum Ca is higher than actual, leading to decreased PTH secretion.

119
Q

1º causes of osteopenia in childhood: (3)

A
  • Osteogenesis imperfecta
  • Idiopathic juvenile osteoporosis
  • Various syndromes of dysplasia and storage
120
Q

2º causes of osteopenia in childhood: (4)

A
  • Corticosteroid excess (Cushings, steroid tx)
  • Immobilization
  • Nutritional deficiency (protein-calorie malnutrition, vitC deficiency)
  • Collagen diseases
121
Q
  • Results from genetic defects in the coding for type I collagen
  • Characterized by osteoporosis and excessive bone fragility
  • Recurrent fractures resulting from minimal trauma, bone pain, deformities, kyphoscoliosis, short stature
  • Conductive hearing loss
  • Blue sclera
A

Osteogenesis imperfecta

122
Q

Management of osteogenesis imperfecta:

A

Orthopedics, bisphosphonates

123
Q
  • MC cause of 2º osteopenia in adults (7.5mg per day and higher) and children
  • High risk of collapsed vertebrae and hip fractures
A

Steroid-induced osteoporosis

124
Q 
Gold standard (but rarely done) to look at bone condition:
What is used as surrogates?
A

Gold standard: bone histology

Surrogates:

  • Bone formation: ALP, osteocalcin
  • Bone resorption: Urine N-telopeptides, serum C-telopeptides
125
Q

Tx for steroid-induced osteoporosis:

A

Bisphosphonates

make sure pt is replenished with Ca and vitD

126
Q
  • Pyrophosphate analogs
  • Bind to hydroxyapatite in bone, inhibiting osteoclast activity
  • Indicated for osteoporosis, hypercalcemia, Paget dz, osteogenesis imperfecta
  • Long-lasting effect
A

Bisphosphonates

e.g., pamidronate

127
Q
  • on chromosome 10
  • mutated in MEN2
  • when activated it promotes growth and differentiation in its associated cells and tissues.
A

RET gene

128
Q

TQ

What do we see in the classical MEN2A dz? (3)

A
  • Medullary Thyroid Carcinoma
  • Pheochromocytoma
  • Parathyroid tumors
129
Q

TQ

What tumor type is a patient most likely to get in MEN2A (highest penetrance)?

A

MTC (medullary thyroid cancer)

1st presenting

130
Q

What cells are cancerous and lead to MTC?

A

Parafollicular cells/”C cells” (migrants from the neural crest)

131
Q

TQ

What percentage of MTC is familial?

A

25% (MEN2) (30 yo +)

75% of MTC will be sporadic in nature (over 60 yo)

132
Q

TQ

When I say high levels of calcitonin, corticotropin, serotonin, melanin, and prostaglandins, you think…

A

MTC

133
Q

TQ

How do we diagnose MTC?

A

Fine Needle Aspiration (FNA)

Calcitonin is NOT used as a screening marker to make a diagnosis of MTC…decr post-tx

134
Q

TQ

Why is it important to include a genetic work up for RET mutations once you have diagnosed MTC?

A

Rule out and/or treat Pheochromocytoma and Hyperparathyroid PRIOR to taking your patient to surgery for MTC tx

135
Q

Tx of MTC?

A

Total thyroidectomy is standard of care regardless of sporadic or familial

MTC: Monitoring

  • Annual Ultrasound of the neck.
  • Annual/ Biannual Calcitonin and CEA
136
Q 
TQ
Dx?
-HTN
-HA
-Palpitations
-Diaphoresis
A

Pheochromocytoma

rare, catecholamine‐ secreting adrenal tumor that may precipitate life‐threatening hypertension.

40% penetrance in MEN2A

137
Q

TQ
Pheo tends to occur 10 years AFTER/BEFORE Medullary
thyroid cancer is found.

A

AFTER!

138
Q

TQ

What is the main difference between sporadic and MEN2A pheochromocytomas?

A

Sporadic Pheo’s are usually unilateral, whereas
MEN2 A tends to be bilateral in 30‐100%.

Pheo’s w/ MEN2A less likely to be malignant

139
Q

TQ
T/F:
Because an undiagnosed Pheo causes severe peri‐operative morbidity and mortality, a pheo MUST be diagnosed and treated FIRST!!!!!

A

TRUE

140
Q

How does the monitoring differ in MEN2A from MEN1?

A

Specific mutations in the RET gene can be found….
Ex:
Pheos and hyperparathyroidism: measure metanephrine, Ca, PTH from the age of 5 annually if have specific codons

141
Q

What dz is associated with MEN2A that results in absensce of autonomic ganglion cells within the distal colonic parasympathetic plexus resulting in chronic obstruction and megacolon

A

Hirschsprung Disease

142
Q
  • Medullary Thyroid Cancer
  • Pheochromocytoma
  • Marfan type body habitus
  • Ganglioneuromas.
  • Hirschsprungs
  • ***NOTassociatedwith hyperparathyroidism
A

MEN2B

143
Q

TQ

Medullary Thyroid Cancer more/less aggressive in Men2B versus MEN2A.

A
  • Medullary Thyroid Cancer IS MUCH more aggressive in Men2B
  • occurs earlier: childhood to early 20’s
  • 50% mortality as opposed to the 9.7% in Men2A.
144
Q

Familial Medullary Thyroid Cancer the “forme fruste” of Men2?

A

Only demonstrates medullary thyroid Cancer but no disposition toward hyperparathyroidism or pheochromocytomas

145
Q

When do we genetically screen for MEN2?

A
  • Clinically proven
  • MTC or pheochromocytoma and a family member with MTC or pheochromocytoma

Apparently sporadic MEN2-related tumors AND:

  • young age (<35 years)
  • multicentric tumors in one organ
  • and/or two different organs affected
  • it can be considered in all patients with sporadic MTC

First and second degree family members of MEN2 patients.

146
Q

Common predisposing factors to diabetes: (5)

A 
Poor glucose control
Insulin resistance (type 2)
Low activity level or immobility
Immune suppression
End-organ damage
147
Q

Organ systems affected by complications of diabetes: (6)

A 
Cardiovascular
Peripheral vascular
Retinopathy
Nephropathy
Neuropathy – peripheral, autonomic
Gastropathy
148
Q

Potential measures to avoid/retard damage: (6)

A

Increase activity
ADA diet to include heart-healthy, low salt
Oral meds
Subcutaneous meds
Counseling
Protective measures (e.g., diabetic shoes)

149
Q

Microalbuminuria = 30 - ? mg

Over 300 mg of albumin in urine referred to as:

A 
Microalbuminuria = 30 - 300 mg
Macroalbuminuria = 300+ mg
150
Q

Satisfactory control of blood sugars is an HbA1c of:

A

7% (140) or less

151
Q

In terms of immune compromise, a glucose level greater than 150 interferes with the function of:

A

neutrophils

152
Q

What does diabetes monitoring entail?

A 
Quarterly:
-HbA1c
-Review self glucose monitoring log
-Foot inspection for ulcers
Annual dilated eye exam
Urine protein screening
Monofilament testing
153
Q

Features shared by both DKA and NKHS: (4)

A

Dehydration (volume depletion)
Insulin deficiency
Glucagon excess
Mental status changes

154
Q

Possible etiologies of DKA: (5)

A 
Inadequate insulin administration
Infection
Infarction (any location)
Surgery
Drugs (cocaine)
155
Q

Initial sx:

  • Anorexia
  • Nausea
  • Vomiting
  • Polyuria
  • Thirst (polydipsia)
A

DKA

156
Q

Progressive sx of DKA: (3)

A

Abdominal pain
Altered mental function
Coma

157
Q

Signs of DKA: (8)

A 
Kussmaul respirations
Fruity odor to breath (acetone)
Dry mucous membranes
Poor skin turgor ("tenting")
Tachycardia
Hypotension
Fever
Abdominal tenderness
158
Q

Labs of DKA:

A 
Hyperglycemia
Ketosis
Metabolic acidosis
Hyperkalemia
Hypertriglyceridemia
Hyperlipoproteinemia
Hyperamylasemia
Leukocytosis
159
Q

High anion gap acidosis: MUDPILES

A 
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isopropyl alcohol, Iron, Isoniazid (INH)
Lactic acidosis
Ethylene glycol
Salicylates
160
Q

What happens to potassium in acidosis?

A

K+ leaves cells, causing hyperkalemia

161
Q

Hyperamylasemia induced by DKA can suggest:

A

Acute pancreatitis

order lipase levels

162
Q

Fluid deficit in DKA:

Fluid replacement rule:

A

3 - 5 L (less than in NKHS)

1-2-3 Rule

163
Q

Initial insulin administration in DKA:

A

10-20 units IV* or IM

164
Q

T/F: Clinical status at least hourly in DKA.

A

TRUE

165
Q

Consider potassium replacement in DKA when serum K+ is less than:

A

5.5 mEq/L

166
Q

Glucose goal in DKA treatment:

A

150-250 mEq/dL

167
Q

Etiologies of NKHS: (3)

A

Insulin deficiency
Inadequate fluid intake
Osmotic diuresis induced by hyperglycemia

168
Q
  • Polyuria
  • Thirst
  • Altered mental state
A

NKHS

169
Q

Fluid deficit in NKHS:

A

8 - 10 L (more than DKA)

170
Q

T/F: More insulin is required in NKHS than in DKA.

A

TRUE

Type 2 diabetics are insulin-resistant, therefore you need to give them more.

171
Q

What drugs can contribute to NKHS? (3)

A

Glucocorticoids
Phenytoin
Thiazide diuretics

172
Q

T/F: N/V, abd pain, ketoacidosis, and Kussmaul respirations are typically ABSENT in NKHS.

A

TRUE

173
Q

Action on kidney when serum osmolality > 295 and/or Na > 143:

  • Increases permeability of collecting duct
  • Increases water reabsorption from urine
  • Decreases serum osmolality back to normal
A

ADH

“vasopressin”

174
Q

The primary clinical manifestation of posterior pituitary deficiency is:

A

diabetes insipidus

175
Q
  • polyuria
  • increased thirst - “preference for ice cold water”
  • nocturia
  • enuresis in children
A

diabetes insipidus

176
Q
  • absence of nocturia
  • intermittent sx
  • 24 urine collection > 18 L suggests:
A

psychogenic polydipsia

177
Q

Etiologies:

  • pituitary tumor - MC craniopharyngioma
  • autoimmune
  • trauma
  • surgery
  • ischemic encephalopathy
  • idiopathic
A

central diabetes insipidus

178
Q

Etiologies:

  • hereditary (ADH receptor mutation)
  • 2º to hypercalcemia
  • lithium (ADH antagonist)
  • demeclocycline (ADH antagonist)
  • cisplatin
  • rifampin
A

nephrogenic diabetes insipidus

179
Q
  • inappropriate excessive fluid intake with functional suppression of ADH secretion
  • may be idiopathic
A

dipsogenic diabetes insipidus

180
Q

Head trauma, multiple sclerosis, TB meningitis, neoplasms, and sarcoidosis may all cause:

A

primary polydipsia

dipsogenic DI

181
Q

in gestational diabetes insipidus, a deficiency of AVP (ADH) can result from increased metabolism by:

A

N-terminal aminopeptidase produced by the placenta

182
Q

if 24 hour urine osmolality is greater than 300, then pt has a solute diuresis.
must then check for:

A

diabetes mellitus

183
Q

if serum osmolality is 280-295, what test should you perform?

A

water deprivation test

184
Q

the absence of response to water deprivation (urine osmol < 300) is diagnostic of:

A

diabetes insipidus

185
Q

abrupt onset of sx suggests:

A

diabetes insipidus

186
Q

absence of nocturia suggests:

A

primary polydipsia

187
Q

cortisol deficiency may mask:

A

DI

188
Q

desmopressin is used in the tx of:

A

central DI

189
Q

greater than 50% increase in urine osmolality after administration of ADH analog (desmopressin)

A

central DI

190
Q
  • urine output 2-5 L/day

- free access to water

A

mild central DI

191
Q

tx for partial central DI: (4)

A
  • AVP agonist (desmopressin acetate)
  • chlorpropamide
  • carbamazepine
  • clofibrate
192
Q

tx of nephrogenic DI: (4)

A
  • HCTZ (thiazide diuretics)
  • indomethacin
  • amiloride
  • hydration
193
Q

causes of SIADH: (4)

A
  • ectopic ADH (e.g., small cell lung cancer, other malignancies***)
  • CNS disorder/head trauma
  • pulmonary dz (COPD, infections)
  • drugs (e.g., cyclophosphamide)
194
Q

Characterized by:

  • hypervolemia
  • hyponatremia
  • hypo-osmolality of serum
  • inappropriately concentrated urine
  • natriuresis
  • absence of edema
  • increased GFR (low serum Cr and uric acid)

Sx may include lethargy, fatigue, anorexia, N/V, irritability, confusion, seizures.

A

SIADH

195
Q
  • urine spot test Na+ is less than 20 (SIADH: Na+ over 20)
  • increased serum Cr, BUN, HCT
  • increased uric acid
  • increased renin and aldosterone
A

hypovolemia

196
Q

tx of SIADH: (3)

if acute neurologic sequelae are present, give:

A

demeclocycline*
conivaptan
tolvaptan

if acute neurologic sequelae are present, give IV hypertonic saline.

197
Q

too rapid correction of hyponatremia can lead to:

A

central pontine myelinolysis (often fatal)

198
Q

glandular enlargement of the male breast often with simultaneous increase of surrounding connective tissue

A

gynecomastia

199
Q

how would you differentiate true gynecomastia from pseudogynecomastia (aka lipomastia)?

A

palpate the anterior axillary fold (adipose tissue) to compare to breast tissue

200
Q

MC ages of males who present with gynecomastia: (3)

A 
neonatal male (maternal/placental estrogens)
adolescent male (median age 14)
senescent (aging) male (40% or more of otherwise healthy men)
201
Q
  • glandular tissue palpated in radially arranged cords usually around the nipple
  • may be discrete button-like or merge gradually with surrounding adipose tissue
  • small areolar glands (glands of Montgomery) oftne prominent
  • more likely to have breast tenderness (mastodynia) if recent onset of enlargement
  • hyperplasia in the epithelial and stromal cells
  • increased duration leads to fibrous tissue, which is more difficult to treat by non-surgical means
A

true gynecomastia

202
Q

2 basic mechanisms of feminization (aka true gynecomastia):

A
  • increased estrogen/androgen ratio

- altered sensitivity of target tissue (decreased androgen sensitivity, increased estrogen sensitivity)

203
Q

increased estrogen/decreased androgen is due in part to stimulation of aromatase activity.

where does this occur?
what does aromatase do?

A

occurs in fibroblasts in the breast tissue

converts androgens to estrogens

204
Q

gonadotropins stimulate estradiol secretion from which cells? where?

A

leydig cells in the testis

  • LH
  • hCG

these are elevated with primary testicular failure (feedback)

205
Q
  • rapid onset
  • very high serum estrogen
  • low serum LH and FSH
  • mass in abd or testicle

these are signs of:

A

malignancy

206
Q
  • usually malignant
  • often large, palpable
  • seen on CT or MRI
  • high serum cortisol
A

feminizing adrenal tumors

207
Q

check ß-hCG and a-fetoprotein in tumors of the:

A

testicles

208
Q
  • fixed
  • indurated
  • irregular
  • firm areas

what do you suspect?

A

primary breast cancer (in the male)

209
Q

systemic causes of gynecomastia: (9)

A 
liver dz
hyperthyroidism
adrenal dz
renal dialysis
pulmonary and cardiac dz
AIDS
EtOH
infections
DRUGS***
210
Q

MC cause of gynecomastia:

A

DRUGS (estrogens)

  • spironolactone
  • digitalis
  • cimetidine
  • alcohol
  • ketoconazole

“Some Drugs Cause Awesome Knockers”

also:

  • omeprazole (PPI)
  • verapamil (Ca channel blockers)
  • ACE inhibitors
  • tricyclic antidepressants
211
Q

spider telangiectasia suggest:

A

chronic EtOH and/or liver dz

212
Q
  • 46XXY
  • eunuchoidal appearance (arm span over 2cm > pts height)
  • small testes
  • increased incidence of breast cancer*
A

klinefelter’s syndrome

213
Q
  • persistent discharge of milk or milk-like substance from the breast in the absence of parturition (giving birth) or breast feeding
  • more commonly benign
A

galactorrhea

214
Q

milky
multicolored
purulent

more likely (benign/malignant)

A

benign

215
Q

yellow or serous
pink or serosanguinous
bloody or sanguinous
clear or watery

more likely (benign/malignant)

A

malignant

216
Q

enhanced prolactin release from: (3)

A

hypothyroidism
sucking reflex
breast trauma (e.g., seatbelt)

217
Q
  • headaches
  • visual disturbances
  • visual field problems
  • abnormalities of temp, thirst, appetite

what do you suspect?

A

pituitary or hypothalamic dz

218
Q

tx of galactorrhea if benign and not infectious:

A

no tx necessary

219
Q

tx of hyperprolactinemia:

A

bromocriptine or cabergoline (dopamine agonists)

220
Q
  • excessive hair growth
  • androgen INdependent areas
  • can be generalized or localized (e.g., pinna of the ear)
  • familial
  • metabolic disorders (thyroid, anorexia nervosa)
  • meds (phenytoin, minoxidil, cyclosporine)
A

hypertrichosis

221
Q

virilization is an ominous sign for:

A

ovarian or adrenal CA

222
Q

hirsutism + defeminizing signs, increased libido, masculinization (voice deepening, clitorimegaly, temporal balding)

A

virilization

223
Q

exogenous (drugs) causes of hirsutism: (7)

A 
phenytoin
minoxidil
diazoxide
danazol
oral contraceptives
anabolic steroids
corticosteroids
224
Q

endocrine causes of hirsutism:

A 
Cushings
hyperprolactinemia (suspect with galactorrhea)
acromegaly
menopause
polycystic ovarian syndrome (PCOS)***
225
Q

MC cause of hirsutism:

A

PCOS

226
Q

MC adrenal cause of hirsutism:

A

congenital adrenal hyperplasia (CAH)

227
Q
  • hirsutism
  • obese
  • menstrual irregularities
  • may not be able to conceive (or might!)
  • large ovaries on pelvic exam
  • multiple cysts on U/S
  • acne
  • hyperinsulinemia and IGF-1 (increased free testosterone)
A

polycystic ovarian syndrome (PCOS)

228
Q

acanthosis nigricans

suspect possible:

A

malignancy

229
Q

androgens + estrogens, hCG, serotonin (carcinoid tumors), or thyroxine (ectopic thyroid tissue)

think:

A

ovarian tumor

230
Q

if mild to moderate hirsutism AND clinical findings consistent with PCOS, normal levels of testosterone, free testosterone, and DHEAS, and LH/FSH > 2:1…

hirsutism is probably due to:

A

PCOS

if LH/FSH < 2:1, think idiopathic hirsutism.

231
Q

possible pharm tx of hirsutism: (5)

A
  • oral contraceptives (progestin/estrogen combo)
  • glucocorticoids (dexamethasone – especially in CAH)**
  • spironolactone (for idiopathic hirsutism)
  • flutamide (hepatotoxicity)
  • cimetidine (least effective)
  • finasteride (5a-reductase inhibitor)

most responses can take 6 months to one year, therefore physical methods (e.g., bleaching, depilatory, epilatory) may be used.

232
Q

TQ
Addisons disease, a primary adrenal insufficiency due to autoimmune adrenalitis, is due to:
A. Humoral immune mechanisms at the adrenal cortex
B. Cell-mediated immune mechanisms at the adrenal cortex
C. Both humoral and cell-mediated immune mechanisms at the adrenal cortex

A

C. Both humoral and cell-mediated

Autoantibodies react most often w/ 21-hydroxylase

233
Q

TQ

What are the two key electrolyte disturbances in Addison’s dz?

A

Hyponatremia

Hyperkalemia

234
Q

Pt presents with dehydration, hypotension, N/V, approaching shock. Also may have assoc hypothyroidism. Hyper-pigmentation on palms

Dx?

A

Addison’s dz

235
Q

MC cause of cushing’s syndrome?

A

Excess glucocorticoids (steroids)

Other: small smell lunch cancer making ACTH

236
Q

Proximal muscle wasting and weakness, bone loss, glucose intolerance, thromboembolic events (incr factor 8), immunity and infection, hirsutism in females

A

Cushings syndrome

237
Q

Adrenocortical tumors are rare, unilateral, and mostly benign. If cancerous, usually aggressive and may cause what?

A

Cushings syndrome or virilization

238
Q

Primary Aldosteronism most frequently causes what?

A

Bilateral idiopathic hyperplasia

239
Q

TQ
T/F
Most patients with pheochromocytomas do NOT have the classic triad symptoms of episodic headache, sweating, and tachycardia

A

TRUE

Endocrine Final (3 decks)

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