ENDO Flashcards

1
Q

The 2 hormones stored in the posterior lobe are

A

ADH (antidiuretic hormone or vasopressin) and oxytocin

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2
Q

Microadenomas are defined as tumors ____ in diameter

A

<1 cm

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3
Q

Pituitary Adenomas by Function

Prolactin_____
Growth hormone (GH) _____
ACTH_____
Gonadotroph ____

A

50–60%

15–20%

10–15%

10–15%

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4
Q

Excess prolactin secretion is a common clinical problem in women and causes the syndrome of

A

galactorrhea-amenorrhea

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5
Q

Why is there amenorrhea in Prolactinemia

A

The amenorrhea appears to be caused by inhibition
of hypothalamic release of gonadotropin-releasing hormone (GnRH) with a decrease in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Prolactin inhibits the LH surge that causes ovulation.

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6
Q

Prolactinemia

The most common presenting symptom in men is

A

erectile dysfunction and decreased libido.

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7
Q

Hyperprolactinemia can be seen in natural physiologic states such as

A

pregnancy, early nursing, hypoglycemia, seizure, exercise, stress, sleep, cirrhosis, nipple stimulation, and
chronic renal failure (due to PRL clearance).

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8
Q

Prolactinemia

They are usually _____ when they occur in women and ______ in men, usually presenting with visual field deficits, etc.

A

microadenomas

macroadenomas

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9
Q

Macroadenomas can obstruct the pituitary stalk, increasing prolactin release by

A

blocking dopamine transport from hypothalamus (stalk effect)

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10
Q

Hyperprolactinemia can also occur with decreased inhibitory action of dopamine.

This occurs with the use of drugs that

A

block dopamine synthesis (phenothiazines, metoclopramide) and dopamine-depleting agents (α-methyldopa, reserpine).

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11
Q

Always check _____in patients with elevated prolactin

A

TSH

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12
Q

Always exclude states such as_______

before starting the work-up of hyperprolactinemia

A

pregnancy, lactation, hypothyroidism and medications

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13
Q

Prolactinomas may co-secrete

A

growth hormone (GH)

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14
Q

Prolactin levels >100 ng/mL suggest probable

A

pituitary adenoma

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15
Q

For prolactinomas, initially treat with _____ both of which reduce prolactin levels in almost all hyperprolactinemic patients.

A

cabergoline or bromocriptine (a dopamine

agonist),

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16
Q

Surgery is reserved only for adenomas

A

not responsive to cabergoline or bromocriptine, or if the tumor is associated with significant compressive
neurologic effects.

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17
Q

T or F

Surgery is more effective for microadenomas than macroadenomas

A

T

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18
Q

About _____of patients treated with cabergoline have a drop in prolactin to <10% of pretreatment levels

A

90%

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19
Q

______ is used if drug therapy and surgery are ineffective in reducing tumor size and prolactin levels

A

Radiation therapy

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20
Q

______ is a syndrome of excessive secretion of growth hormone. In children this is called____

A

Acromegaly

gigantism

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21
Q

______ is an insidious, chronic debilitating disease associated with bony and soft tissue overgrowth, and increased mortality

A

Acromegaly

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22
Q

Acromegaly is caused by

A

pituitary adenomas, usually a macroadenoma in 75% of

the cases that produce growth hormone

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23
Q

Other SSX associated with acromegaly

A

Obstructive sleep apnea can also develop.

Interstitial edema, osteoarthritis, and entrapment neuropathy (carpal tunnel syndrome)
are seen

About 10-20% of patients develop cardiac anomalies such as hypertension, arrhythmias, hypertrophic cardiomyopathy, and accelerated atherosclerosis.

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24
Q

Metabolic changes asstd with acromegaly

A

impaired glucose tolerance (80%) and diabetes (13–20%).

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25
Q

Dx of Acromegaly

The best initial test is

A

IGF-1 level. A significantly elevated IGF level compared to

the average IGF-1 for age-matched equivalents is a positive screen for acromegaly

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26
Q

The most common cause of death in acromegaly is

_______

A

cardiovascular mortality.

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27
Q

Confirmatory test for acromegaly

Confirmatory testing involves the

A

measurement of GH after 100 g of glucose is given orally;

this test is positive if GH remains high (>5 ng/mL) and suggests acromegaly

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28
Q

Measurement of ______ and _______correlates with disease activity

A

insulin-like growth factor (IGF) or somatomedin

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29
Q

Goal of Tx for acromegaly

A

The objectives are to decrease GH levels to normal, stabilize or decrease tumor size, and preserve normal pituitary function

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30
Q

Mx of acromegaly for pit ad

A

Transsphenoidal surgery provides a rapid

response.

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31
Q

Mx of acromegaly

Drug of Choice (DOC)

______are the drugs of choice

A

Somatostatin analogues

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32
Q

Mx of acromegaly

__________ reduce GH values
in around 70% of patients and cause partial tumor regression in 20–50% of patients.

A

Octreotide and lanreotide

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33
Q

_____ is the best medical therapy for acromegaly

A

Octreotide

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34
Q

The main side effect of concern with

somatostatin analogues is

A

cholestasis, leading to cholecystitis.

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35
Q

_________ are used if surgery is not curative.

10% of patients respond to these drugs

A

Dopamine agonists such as bromocriptine and cabergoline

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36
Q

______is a growth hormone analogue that antagonizes endogenic GH by blocking peripheral GH binding to its receptor in the liver. It is a second- line agent.

A

Pegvisomant

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37
Q

Other complications of acromegaly include

A
cardiac failure (most common cause of death in acromegaly), diabetes mellitus,
cord compression, and visual field defects.
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38
Q

Large pituitary tumors, or cysts, as well as hypothalamic tumors (craniopharyngiomas, meningiomas, gliomas) can lead to _______

A

hypopituitarism

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39
Q

______ are the most common cause of panhypopituitarism.

A

Pituitary adenomas

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40
Q

Hypopituitarism

_____ is a syndrome associated with acute hemorrhagic infarction of a preexisting pituitary adenoma, and manifests as severe headache, nausea or vomiting, and depression of consciousness. It is a medical and neurosurgical emergency

A

Pituitary apoplexy

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41
Q

Hypopituitarism

Vascular diseases such as ______ (initial sign being the inability to lactate) and infiltrative diseases including _____ and ________ may induce this
state as well

A

Sheehan postpartum necrosis

hemochromatosis and amyloidosis

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42
Q

1st hormone lost in panhypopit

________ can occur in women and lead to amenorrhea,
genital atrophy, infertility, decreased libido, and loss of axillary and pubic hair

A

Gonadotropin deficiency (LH and FSH)

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43
Q

1st hormone lost in panhypopit

In men, decreased ______ results in impotence, testicular atrophy, infertility, decreased libido, and loss of axillary and pubic hair

A

LH and FSH

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44
Q

2nd hormone lost in panhypopit

______ gives an asymptomatic increase in lipid levels and a decrease in muscle, bone, and heart mass. It also may accelerate atherosclerosis, and it increases visceral obesity

A

GH deficiency

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45
Q

3rd hormone lost in panhypopit

____ results in hypothyroidism with fatigue, weakness,
hyperlipidemia, cold intolerance, and puffy skin without goiter

A

Thyrotropin (TSH) deficiency

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46
Q

4th hormone lost in panhypopit

____ deficiency occurs last and results in secondary adrenal insufficiency caused by pituitary disease

A

Adrenocorticotropin (ACTH)

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47
Q

The first step in diagnosing pituitary insufficiency is to measure _____

A

GH, TSH, LH, and

IGF-1.

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48
Q

The most reliable stimulus for GH secretion is

A

insulin-induced hypoglycemia

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49
Q

How to Dx GH deficiency

A

After injecting 0.1 μ/kg of regular insulin, blood glucose declines to <40 mg/dL; in normal conditions
that will stimulate GH levels to >10 mg/L and exclude GH deficiency

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50
Q

Random _______

are not sensitive enough to diagnose GH deficiency.

A

GH and IGF levels

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51
Q

______can also stimulate growth hormone release. This is less dangerous because it does not lead to ____

A

Arginine infusion

hypoglycemia.

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52
Q

To diagnose ACTH deficiency,_______may be preserved (the problem could be only in response to stress).

A

basal cortisol levels

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53
Q

How to Dx ACTH deficiency

Insulin tolerance test is diagnostic and involves giving 0.05–0.1 U/kg of regular insulin and measuring serum cortisol; plasma cortisol should increase to ______

A

> 19 mg/dL.

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54
Q

A failure of ACTH levels to rise after giving ___would indicate pituitary insufficiency.

A

metyrapone (blocks cortisol production, which

should increase ACTH levels. )

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55
Q

_____may give abnormally low cortisol output if pituitary insufficiency has led to adrenal atrophy

A

Cosyntropin (ACTH) stimulation

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56
Q

To diagnose gonadotropin deficiency in women, measure _______.

In males, gonadotropin deficiency can be detected by measuring ______

A

LH, FSH, and estrogen

LH, FSH, and testosterone

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57
Q

To diagnose TSH deficiency, measure ______

A

serum thyroxine (T4) and free triiodothyronine (T3), which are low, with a normal to low TSH.

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58
Q

Management of hypopituitarism involves treating the underlying causes. Multiple hormones must be replaced, but the most important is______

A

cortisol replacement

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59
Q

____the sella has no bony erosion. It is caused by herniation of the suprasellar subarachnoid space
through an incomplete diaphragm sella. No pituitary gland is visible on CT or MRI

A

Empty Sella Syndrome (ESS)

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60
Q

MCC of Empty Sella Syndrome (ESS)

A

The syndrome can be primary (idiopathic) and is also associated with head trauma and radiation
therapy.

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61
Q

MC Sx of Pts with ESS

A

Most patients with these syndromes are obese, multiparous women with headaches;
30% will have hypertension; endocrine symptoms are absent

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62
Q

Vasopressin or ADH and oxytocin are synthesized in neurons of the _______ and _____, then transported to the posterior pituitary lobe to be released into the circulatory system

A

supraoptic and paraventricular

nuclei in the hypothalamus

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63
Q

The syndrome associated with an excess secretion of

ADH is called ______ and the syndrome associated with a deficiency of ADH is called ____

A

SIADH (syndrome of inappropriate secretion of ADH),

diabetes insipidus (DI).

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64
Q

____is a disorder of the neurohypophyseal system
caused by a partial or total deficiency of vasopressin (ADH), which results in excessive, dilute
urine and increased thirst associated with hypernatremia

A

Central diabetes insipidus (CDI)

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65
Q

_____ is caused by renal

resistance to the action of vasopressin.

A

Nephrogenic DI

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66
Q

The differential diagnosis of DI includes primary disorders of water intake _______ and hypothalamic diseases

A

(psychogenic polydipsia, drug-induced polydipsia from chlorpromazine, anticholinergic
drugs, or thioridazine)

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67
Q

For nephrogenic DI,_____ or ____ may be used, which enhances the reabsorption of fluid from the proximal tubule.

A

HCTZ or amiloride

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68
Q

SIADH SSx include

A

This includes adrenal insufficiency, excessive fluid loss, fluid deprivation, and probably positive-pressure respiration

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69
Q

The etiology of SIADH includes malignancies such as
1
2
3

A

small cell carcinomas, carcinoma

of the pancreas, and ectopic ADH secretion

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70
Q

Drugs such as _________ can induce SIADH

A

chlorpropamide clofibrate, vincristine, vinblastine, cyclophosphamide, and carbamazepine

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71
Q

The _____ and ______ both cause hyponatremia, which is a key feature in SIADH.

A

water retention

and sodium loss

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72
Q

Laboratory findings in diagnosis of SIADH include _____ and ______

A

hyponatremia <130 mEq/L, and Posm <270 mOsm/kg.

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73
Q

Other findings of SIADH are______

A

urine sodium concentration >20 mEq/L (inappropriate
natriuresis), maintained hypervolemia, suppression of renin–angiotensin system, and no equal concentration of atrial natriuretic peptide

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74
Q

Initial MX for SIADH

A

Fluid restriction to 800–1,000 mL/d should be obtained to increase serum sodium.

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75
Q

Mx of SIADH in chronic situations

_____ can be used in chronic situations when fluid restrictions are difficult to maintain.

A

Demeclocycline

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76
Q

Demeclocycline MOA________

A

inhibits ADH action at the collecting duct (V2).

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77
Q

_____ and _______ are V2 receptor blockers indicated for moderate to severe SIADH.

A

Conivaptan and tolvaptan

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78
Q

For very symptomatic patients (severe confusion, convulsions, or coma),_______ should be used.

A

hypertonic saline (3%) 200–300 mL intravenously in 3–4 h

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79
Q

The rate of correction should be between _______

A

0.5–1 mmol/L/h of serum Na.

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80
Q

The normal function of the thyroid gland is directed toward the secretion of_________), which influence a diversity of metabolic processes.

A

l-thyroxine (T4) and l-3,5,5′-triiodothyronine (T3

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81
Q

The most sensitive test in thyroid diseases is the _____

A

TSH.

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82
Q

T4 and T3 do not always reflect actual thyroid function. For example, increased TBG levels are seen in ________ This will increase total T4 but free or active T4 level is normal

A

pregnancy and the use of oral contraceptives.

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83
Q

Decreased TBG levels are seen in______ and the use of androgens. This will decrease total T4 but free or active T4 level is normal with the patient being euthyroid

A

nephrotic syndrome

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84
Q

Always check free ____to assess thyroid function.

A

T4

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85
Q

________ varies directly with the functional state of the thyroid

A

RAIU ( thyroid-reactive iodine uptake)

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86
Q

RAIU is increased in _____ or ______and decreased in thyroiditis or surreptitious ingestion of thyroid hormone.

A

Graves’ disease or toxic nodule

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87
Q

Other tests include______ and _______, which are detected in Hashimoto thyroiditis

A

antimicrosomal and antithyroglobulin antibodies

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88
Q

In Graves’ disease, ______

A

thyroid-stimulating immunoglobulin (TSI) is

found.

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89
Q

Serum________ concentration can be used to assess the adequacy of treatment and follow-up of thyroid cancer, and to confirm the diagnosis of thyrotoxicosis factitia

A

thyroglobulin

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90
Q

Graves’ causes the production of ______ which stimulate the thyroid to secrete T4 and T3.

A

antibodies (thyroid stimulating immunoglobulin [TSI]),

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91
Q

What condition

A toxic multinodular goiter non-autoimmune
disease of the elderly associated commonly with arrhythmia and CHF and sometimes the
consequence of simple goiter.

A

(Plummer disease),

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92
Q

Drugs such as _____, ______, and ______can induce thyrotoxicosis

A

amiodarone, alpha interferon, and lithium

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93
Q

Extrathyroid source of hormones include

A

thyrotoxicosis factitia and ectopic thyroid tissue (struma ovarii, functioning follicular carcinoma).

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94
Q

Graves’ disease

Patients with another autoimmune disease such as ______ and _______
are more likely to be affected

A

type 1 diabetes or pernicious anemia

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95
Q

Graves’ disease

_____causes increased risk of disease and may make the exopthalmos worse

A

Smoking

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96
Q

Graves

______ predominate in younger patients, whereas _______symptoms are more common in older patient

A

Nervous symptoms

cardiovascular and myopathic

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97
Q

Graves

Osteoporosis and hypercalcemia can occur from increases in ______

A

osteoclast activity.

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98
Q

Graves Tx

______ is preferred, as it has a longer half-life, reverses hyperthyroidism more quickly, and has fewer side effects

A

Methimazole

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99
Q

Methimazole requires an average of _______to lower T4 levels to normal and is often
given before radioactive iodine treatment; it can be taken 1x/ day

A

6 weeks

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100
Q

WHy is PTU CI in pregnancy?

A

is because there have been rare cases of liver damage in people taking propylthiouracil

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101
Q

For women who are nursing, ______ is probably a better choice than propylthiouracil (to avoid liver side effects).

A

methimazole

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102
Q

PTU and Methimazole can cause ______

A

agranulocytosis.

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103
Q

The most commonly used ‘permanent’ therapy for Graves’ disease is ______

A

radioactive iodine

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104
Q

Indications for RAI

A
  • Large thyroid gland
  • Multiple symptoms of thyrotoxicosis
  • High levels of thyroxine
  • High titers of TSI
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105
Q

Patients currently taking antithyroid drugs must discontinue the medication at least 2 days prior to taking
the radiopharmaceutical since_______

A

pretreatment with antithyroid drugs reduces the cure rate

of radioiodine therapy in hyperthyroid diseases.

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106
Q

Graves

______is indicated only in pregnancy (second trimester), in children, and in cases when the thyroid is so large that there are compressive
symptoms

A

Subtotal thyroidectomy (and rarely total thyroidectomy)

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107
Q

Thyroid storm

Therapy for hyperthyroidism is also used and includes first, ______.

Next,______ should be given to inhibit
hormone release.

This should be followed by ______.

Finally,___________is given to provide adrenal support

A

propylthiouracil

iodine

adrenergic antagonists (e.g., b-adrenergic blockers)

dexamethasone

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108
Q

Primary hypothyroidism can occur secondary to chronic thyroiditis (Hashimoto disease); this is the most common cause of goitrous hypothyroidism and is associated with _______

A

antimicrosomal antibodies

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109
Q

Drugs such as _______ can elicit primary hypothyroidism.

A

lithium and acetylsalicylic acid, Amiodarone, interferon, and sulfonamides

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110
Q

with the lower doses of amiodarone, incidence of thyroid

dysfunction is around______

A

4%

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111
Q

T or F

Amiodarone can both cause amiodarone- induced thyrotoxicosis or amiodarone-induced hypothyroidis

A

T

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112
Q

Amiodarone-induced thyrotoxicosis

Type 1________

A

Type 1 occurs in patients with underlying thyroid pathology such as autonomous nodular goiter or Graves’; treatment is anti-thyroid therapy

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113
Q

Amiodarone-induced thyrotoxicosis

Type 2________

A

is a result of amiodarone causing a subacute thyroiditis, with release of preformed thyroid hormones into the circulation; treatment is a trial of glucocorticoids

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114
Q

Amiodarone-induced hypothyroidism due to

A

inhibition of peripheral conversion of T4 to T3

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115
Q

Dx of Primary Hypothyroidism

A

↑ TSH, ↓ T4, ↓ FT4, T3 decreases in lesser extent

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116
Q

Dx of 2° or 3° Hypothyroidism

A

Normal or ↓ TSH, ↓ T4, ↓ FT4, Accompanied by decreased secretion of other hormones

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117
Q

The goal in management of hypothyroidism is to restore metabolic state with levothyroxine. This has to be done gradually in the _______ and ______

A

elderly and patients with coronary artery

disease.

118
Q

If there is a strong suspicion of suprathyroid hypothyroidism of hypothalamic or pituitary
origin, give _________

A

hydrocortisone with thyroid hormones

119
Q

In patients with suprathyroid hypothyroidism, _____ level rather than TSH is used to guide treatment

A

T4

120
Q

Levothyroxine should be taken on an empty stomach with no other drugs or vitamins; multivitamins, including ______ and _____, can decrease its absorption

A

calcium and iron

121
Q

Hypothyroidism during pregnancy should be treated with levothyroxine, with serum TSH goal to be _______

A

kept in the lower reference range

122
Q

How to measure TSH during pregnancy

A

Serum TSH should be measured at 4−6 weeks’ gestation, then every 4−6 weeks until 20 weeks’ gestation

123
Q

Myxedema coma is precipitated by

A

cold exposure, trauma, infections, and CNS depressants

124
Q

Myxedema coma Tx

A

Treatment includes very high doses of T4 along with T3.

125
Q

Subacute thyroiditis includes

A

granulomatous, giant cell, or de Quervain thyroiditis.

126
Q

Labs of subacute thyroiditis

A

elevated erythrocyte sedimentation rate (ESR),
decreased radioactive iodine uptake,
initial elevation in T4 and T3 (caused by leak of hormone
from the gland), followed by hypothyroidism as the hormone is depleted.

127
Q

Tx of subacute thyroiditis

A

Treatment is symptomatic with NSAIDs, prednisone, and propranolol

128
Q

____ is a chronic inflammatory process of the thyroid

with lymphocytic infiltration of the gland, and is thought to be caused by autoimmune factors

A

Hashimoto thyroiditis

129
Q

most common cause of sporadic goiter in children

A

Hashimoto Thyroiditis

130
Q

SSx of Hashimoto Thyroiditis

A

Clinical findings include agoiter that is painless, which is the main feature of this disease. The goiter is rubbery and not always symmetrical. Hypothyroidism occurs

131
Q

Hashimoto thyroiditis is managed by ____

A

replacement with l-thyroxine

132
Q

______is a selflimiting episode of thyrotoxicosis associated with chronic lymphocytic thyroiditis

A

Lymphocytic thyroiditis

133
Q

Labs of Lymphocytic thyroiditis

A

The thyroid is nontender, firm, symmetrical, and slightly to

moderately enlarged. T4 and T3 are elevated, RAIU is low, and ESR normal

134
Q

Lymphocytic thyroiditis

This disease may last for ____ and be recurrent (as in postpartum thyroiditis)

A

2–5 months

135
Q

_____results from intense fibrosis of the thyroid and surrounding structures (including mediastinal and retroperitoneal fibrosis).

A

Reidel thyroiditis

136
Q

______ is the most common thyroid cancer. It is associated with history of radiation exposure

A

Papillary carcinoma

137
Q

______ of all thyroid cancers are papillary

A

60–70%

138
Q

Mx of papillary CA

A

The treatment is surgery when the tumor is small

and limited to a single area of the thyroid

139
Q

____accounts for 15–20% of all thyroid cancers.

A

Follicular carcinoma

140
Q

Follicular carcinoma spreads hematogenously with distant metastasis_______

A

to the lung and bone.

141
Q

Mets of papillary CA

A

lymphatics

142
Q

Mx of Follicular CA

A

Treatment requires near total thyroidectomy with postoperative radioiodine ablation

143
Q

____ accounts for 1–2% of all thyroid cancer. It

occurs mostly in elderly patients

A

Anaplastic carcinoma

144
Q

Anaplastic carcinoma Ssx

A

Anaplastic carcinoma is highly malignant with rapid and painful enlargement

145
Q

Anaplastic CA

______of patients die within 1 year of diagnosis

A

Eighty percent

146
Q

Anaplastic CA mets

A

This cancer spreads by direct extension

147
Q

Medullary carcinoma accounts for___ of all thyroid cancers

A

5%

148
Q

Medullary CA

This tumor arises from________ of the thyroid
and is more malignant than follicular carcinoma

A

parafollicular cells

149
Q

Medullary carcinoma is the component of two types of MEN (multiple endocrine neoplasia).

In _______ pheochromocytoma, medullary thyroid carcinoma, and (in one-half of cases) parathyroid hyperplasia occur

A

type IIa (Sipple syndrome),

150
Q

In MEN type IIb, ______, _______, _____ occur

A

pheochromocytoma,

medullary carcinoma, and neuromas

151
Q

Medullary CA

The only effective therapy is ______

A

thyroidectomy

152
Q

The only thyroid cancer with an elevated calcitonin level is __________

A

medullary cancer

153
Q

Calcifications on x-rays such as psammoma bodies suggest ______ increased density is seen in
______

A

papillary carcinoma;

medullary carcinoma.

154
Q

T or F

cancer is never hyperfunctioning

A

T

155
Q

______ is the initial procedure of choice in the evaluation of most patients solitary nonfunctioning nodule

A

Fine-needle aspiration (FNA) for cytology

156
Q

_____ of nonfunctioning thyroid nodules prove to be malignant

A

Five percent

157
Q

The first test to do in a patient with a thyroid nodule is

____ if this is normal, then proceed to ____. U/S is useful to distinguish cysts from solid nodules.

A

TSH;

FNA

158
Q

PTH acts directly on the ____ and indirectly on _____
(through its effects on synthesis of 1,25-dihydroxycholecalciferol [1,25(OH)2D3]) to increase
serum calcium.

A

bone and kidney,

intestine

159
Q

PTH increases____ which releases calcium

A

osteoclast activity,

160
Q

PTH also inhibits ______ in the kidney tubule.

A

phosphate reabsorption

161
Q

PTH activates_____ which increases the GI absorption of calcium.

A

vitamin D,

162
Q

Calcium is absorbed from the ______

A

proximal portion of the small intestine, particularly

the duodenum

163
Q

Calcium

Of the 2% that is circulating in blood, free calcium is ___ protein bound is ____, with only ____ bound to citrate or phosphate buffers.

A

50%,

40%

10%

164
Q

The most common cause of hypercalcemia is____

A

primary hyperparathyroidism

165
Q

The hypercalcemia of malignancy is due to a PTH-like protein produced

A

by squamous cell carcinoma of the lung or metastatic disease to the bone

166
Q

Neutrophils in granulomas have their own 25-vitamin

D hydroxylation, producing active ______

A

1,25 vitamin D.

167
Q
Rare causes of hypercalcemia include
1
2
3
4
5
A

vitamin D intoxication, thiazide diuretics, lithium use, and Paget disease, as well as prolonged immobilization

168
Q

______is associated with hypercalcemia because there is a partial effect of thyroid hormone on osteoclasts

A

Hyperthyroidism

169
Q

_____ is a benign form of hypercalcemia. It presents
with mild hypercalcemia, family history of hypercalcemia, urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day (hypocalciuria).

A

Familial hypocalciuric hypercalcemia (FHH)

170
Q

Familial hypocalciuric hypercalcemia (FHH) is associated with:

A

Most cases are associated with loss of function mutations in the CaSR gene, which encodes a calcium sensing receptor (expressed in kidney and parathyroid tissue).

171
Q

Tx of FHH

A

none. they are asymptomatic

172
Q

Why is there pancreatitis with hypercalcemia?

A

Pancreatitis occurs because of the precipitation of calcium in the pancreas.

173
Q

Severe pancreatitis, however, is associated with

hypocalcemia because of_______

A

binding of calcium to malabsorbed fat in the intestine

174
Q

Hypercalcemia results in polyuria and polydipsia because of the induction of ______

A

nephrogenic diabetes insipidus

175
Q

Calcium also precipitates in the kidney, resulting in

both kidney stones as well as ______

A

nephrolithiasis

176
Q

Hypertension occurs in 30–50% of patients with hypercalcemia. The EKG will show a _____

A

short QT

177
Q

Severe, life-threatening hypercalcemia is treated first with

A

vigorous fluid replacement with normal saline or half-normal saline

178
Q

_______ inhibit osteoclasts and stimulate osteoblasts

A

IV bisphosphonates such as zoledronate and

pamidronate

179
Q

The maximum effect of bisphosphonates takes_____

A

2–3 days

180
Q

Hyperparathyroidism

Etiology. It is most commonly due to ______ but hyperplasia of all 4 glands can lead to primary hyperparathyroidism (20%)

A

one gland adenoma (80%),

181
Q

In MEN type I, _______, _______, _____are seen.

A

hyperparathyroidism, pituitary tumors (3 “Ps”), and pancreatic tumors

182
Q

____ with hyperparathyroidism occurs because of increased rate of osteoclastic bone resorption and results in bone pain, fractures, swelling, deformity, areas of demineralization, bone cysts, and brown tumors (punched-out lesions producing a salt-and-pepper-like appearance).

A

Osteitis

fibrosa cystica

183
Q

Dx of primary hyperparathyroidism

A

Diagnosis can be made by laboratory findings of serum calcium >10.5 mg/dL, with elevated PTH level.

184
Q

A _______ can be used to localize the adenoma.

A

nuclear parathyroid scan (sestamibi)

185
Q

The dietary calcium should be reduced to____ in pts with primary hyperparathyroidism

A

400 mg/d

186
Q

In primary hyperparathyroidism, surgery is indicated if any of the following are present:

A
  • Symptomatic hypercalcemia
  • Calcium >11.5 mg/dL
  • Renal insufficiency
  • Age <50 years
  • Nephrolithiasis
  • Osteoporosis
187
Q

_____ is hypocalcemia that occurs after surgical removal of a hyperactive parathyroid gland, due to increased osteoblast activity

A

Hungry bones syndrome

188
Q

Hungry bones syndrome

It usually presents with :

A

rapidly decreasing calcium, phosphate, and magnesium 1–4 weeks post-parathyroidectomy

189
Q

______ agent that has some effect in hyperparathyroidism by shutting off the parathyroids

A

Cinacalcet is a calcimimetic

190
Q

Fn of Cinacalcet

A

This increases the sensitivity of calcium sensing (basolateral membrane potential) on the parathyroid

191
Q

Cinacalcet is also indicated in:

A

It is also indicated for the treatment of hypercalcemia in patients with parathyroid carcinoma and in moderate-to-severe primary hyperparathyroidism unamenable to surgery.

192
Q

________ results from a hyperfunction of the parathyroid glands themselves

A

Primary hyperparathyroidism

193
Q

________ is due to physiologic (i.e., appropriate) secretion of PTH by the parathyroid glands in response to hypocalcemia (resulting vitamin D deficiency, chronic kidney disease, etc.)

A

Secondary hyperparathyroidism

194
Q

_______is seen with long-term secondary hyperparathyroidism, which can
lead to hyperplasia of the parathyroid glands and a loss of response to serum calcium levels

A

Tertiary hyperparathyroidism

195
Q

_____is most commonly caused by hypoparathyroidism, renal failure, hyperphosphatemia, and hypomagnesemia

A

Hypocalcemia

196
Q

Drugs such as ________ will also lower calcium levels.

A

loop diuretics, phenytoin, alendronate, and

foscarnet

197
Q

Renal failure causes hypocalcemia because of the _______

A

loss of

activated 1,25-dihydroxy-vitamin D.

198
Q

_____ decreases free calcium levels by causing increased binding of calcium to albumin

A

Alkalosis

199
Q

___ occurs with low albumin levels. The free calcium level

remains normal, while the total calcium level decreases

A

Pseudo hypocalcemia

200
Q

Ca correction for hypoalb

A

To correct for albumin, add 0.8 to calcium level for every 1 gram below 4 of albumin

201
Q

Hypocalcemia results in ________

A

increased neural hyperexcitability such as seizures,

tetany, circumoral numbness, and tingling of the extremities

202
Q

Treatment of hypocalcemia is ________

A

IV or oral calcium replacement, and vitamin D replacement as necessary.

203
Q

The most common cause of hypoparathyroidism is ______

A

surgical removal of the thyroid

204
Q

_____ deficiency prevents release of PTH

from the gland.

A

Magnesium

205
Q

Hypoparathyroidism

______ is seen, such as tetany, laryngospasm, cramping, seizures, and
impaired memory function

A

Neuromuscular irritability

206
Q

Hypoparathyroidism eye findings

A

Ocular findings such as cataracts and soft tissue calcifications can occur.

207
Q

Hyperventilation worsens symptoms of hypocalcemia

because the_________

A

alkalosis decreases free calcium levels

208
Q

DX of hypoparathyroidism is made when?

A

Diagnosis is suggested when the serum calcium is low; it

209
Q

Low calcium with high phosphorous can be due to______

A

renal failure, massive tissue destruction, hypoparathyroidism, and pseudohypoparathyroidism

210
Q

Low calcium with low phosphorous is due to absent or ________

A

ineffective vitamin D

211
Q

In the acute stage of hypocalcemia, _____can be given IV.

A

calcium gluconate

212
Q

As many as _____ of diabetic patients can be kept off of medication with diet and exercise alone

A

25%

213
Q

_____is the drug of choice and along with lifestyle intervention should be used in all newly diagnosed patients

A

Metformin

214
Q

If a patient is initiated on metformin yet the diabetes does not become well-controlled, add a_______

A

sulfonylurea

215
Q

If a patient is already taking both metformin and a sulfonylurea yet there is still poor glycemic control, then either switch to ________

A

insulin or add a glitazone

216
Q

Glitazones can lead to ______

A

fluid retention.

217
Q

If metformin cannot be used, use a new _____

A

glucagon-like peptide (GLP-1) agonist (exenatide

or liraglutide).

218
Q

Sulfonylureas (glyburide, glipizide, glimepiride SE):

A

increase weight, cause hypoglycemia; sulfa drugs

219
Q

Thiazolidinediones (rosiglitazone or pioglitazone): can worsen _______

A

CHF

220
Q

Recent studies suggest pioglitazone may be linked to _______

A

bladder cancer

221
Q

Augment the naturally occurring hormones that are secreted from the GI tract in response to food

A

Incretin mimetics (exenatide, liraglutide

222
Q

Incretin is also called______

A

Also called gastric inhibitory peptide or glucose-dependent insulinotropic peptide (both abbreviated as GIP);

223
Q

The “incretin mimetic” drugs exenatide and liraglutide are direct analogues of GIP and GLP, except that _______

A

their actions last much longer

224
Q

Dipeptidyl peptidase IV (DPP-IV) inhibitors (sitagliptin, saxagliptin, linagliptin):

A

natural hormones which prevent the metabolism of the incretins GIP and GLP

225
Q

The main problems in DKA stem from ______

A

acidosis with increased anion gap and dehydration

226
Q

The adrenal cortex is divided into 3 areas, the outer zone (glomerulosa), which is the site of ______

the central zone (fasciculata), which is the site of __________;

and the inner zone (reticularis), which
is the site of ______

A

aldosterone synthesis;

cortisol synthesis

androgen biosynthesis

227
Q

The etiology of Cushing syndrome includes ________. This can be secondary to pituitary ACTH production, which occurs in pituitary-hypothalamic dysfunction, and pituitary ACTH-producing adenomas (microadenoma, e.g., Cushing disease).

A

adrenal hyperplasia

228
Q

Dx test for Cushing sundrome

The diagnostic tests used to establish the syndrome of cortisol excess are the:

A

1-mg overnight dexamethasone suppression test and the 24-hour urine-free cortisol

229
Q

The tests used to establish a precise etiology of the cortisol excess are the

A

ACTH level, high-dose dexamethasone suppression test, CT and MRI scanning, and occasionally sampling of the petrosal venous sinus, which drains out of the pituitary

230
Q

What is the normal result of the 1-mg overnight dexamethasone suppression test

A

If you give a milligram of dexamethasone at 11 p.m., the
cortisol level at 8 a.m. should come to normal if there is the normal ability to suppress ACTH production over several hours

231
Q

False positive of the 1-mg overnight dexamethasone suppression test

A

Any drug that increases the metabolic breakdown of dexamethasone will prevent its ability to suppress cortisol levels.

Examples of drugs increasing the metabolism of dexamethasone are phenytoin, carbamazepine, and rifampin.

Stress increases glucocorticoid levels

232
Q

An abnormality on the 1-mg overnight test should be confirmed with a ______

A

24-hour urine-free

cortisol

233
Q

The ________is more accurate and is the gold standard for confirming or excluding Cushing’s syndrome.

A

24-hour urine-free

cortisol

234
Q

A third screening test for Cushing is the ______

A

midnight salivary cortisol

235
Q

The precise etiology of the Cushing syndrome is established by ______

A

using ACTH levels, sometimes in combination with high-dose dexamethasone suppression testing

236
Q

ACTH levels are elevated with either a pituitary source of ACTH such as an _______

A

adenoma or with an ectopic source.

237
Q

Highdose dexamethasone suppression testing can distinguish the difference between an adenoma or with an ectopic source.

The output of a pituitary adenoma will suppress with ______The output of an ectopic source will __________

A

high-dose dexamethasone.

not suppress with high-dose dexamethasone.

238
Q

If the ACTH level is low, then the etiology is most likely from an adrenal tumor such as an ______

A

adenoma, cancer, or from adrenal hyperplasia

239
Q

When there is a low ACTH level, the precise etiology is confirmed with a ________

A

CT scan of the adrenals.

240
Q

When there is a high ACTH level, the precise etiology is confirmed with an ______

A

MRI of the pituitary looking for an adenoma or a CT scan of the chest looking for an ectopic focus

241
Q

T or F

Single random cortisol levels are not reliable.

A

T

242
Q

The normal function of aldosterone is to _______

A

reabsorb sodium and excrete potassium and acid (H+).

243
Q

Hyperaldosteronism can be divided into the following:

  • Primary aldosteronism,_______
  • Secondary aldosteronism,_______
A

in which the stimulus for the excessive aldosterone production is within the adrenal gland

in which the stimulus is extraadrenal

244
Q

The most common cause of primary hyperaldosteronism is a _______ (70%). _______ accounts for 25–30%.

A

unilateral adrenal adenoma

Bilateral hyperplasia

245
Q

Primary hyperaldosteronism is characterized by _____ and ________

A

hypertension and low potassium levels.

246
Q

Other Sx of Primary hyperaldosteronism:

A

muscle weakness, polyuria, and polydipsia, are

from the hypokalemia.

247
Q

Metabolic alkalosis occurs because ______

A

aldosterone increases hydrogen ion (H+) excretion.

248
Q

______is uncommon with primary hyperaldosteronism

because of sodium release into the urine

A

Edema

249
Q

The preliminary screen for hyperaldosteronism is a _________

A

plasma aldosterone concentration (PAC) and plasma renin activity (PRA).

250
Q

Hyperaldosteronism

Plasma aldosterone concentration (PAC) and plasma renin activity (PRA).

A positive screen is a PAC/PRA ratio ___ and a
PAC ______.

A

> 20:1

> 15

251
Q

To confirm hyperaldosteronism, an ______ is required

This can be via normal saline, NaCl tabs, or fludrocortisone.

A

NaCl challenge

252
Q

After an NaCl challenge, PAC should be_______

A

suppressed as in a normal individual. If PAC is still elevated, this confirms the diagnosis

253
Q

Adrenal adenomas are removed surgically. Bilateral hyperplasia is treated with _______

A

spironolactone, which blocks aldosterone.

254
Q

The exception of secondary hyperaldosteronism without edema or hypertension is________

A

Bartter syndrome

255
Q

Bartter syndrome is caused by a defect in the __________This is like having a furosemide-secreting tumor.

A

loop of Henle in which it loses NaCl. This is due to a defect in the Na-K-2Cl cotransporter.

256
Q

What are the problems in Bartters syndrome

A

juxtaglomerular hyperplasia, normal to low blood pressure, no edema, severe hypokalemic alkalosis, defect in renal conservation of sodium or chloride, and
renal loss of sodium, which stimulates renin secretion and aldosterone production

257
Q

______ is a syndrome associated with increased adrenal androgen production because of enzymatic defects

A

Congenital adrenal hyperplasia

258
Q

CAH

Enzymatic defects include ______ in 95% of all cases

A

C-21 hydroxylase

deficiency

259
Q

C-21 hydroxylase deficiency is associated with _____

A

reduction in aldosterone secretion in one-third of patients

260
Q

SSx of CAH from C-21 hydroxylase deficiency

A

Patients are female at birth with ambiguous external genitalia (female pseudohermaphrodism),
enlarged clitoris, and partial or complete fusion of the labia

261
Q

Manifestations of C-11 hydroxylase deficiency in early infancy

A

In early infancy, despite having excessive mineralocorticoid hormones, patients sometimes present with relative ‘salt wasting’ (aldosterone deficiency).

This is because some infants have inefficient salt conservation as well as immature aldosterone
production.

During this phase, infants can present with hypotension and hyperkalemia (very similar to 21 hydroxylase deficiency).

262
Q

Manifestations of C-11 hydroxylase deficiency Later in life (childhood and adulthood)

A

there is better ability to hold onto salt, so the patient develops the typical C-11 deficiency syndrome: hypertension and hypokalemia

263
Q

C-17 hydroxylase deficiency can occur as well, and is characterized by hypogonadism, hypokalemia,
and hypertension resulting from increased production of ________

A

11-deoxycorticosterone

264
Q

CAH should be considered in all infants exhibiting_______

A

failure to thrive, especially those with episodes of acute adrenal insufficiency, salt wasting, or hypertension

265
Q

CAH

The most useful measurements are of _____

A

serum testosterone, androstenedione, dehydroepiandrosterone, 17-hydroxyprogesterone, urinary 17-ketosteroid, and pregnanetriol.

266
Q

Tx of CAH

A

Treatment is glucocorticoid (hydrocortisone) replacement

267
Q

Adrenal insufficiency can be divided into
1
2

A

primary adrenocorticoid insufficiency (Addison disease) and secondary failure in the elaboration of ACTH

268
Q

MC etiology of Addison

A

Idiopathic atrophy is the most common cause of anatomic

destruction, and autoimmune mechanisms are probably responsible.

269
Q

The clinical findings in Addison disease include :

A

weakness, paresthesias, cramping, intolerance to stress, and personality changes such as irritability and restlessness.

270
Q

______ is characterized by fever and hypotension.

A low sodium with a high potassium level and mild acidosis are also present

A

Acute Addisonian crisis

271
Q

The diagnosis of Addison disease is made through _______

A

rapid ACTH administration and measurement of cortisol

272
Q

Lab findings of Addison disease

A

Laboratory findings include white blood cell count with moderate neutropenia, lymphocytosis, and eosinophilia; elevated serum potassium and urea nitrogen;
low sodium; low blood glucose; and morning low plasma cortisol

273
Q

The definitive dx of Addison disease is:

A

cosyntropin or ACTH stimulation test.

274
Q

Normal results of the cosyntropin or ACTH stimulation test.

A

A cortisol level is obtained before and after administering ACTH. A normal person should show a brisk rise in
cortisol level after ACTH administration.

275
Q

The management of Addison disease involves

A

glucocorticoid, mineralocorticoid, and sodium chloride replacement, in addition to patient education.

276
Q

Who may suffer adrenal crisis

A

• Previously undiagnosed patient with adrenal insufficiency who has undergone surgery,
serious infection, and/or major stress
• Bilateral adrenal infarction or hemorrhage
• Patient who is abruptly withdrawn from chronic glucocorticoid therapy

277
Q

What is the rule of 10 for Phaeochrom

A

The rule of 10% applies in pheochromocytoma with 10% being extraadrenal, 10% malignant, 10% in children, and 10% bilateral or multiple (>right side).
Also, 10% are not associated with hypertension.

278
Q

Familial pheochromocytoma occurs in 5% of cases, and is transmitted as an autosomal dominant trait alone or in combination with

A

MEN type II or III, von Recklinghausen neurofibromatosis, or von Hippel-Lindau retinal cerebellar hemangioblastomatosis.

279
Q

In adults, _____ of pheochromocytomas occur as a unilateral solitary lesion with ___ being bilateral and ____ extraadrenal

A

80%

10%

10%

280
Q

Extraadrenal pheochromocytomas are mostly located within the ______

A

abdomen and near the celiac, superior mesenteric, and inferior mesenteric ganglia

281
Q

Clinical findings of pheochromocytoma include _____

A

paroxysms or crisis.

282
Q

> 33% of pheochromocytomas cause death prior to diagnosis; death is often due to

A

cardiac arrhythmia and stroke

283
Q

pheochromocytoma

__________are tests of choice.

A

Urinary-free catecholamines, urinary metanephrines, vanillylmandelic acid, and plasma catecholamines

284
Q

pheochromocytoma

__________s are the best initial tests. Recently, plasma metanephrine levels have been used in conjunction with urinary tests

A

A 24-hour urinary VMA, metanephrines, and

free catecholamines

285
Q

Overall, _______ are the most sensitive and specific

individual test

A

metanephrines

286
Q

Failure of epinephrine levels to fall after _____

administration is highly suggestive of pheochromocytoma

A

clonidine

287
Q

________ is used to locate a pheochromocytoma

not found on a CT scan.

A

MIBG (metaiodobenzylguanidine) scanning

288
Q
1
2
3
, is
required to control BP and prevent a hypertensive crisis, since high circulating catecholamine levels stimulate alpha receptors on blood vessels and cause vasoconstriction
A

Alpha-adrenergic blockade, phentolamine, and/or phenoxybenzamine

289
Q

Phaechrom

______are not administered until adequate alpha blockade has been established, since unopposed alpha-adrenergic receptor stimulation can precipitate a hypertensive crisis.

A

beta blockers

290
Q

Choice of BB in Phaeochrom

A
Noncardioselective beta blockers (propranolol, nadolol) are the usual choice, though
cardioselective agents (atenolol, metoprolol) may be used
291
Q

______has been associated with paradoxic episodes of hypertension thought to be secondary to incomplete alpha blockade.

A

Labetalol