Endocrinology Flashcards

1
Q

When should you screen for T2DM?

A

Age 45, screen ever 3 yrs or earlier in high risk groups

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2
Q

What is a sensitive indicator of thyroid function, it is generally recommended as a first-line test for thyroid disorders.

A

TSH

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3
Q

Blood supply of the posterior pituitary

A

The posterior pituitary is supplied by the inferior hypophyseal arteries

In contrast to the anterior pituitary, the posterior lobe is directly innervated by hypothalamic neurons (supraopticohypophyseal and tuberohypophyseal nerve tracts) via the pituitary stalk

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4
Q

Lactotropes constitute __% of anterior pituitary cells

A

20

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5
Q

Peak serum PRL levels (up to 30 μg/L) occur between ____ a.m.

A

4:00 and 6:00

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6
Q

What makes prolactin unique among the pituitary hormones?

A

PRL is unique among the pituitary hormones in that the predominant hypothalamic control mechanism is inhibitory, reflecting tonic dopamine-mediated suppression of PRL release.

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7
Q

In what instances does serum prolactin rise?

A

after exercise, meals, sexual intercourse, minor surgical procedures, general anesthesia, chest wall injury, acute myocardial infarction, and other forms of acute stress

Also increases (10 fold) during pregnancy then declines rapidly within 2 weeks of parturition

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8
Q

What is the function of prolactin?

A

PRL acts to induce and maintain lactation and to suppress both reproductive function and sexual drive.

PRL inhibits reproductive function by suppressing hypothalamic (GnRH) and pituitary gonadotropin secretion and by impairing gonadal steroidogenesis in both women and men.

In the ovary, PRL blocks folliculogenesis and inhibits granulosa cell aromatase activity, leading to hypoestrogenism and anovulation.

PRL also has a luteolytic effect, generating a shortened, or inadequate, luteal phase of the menstrual cycle. In men, attenuated LH secretion leads to low testosterone levels and decreased spermatogenesis.

These hormonal changes decrease libido and reduce fertility in patients with hyperprolactinemia.

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9
Q

Most abundant anterior pituitary hormone

A

Growth hormone

Somatotrope -50%

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10
Q

How does ghrelin affect GH?

A

Induces GHRH and GH release

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11
Q

Peripheral target for GH

A

IGF-1

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12
Q

Peak levels of GH secretion occurs when?

A

GH secretion is pulsatile, with highest peak levels occurring at night, generally correlating with sleep onset.

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13
Q

In what instances does GH secretion increase?

A

Elevated GH levels occur within an hour of deep sleep onset as well as after exercise, physical stress, and trauma and during sepsis.

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14
Q

What stimulates GH release?

A

GH is stimulated by oral ghrelin receptor agonists, intravenous l-arginine, dopamine, and apomorphine (a dopamine receptor agonist), as well as by α-adrenergic pathways.

β-Adrenergic blockade induces basal GH and enhances GHRH- and insulin-evoked GH release.

On the other hand, glucose decreases GH secretion

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15
Q

Which organs express the highest amount of GH receptors?

A

The liver and cartilage express the greatest
number of GH receptors.

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16
Q

Organ that is the major source of IGF-1

A

Liver

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17
Q

What is the effect of IGF-1 on glucose levels

A

induces hypoglycemia and improves insulin sensitivity

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18
Q

Peak time of ACTH secretion

A

ACTH secretion is pulsatile and exhibits a characteristic circadian rhythm, peaking at about 6:00 a.m. and reaching a nadir about midnight

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19
Q

What peptide regulates GnRH release?

A

Brain kisspeptin, a product of the KISS1 gene, regulates hypothalamic GnRH release

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20
Q

syndrome that results from defective hypothalamic (GnRH) synthesis and is associated with anosmia or hyposmia due to olfactory bulb agenesis or hypoplasia

A

Kallman syndrome

Classically, the syndrome may also be associated with color blindness, optic atrophy, nerve deafness, cleft palate, renal abnormalities, cryptorchidism, and neurologic abnormalities such as mirror movements

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21
Q

Syndrome characterized by intellectual disability, renal abnormalities, obesity, and hexadactyly, brachydactyly, or syndactyly

A

Bardet-Biedl Syndrome

Retinal degeneration begins in early childhood, and most patients are blind by age 30.

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22
Q

Syndrome associated with hypogonadotropic hypogonadism, hyperphagia-obesity, chronic muscle hypotonia, mental retardation, and adult-onset diabetes mellitus

A

Prader Willi

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23
Q

Hormone that is more likely to be affected by cranial irradiation

A

GH

GH deficiency is most common, followed by gonadotropin, thyroid, and ACTH deficiency

The development of hypopituitarism occurs over 5–15 years and usually reflects hypothalamic damage rather than primary destruction of pituitary cells.

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24
Q

Lymphocytic hypophysitis occur most commonly in which subset of the population

A

post partum women

Most patients manifest symptoms of progressive mass effects with headache and visual disturbance.

The ESR often is elevated. Because it may be indistinguishable from a pituitary adenoma on MRI, hypophysitis should be considered in a postpartum woman with a newly diagnosed pituitary mass before an unnecessary surgical intervention is undertaken.

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25
Q

Syndrome that occurs during post partum and presents with acute intrapituitary hemorrhagic vascular events can cause substantial damage to the pituitary and surrounding sellar structures.

A

Sheehan’s syndrome

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26
Q

ACTH reserve is most reliably assessed by measuring

A

ACTH and cortisol levels during insulin-induced hypoglycemia

Administering insulin to induce hypoglycemia is contraindicated in patients with active coronary artery disease or known seizure disorders

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27
Q

Syndrome with Homozygous or heterozygous mutations of the GH receptor are associated with partial or complete GH insensitivity and growth failure

A

(Laron syndrome)

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28
Q

Short stature should be evaluated comprehensively if a patient’s height is > __ standard deviations below the mean for age or if the growth rate has decelerated

A

3

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29
Q

Sequence of hormone loss in pituitary deficiency

A

The sequential order of hormone loss is usually GH → FSH/LH → TSH → ACTH.

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30
Q

The most validated test to distinguish pituitary-sufficient patients from those with AGHD is

A

insulin-induced (0.05–0.1 U/kg) hypoglycemia

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31
Q

Expected response of AGHD after insulin induced hypoglycemia

A

About 90% of healthy adults exhibit GH responses >5 μg/L; AGHD is defined by a peak GH response to hypoglycemia of <3 μg/L.

Contraindicated in patients with diabetes, ischemic heart disease, cerebrovascular disease, or epilepsy and in elderly patients.

Alternative stimulatory tests include intravenous arginine (30 g), GHRH (1 μg/kg), oral ghrelin receptor agonist (0.5 mg/kg), and glucagon (1 mg).

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32
Q

Contraindications to GH therapy

A

Contraindications to therapy include the presence of an active neoplasm, intracranial hypertension, and uncontrolled diabetes and retinopathy

Women require higher doses than men, and elderly patients require less GH.

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33
Q

Type of cholesterol increased by GH administration

A

HDL

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34
Q

In ACTH deficiency, The total daily dose of hydrocortisone replacement preferably should generally not exceed _ mg daily, divided into two or three doses.

A

20

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35
Q

most common presenting feature of adult hypopituitarism even when other pituitary hormones are also deficient.

A

Hypogonadism

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36
Q

Screening test for
Acromegaly?
Prolactinoma?

A

See table

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37
Q

Screening test for Cushing’s dse

A

See table

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38
Q

Screening test for Gonadotropinoma

A

See table

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39
Q

Screening test for TSH-producing adenoma

A

See table

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40
Q

Transsphenoidal resection is the desired surgical approach for pituitary tumors, except for

A

rare invasive suprasellar mass surrounding the frontal or middle fossa or the optic nerves or invading posteriorly behind the clivus, which may require transcranial approaches.

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41
Q

Treatment of choice for prolactinoma

A

Dopamine agonists

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42
Q

Treatment for acromegaly

A

For acromegaly, somatostatin receptor ligands
(SRLs) and a GH receptor antagonist are indicated.

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43
Q

______ are benign, suprasellar cystic masses that present with headaches, visual field deficits, and variable degrees of hypopituitarism. They are derived from Rathke’s pouch and arise near the pituitary stalk, commonly extending into the suprasellar cistern.

A

Craniopharyngiomas

Hypopituitarism is documented in ~90%, and diabetes insipidus occurs in ~10% of patients.

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44
Q

Treatment for craniopharyngioma

A

Treatment usually involves transcranial or transsphenoidal surgical resection followed by postoperative radiation of residual tumor.

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45
Q

the most common cause of pituitary hormone hypersecretion and hyposecretion syndromes in adults.

A

Pituitary adenomas

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46
Q

Syndrome associated with Pituitary hyperplasia and adenomas (10%), Atrial myxomas, Schwannomas, Adrenal hyperplasia, Lentigines

A

Carney Complex

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47
Q

autosomal dominant syndrome characterized primarily by a genetic predisposition to parathyroid, pancreatic islet, and pituitary adenomas

A

MEN 1

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48
Q

syndrome that consists of polyostotic fibrous dysplasia, pigmented skin patches, and a variety of endocrine disorders, including acromegaly, adrenal adenomas, and autonomous ovarian function

A

McCune Albright

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49
Q

most common pituitary hormone hypersecretion syndrome in both men and women

A

Hyperprolactinemia

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50
Q

Effect of chronic renal failure on prolactin levels

A

Elevates by decreasing clearance

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51
Q

the hallmarks of hyperprolactinemia in women.

A

Amenorrhea, galactorrhea, and infertility

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52
Q

When is galactorrhea suspected in patients who just gave birth?

A

the inappropriate discharge of milk-containing fluid from the breast, is considered abnormal if it persists longer than6 months after childbirth or discontinuation of breast-feeding.

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53
Q

In patients with markedly elevated PRL levels (____ μg/L), reported results may be falsely lowered because of assay artifacts;

A

> 1000

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54
Q

Macroadenomas are >___ in diameter and may be locally invasive and impinge on adjacent structures.

A

1 cm

Tumor size generally correlates directly with PRL concentrations; values >250 μg/L usually are associated with macroadenomas.

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55
Q

The drug Cabergoline effectively suppresses PRL for >___days after a single oral dose and induces prolactinoma shrinkage in most patients.

A

14

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56
Q

Preferred dopamine agonists in pregnant patients

A

Bromocriptine

B for buntis

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57
Q

What level of prolactin should you consider surgery in microadenoma

A

> 50 ug/L

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58
Q

When should you repeat MRI after starting patient with macroadenoma on dopamine agonist?

A

4 months

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59
Q

The most significant clinical impact of GH excess occurs with respect to the ____ system

A

cardiovascular

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60
Q

Confirmatory test for acromegaly

A

The diagnosis of acromegaly is confirmed by demonstrating the failure of GH suppression to <0.4 μg/L within 1–2 h of an oral glucose load (75 g)

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61
Q

Initial tx for acromegaly

A

Surgical resection of GH-secreting adenomas is the initial treatment for most patients

Transsphenoidal surgical resection by an experienced surgeon is the preferred primary treatment for both microadenomas (remission rate ~70%) and macroadenomas (<50% in remission).

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62
Q

Drug that antagonizes endogenous GH action by blocking peripheral GH binding to its receptor. Consequently, serum IGF-1 levels are suppressed, reducing the deleterious effects of
excess endogenous GH.

A

Pegvisomant

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63
Q

Next step after surgery of acromegaly

A

Somatostatin receptor ligands eg. octreotide, lanreotide, pasireotide

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64
Q

Account for 70% of patients with endogenous causes of Cushing’s syndrome.

A

Pituitary corticotrope adenomas (Cushing’s
disease)

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65
Q

most common cause of cushingoid features

A

iatrogenic hypercortisolism

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66
Q

Primary cause of death in Cushing’s syndrome

A

Cardiovascular

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67
Q

Most common clinical feature of Cushing syndrome

A

Obesity and Thick skin

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68
Q

Screening test for Cushing syndrome

A

24hr urinary free cortisol
Alternatively, overnight 1mg dexa test

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69
Q

how do you differentiate ACTH secreting tumor vs ectopic ACTH secretion

A

see table

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70
Q

Treatment of choice for cushing disease

A

Selective transphenoidal resection

The remission rate for this procedure
is ~80% for microadenomas but <50% for macroadenomas

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71
Q

What is the effect of pasireotide on sugar levels

A

Notably, hyperglycemia and new-onset diabetes develop in up to 70% of patients, likely due to suppressed pancreatic secretion of insulin and incretins.

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72
Q

What is an oral 11β-hydroxylase inhibitor used for Cushing dse that blocks adrenal gland cortisol biosynthesis, normalizes 24-h UFC in 86% of patients.

A

Osilodrostat (2 mg twice daily titrated up to 30 mg twice daily)

Elevated adrenal hormone precursors may lead
to hypokalemia and hypertension.

QTc prolongation and possibly
increased tumor volume are also reported.

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73
Q

What is a drug used in Cushing syndrome that is a glucocorticoid receptor antagonist, blocks peripheral cortisol action and is approved to treat hyperglycemia in Cushing’s disease?

A

Mifepristone (300–1200 mg/d)

Because the drug does not target the pituitary tumor, both ACTH and cortisol levels remain elevated, thus obviating a reliable circulating biomarker.

Side effects are largely due to general antagonism of other steroid hormones and include hypokalemia, endometrial hyperplasia, hypoadrenalism, and hypertension.

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74
Q

Drug that inhibits 11β-hydroxylase activity and normalizes plasma cortisol in up to 75% of patients with Cushing syndrome

A

Metyrapone (2–4 g/d)

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75
Q

Adrenalectomy in the setting of residual corticotrope adenoma tissue predisposes to the development of _____ syndrome, a disorder characterized by rapid pituitary tumor enlargement and increased pigmentation secondary to high ACTH levels.

A

Nelson’s

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76
Q

most common type of pituitary adenoma and are usually macroadenomas at the time of diagnosis

A

non functioning pituitary adenoma

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77
Q

If PRL levels are <100 μg/L in a patient harboring a pituitary mass, what should be considered?

A

a nonfunctioning adenoma causing pituitary stalk compression should be considered

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78
Q

Sources of ectopic ACTH secretion

A

Bronchial, abdominal carcinoid
Small-cell lung cancer
Thymoma

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79
Q

critical first step in thyroid hormone synthesis.

A

Iodide uptake

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80
Q

Mutation of the _____ gene causes Pendred syndrome, a disorder characterized by defective organification of iodine, goiter, and sensorineural deafness.

A

pendrin gene

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81
Q

The Recommended Dietary Allowance (RDA) is
___ μg iodine per day for pregnant women and ____ μg iodine per dayfor breastfeeding women

A

220, 290

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82
Q

Urinary iodine is > ___ in iodine-sufficient populations.

A

100 μg/L

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83
Q

Excess iodide transiently inhibits thyroid iodide organification, a phenomenon known as the ____

A

Wolff-Chaikoff effect

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84
Q

Five factors alter thyroid function in pregnancy

A

(1) the transient increase in hCG during the first trimester, which weakly stimulates the TSH-R
(2) the estrogen-induced rise in TBG during the first trimester, which is sustained during pregnancy
(3) alterations in the immune system, leading to the onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease
(4) increased thyroid hormone metabolism by the placental type III deiodinase; and
(5) increased urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine sufficiency.

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85
Q

Women with a precarious iodine intake (<___) are most at risk of developing a goiter during pregnancy or giving birth to an infant with a goiter and hypothyroidism.

A

50 μg/d

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86
Q

Thyroid hormone requirements are increased by up to __% during pregnancy in levothyroxine-treated hypothyroid women.

A

45

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87
Q

What are the differentiating factors of t3 vs t4

A

see table

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88
Q

Medications that decrease conversion of T4 to T3

A

propranolol, ipodate, iopanoic acid,
amiodarone

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89
Q

Expected TFT in thyroid hormone resistance

A

Increased unbound T4, T3
Normal or increased TSH

Individuals with RTH do not, in general, exhibit signs and symptoms that are typical of hypothyroidism because hormone resistance is partial and is compensated by increased levels of thyroid hormone.

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90
Q

Large retrosternal goiters can cause venous distention over the neck and difficulty breathing, especially when the arms are raised _____

A

(Pemberton’s sign)

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91
Q

What is the effect of biotin supplement on TSH levels

A

falsely low

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92
Q

What is the effect of androgens and nephrotic syndrome on TBG

A

dec

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93
Q

Serum Tg levels are increased in all types of thyrotoxicosis except

A

thyrotoxicosis factitia

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94
Q

Sonographic findings that are highly suggestive of thyroid malignancy

A

Sonographic patterns that combine suspicious sonographic features are highly suggestive of malignancy (e.g., hypoechoic solid nodules with infiltrative borders and microcalcifications, >90% cancer risk)

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95
Q

Sonographic findings that are highly suggestive of benign pattern of thyroid mass

A

(isoechoic solid nodules, 5–10% cancer risk).

Some patterns suggest benignity (e.g., spongiform nodules, defined as those with multiple small internal cystic areas, or simple cysts, <3% cancer risk)

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96
Q

Starting dose for LT4 for congenital hypothyroidism

A

When the diagnosis is confirmed, T4 is instituted at a dose of 10–15 μg/kg per d,

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97
Q

Most common symptom and sign of hypothyroidism

A

symptom: tiredness, weakness
sign: dry coarse skin, weak peripheral pulses

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98
Q

Next step when TSH is high but FT4 is normal or low

A

Request for TPO antibodies

if symptomatic, consider LT4 tx
if asymptomatic, annual ff up

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99
Q

Dose of LT4 for clinical hypothyroidism

A

If there is no residual thyroid function, the daily replacement dose of LT4 is usually 1.6 μg/kg body weight (typically 100–150 μg), ideally taken at least 30 min before breakfast.

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100
Q

when does symptoms of hypothyroidism resolve after treatment with LT4

A

Patients may not experience full relief from symptoms until 3–6 months after normal TSH levels are restored

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101
Q

In patients of normal body weight who are taking ≥ ____ of LT4 per d, an elevated TSH level is often a sign of poor adherence to treatment.

A

200 μg

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102
Q

What should be done if you missed 1 dose of LT4?

A

Because T4 has a long half-life (7 days), patients who miss a dose can be advised to take two doses of the skipped tablets at once

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103
Q

When should subclinical hypothyroidism be treated

A

There are no universally accepted recommendations for the management of subclinical hypothyroidism, but LT4 is recommended if the patient is a woman who wishes to conceive or is pregnant or when TSH levels are >10 mIU/L.

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104
Q

Target TSH in pregnant women

A

Because of the known increase in thyroid hormone requirements during pregnancy in hypothyroid women, LT4 therapy should be targeted to maintain a serum TSH in the normal range but <2.5 mIU/L prior to conception

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105
Q

When should be TSH be checked during pregnancy?

A

thyroid function should be evaluated immediately after pregnancy is confirmed and every 4 weeks during the first half of the pregnancy, with less frequent testing after 20 weeks’ gestation (every 6–8 weeks depending on whether LT4 dose adjustment is ongoing).

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106
Q

Elderly patients may require ___% LESS thyroxine than younger patients

A

20

In the elderly, especially patients with known coronary artery disease, the starting dose of LT4 is 12.5–25 μg/d with similar increments every 2–3 months until TSH is normalized

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107
Q

How do you treat myxedema coma?

A

LT4 can initially be administered as a single IV bolus of 200–400 μg, which serves as a loading dose, followed by a daily oral dose of 1.6 μg/kg per d, reduced by 25% if administered IV

Because T4 → T3 conversion is impaired in myxedema coma, there is a rationale for adding liothyronine (T3 ) intravenously or via nasogastric tube to LT4 treatment, although excess liothyronine has the potential to provoke arrhythmias. An initial loading dose of 5–20 μg liothyronine should be followed by 2.5–10 μg every 8 h, with lower doses chosen for smaller or older patients and those at cardiovascular risk

Parenteral hydrocortisone (50 mg every 6 h) should be administered because there is impaired adrenal reserve in profound hypothyroidism

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108
Q

Most common cause of thyrotoxicosis

A

Graves’ disease accounts for 60–80% of thyrotoxicosis

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109
Q

_____ is a minor risk factor for Graves’ disease and a major risk factor for the development of ophthalmopathy

A

Smoking

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110
Q

Most common symptom and sign of hyperthyroidism

A

symptom: hyperactivity, irritability, dysphoria
sign: tachycardia, AF in elderly

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111
Q

Most common cardiovascular manifestation of Graves

A

The most common cardiovascular manifestation is sinus tachycardia, often associated with palpitations, occasionally caused by supraventricular tachycardia

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112
Q

Where should you auscultate for thrill/bruit of thyroid in Grave’s dse

A

There may be a thrill or bruit, best detected at the inferolateral margins of the thyroid lobes, due to the increased vascularity of the gland and the hyperdynamic circulation

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113
Q

Earliest manifestation of Grave’s ophthalmopathy

A

The earliest manifestations of ophthalmopathy are usually a sensation of grittiness, eye discomfort, and excess tearing

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114
Q

_____ refers to a form of clubbing found in <1% of patients with Graves’ disease

A

Thyroid acropachy

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115
Q

What is the site involved in thyroid dermopathy?

A

Thyroid dermopathy occurs in <5% of patients with Graves’ disease , almost always in the presence of moderate or severe ophthalmopathy. Although most frequent over the anterior and lateral aspects of the lower leg (hence the term pretibial myxedema), skin changes can occur at other sites, particularly after trauma.

The typical lesion is a noninflamed, indurated plaque with a deep pink or purple color and an “orange skin” appearance

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116
Q

What should you suspect if TFTs revealed TSH normal or increased, high unbound T4

A

TSH-secreting pituitary adenoma or thyroid hormone resistance syndrome

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117
Q

Next step when TSH is low but FT4 is normal

A

measure unbound t3

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118
Q

When should you schedule ff up for subclinical hyperthyroidism

A

6-12 weeks

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119
Q

Clinical course of Grave’s ophthalmopathy

A

The clinical course of ophthalmopathy does not follow that of the thyroid disease, although thyroid dysfunction can worsen eye signs. Ophthalmopathy typically worsens over the initial 3–6 months, followed by a plateau phase over the next 12–18 months, and then some spontaneous improvement, particularly in the soft tissue changes

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120
Q

When should you follow up patients with hyperthyroidism after starting treatment

A

Thyroid function tests and clinical manifestations are reviewed 4–6 weeks after starting treatment, and the dose is titrated based on unbound T4 levels.

Most patients do not achieve euthyroidism until 6–8 weeks after treatment is initiated

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121
Q

When should methimazole be stopped prior to RAI and when can it be restarted?

A

Carbimazole or methimazole must be stopped 2–3 days before radioiodine administration to achieve optimum iodine uptake and can be restarted 3–7 days after radioiodine in those at risk of complications from worsening thyrotoxicosis

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122
Q

% risk of hypothyroidism after RAI

A

The risk of hypothyroidism after radioiodine depends on the dosage but is at 10–20% in the first year and 5% per year thereafter.

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123
Q

How long shoud you avoid close prolonged contact with children and women after RAI

A

In general, patients need to avoid close, prolonged contact with children and pregnant women for 5–7 days because of possible transmission of residual isotope and exposure to radiation emanating from the gland

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124
Q

What precautions should be done to avoid thyrotoxic crisis prior to thyroidectomy

A

Careful control of thyrotoxicosis with antithyroid drugs, followed by potassium iodide (SSKI; 1–2 drops orally tid for 10 days), is needed prior to surgery to avoid thyrotoxic crisis and to reduce the vascularity of the gland

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125
Q

Birth defect associated with methimazole

A

Aplasia cutis

PTU should be used until 14-16 weeks

However, because of its rare association with hepatotoxicity, propylthiouracil should be limited to the first trimester and then maternal therapy should be converted to methimazole (or carbimazole) at a ratio of 15–20 mg of propylthiouracil to 1 mg of methimazole

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126
Q

How do you manage thyroid storm

A

Large doses of propylthiouracil (500–1000 mg loading dose and 250 mg every 4 h) should be given orally or by nasogastric tube or per rectum; the drug’s inhibitory action on T4 → T3 conversion makes it the antithyroid drug of choice.

If not available, methimazole can be used in doses of 20 mg every 6 h.

One hour after the first dose of propylthiouracil, stable iodide (5 drops SSKI every 6 h) is given to block thyroid hormone synthesis via the Wolff-Chaikoff effect (the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone).

Propranolol should also be given to reduce tachycardia and other adrenergic manifestations (60–80 mg PO every 4 h, or 2 mg IV every 4 h).

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127
Q

Treatment for severe Grave’s ophthalmopathy

A

Pulse therapy with IV methylprednisolone (e.g., 500 mg of methylprednisolone once weekly for 6 weeks, then 250 mg once weekly for 6 weeks) is preferable to oral glucocorticoids, which are used for moderately active disease

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128
Q

In children and young adults, the most common cause of acute thyroiditis

A

presence of a piriform sinus

usually due to a bacterial infection

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129
Q

Other name for subacute thyroiditis

A

de Quervain’s thyroiditis, granulomatous thyroiditis, or viral thyroiditis

The patient usually presents with a painful and enlarged thyroid, sometimes accompanied by fever

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130
Q

treatment for subacute thyroiditis

A

Relatively large doses of aspirin (e.g., 600 mg every 4–6 h) or nonsteroidal anti-inflammatory drugs (NSAIDs) are sufficient to control symptoms in many cases.

If this treatment is inadequate, or if the patient has marked local or systemic symptoms, glucocorticoids should be given. The usual starting dose is 15–40 mg of prednisone, depending on severity. The dose is gradually tapered over 6–8 weeks, in response to improvement in symptoms and the ESR

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131
Q

What subset of population is silent thyroiditis associated?

A

Painless thyroiditis, or “silent” thyroiditis, occurs in patients with underlying autoimmune thyroid disease and has a clinical course similar to that of subacute thyroiditis. The condition occurs in up to 5% of women 3–6 months after pregnancy and is then termed postpartum thyroiditis

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132
Q

Treatment for silent thyroiditis

A

Glucocorticoid treatment is not indicated for silent thyroiditis. Severe thyrotoxic symptoms can be managed with a brief course of propranolol, 20–40 mg three or four times daily. Thyroxine replacement may be needed for the hypothyroid phase but should be withdrawn after 6–9 months, as recovery is the rule

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133
Q

The most common clinically apparent cause of chronic thyroiditis is ___________ , an autoimmune disorder that often presents as a firm or hard goiter of variable size

A

Hashimoto’s thyroiditis

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134
Q

The most common hormone pattern in sick euthyroid syndrome (SES), also called nonthyroidal illness (NTI), is

A

a decrease in total and unbound T3 levels (low T3 syndrome) with normal levels of T4 and TSH.

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135
Q

TFT abnormalities in the ff
Acute liver disease?
Acutely ill psyciatric patients?
HIV infection?
Renal disease?

A

Acute liver disease is associated with an initial rise in total (but not unbound) T3 and T4 levels due to TBG release

. A transient increase in total and unbound T4 levels, usually with a normal T3 level, is seen in 5–30% of acutely ill psychiatric patients. TSH values may be transiently low, normal, or high in these patients.

In the early stage of HIV infection, T3 and T4 levels rise, even if there is weight loss. T3 levels fall with progression to AIDS, but TSH usually remains normal.

Renal disease is often accompanied by low T3 concentrations, but with normal rather than increased rT3 levels, due to an unknown factor that increases uptake of rT3 into the liver

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136
Q

Moreover, because amiodarone is stored in adipose tissue, high iodine levels persist for >___ months after discontinuation of the drug

A

6

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137
Q

Most effective long term solution for amiodarone induced thyroiditis

A

thyroidectomy

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138
Q

T/F

Thyroid function tests should be performed in all patients with goiter

A

True

to exclude thyrotoxicosis or hypothyroidism

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139
Q

Low urinary iodine levels (____) support a diagnosis of iodine deficiency

A

<50 μg/L

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140
Q

What are the UTZ findings suggestive of malignant thyroid mass in terms of composition, echogenicity, shape, margin and echogenic foci

A
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141
Q

In patients with thyroid mass, Tracheal deviation is common, but compression must usually exceed ___ % of the tracheal diameter before there is significant airway compromise

A

70

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142
Q

In hyperfunctioning solitary nodule, Thyrotoxicosis is usually mild and is generally only detected when a nodule is >____

A

3 cm

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143
Q

Tx of choice for hyperfunctioning solitary nodule

A

RAI

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144
Q

the most common malignancy of the endocrine system

A

Thyroid carcinoma

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145
Q

Risk Factors for Thyroid Carcinoma in Patients with Thyroid Nodule from History and Physical Examination

A
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146
Q

Activation of the _____ signaling pathway is seen in up to 70% of PTCs, although the types of mutations are heterogeneous

A

RET-RAS-BRAF

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147
Q

Most common type of thyroid CA

A

PTCA

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148
Q

T/F

Micrometastases is associated with poorer prognosis in PTCA

A

F

Micrometastases, defined as <2 mm of cancer in a lymph node, do not affect prognosis

However, gross metastatic involvement of multiple 2- to 3-cm lymph nodes indicates a 25–30% chance of recurrence and may increase mortality in older patients

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149
Q

Therefore, near-total thyroidectomy is appropriate for tumors >___ or in the presence of metastases or clinical evidence of extrathyroidal invasion.

A

4 cm

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150
Q

Mainstay of thyroid CA tx

A

Because most tumors are still TSH-responsive, LT4 suppression of TSH is a mainstay of thyroid cancer treatment

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151
Q

Target TSH for PTCA with the ff risk
Low risk?
Intermediate ?
High?
Known mets?

A

low risk = 0.5–2.0 mIU/L
Intermediate = 0.1–0.5 mIU/L
high risk of recurrence and known mets <0.1 mIU/L

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152
Q

Ideal TSH level before RAI for well differentiated thyroid CA

A

> 25 mIU/L

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153
Q

sensitive marker of residual/recurrent thyroid cancer after ablation of the residual postsurgical thyroid tissue

A

Serum thyroglobulin

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154
Q

Prognosis of anaplastic thyroid CA

A

The prognosis is poor, and most patients die within 6 months of diagnosis

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155
Q

Most common type of lymphoma of the thyroid

A

DLBCL

highly sensitive to external radiation
Surgery should be avoided (may spread dse)

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156
Q

which type of MEN has more aggresive form of MTC

A

MEN2B>2A

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157
Q

Next step if FNAB showed follicular neoplasm

A

consider molecular testing

25–40% risk of malignancy

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158
Q

Next step if FNAB showed Atypia or follicular lesion of undetermined significance

A

Repeat or consider molecular testing

~10–30% risk of malignancy

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159
Q

In dibetes insipidus, The 24-h urine volume exceeds __mL/kg body weight, and the 24-h urine osmolarity is < ___ mosm/L

A

The 24-h urine volume exceeds 40 mL/
kg body weight, and the 24-h urine osmolarity is <280 mosm/L

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160
Q

If symptoms of urinary frequency, enuresis, nocturia, and/or persistent thirst are present in the absence of glucosuria, the possibility of DI should be evaluated by

A

collecting a 24-h urine on unrestricted fluid intake

If the osmolarity is <280 mosm/L and the volume >50 mL/kg per day, the patient has DI and should be evaluated further to determine the type.

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161
Q

Next step in evaluating for DI after 24 hr urine volume and osmolarity

A

Get the basal plasma AVP

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162
Q

How do you differentiate primary polydipsia from pituitary DI

A

Pituitary bright spot is present in primary polydipsia since it reflects AVP stores

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163
Q

When treating DI with desmoperessin, Hyponatremia rarely develops unless urine volume is reduced to < ____ per day or fluid intake is excessive due to an associated abnormality in thirst or cognition

A

10 mL/kg

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164
Q

Treatment for hypodipsic hypernatremia

A

administering water orally if the patient is alert and cooperative or by infusing hypotonic fluids (0.45% saline or 5% dextrose and water) if the patient is not

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165
Q

Most common form of SIADH

A

The most common is one in which the AVP secretion responds normally to osmotic stimulation and suppression but the threshold or set point of the system is lower than normal

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166
Q

In SIADH, the excess body water should be eliminated. If the hyponatremia is mild and largely asymptomatic, restricting total water intake to ~_______ less than urine output for several days or until the syndrome remits spontaneously will usually suffice

A

30 mL/kg per day

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167
Q

Alternative treatment for SIADH if water restriction does not suffice

A

Infusion of 3% saline at a rate of ~0.05 mL/kg body weight per min raises serum sodium at a rate of ~1–2 meq/L per h, not only by replacing the slight sodium deficit but also by promoting a solute diuresis, which reduces total body water.

Alternatively, a vaptan can be used to reduce body water by increasing urine output.

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168
Q

How do you assess glucorticoid deficiency

A

to assess glucocorticoid deficiency, ACTH stimulation of cortisol production is used

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169
Q

How is ACTH stimulation done?

A

The standard ACTH stimulation test involves administration of cosyntropin (ACTH 1-24), 0.25 mg IM or IV, and collection of blood samples at 0, 30, and 60 min for cortisol.

A normal response is defined as a cortisol level >15–20 μg/dL (>400–550 nmol/L) 30–60 min after cosyntropin stimulation, with the precise cutoff dependent on the assay used

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170
Q

How is insulin tolerance test done?

A

The ITT involves administration of regular insulin 0.1 U/kg IV (dose should be lower if hypopituitarism is likely) and collection of blood samples at 0, 30, 60, and 120 min for glucose, cortisol, and growth hormone (GH), if also assessing the GH axis.

Oral or IV glucose is administered after the patient has achieved symptomatic hypoglycemia (usually plasma glucose <40 mg/dL).

A normal response is defined as a cortisol >20 μg/dL and GH >5.1 μg/L, again with assay-specific cutoff variability.

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171
Q

Cortisol is inactivated to cortisone by this microsomal enzyme

A

11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2)

Cortisol and aldosterone bind the mineralocorticoid receptor (MR) with equal affinity; however, cortisol circulates in the bloodstream at about a 1000-fold higher concentration.

Thus, only rapid inactivation of cortisol to cortisone by 11β-HSD2 prevents MR activation by excess cortisol, thereby acting as a tissue-specific modulator of the MR pathway

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172
Q

Ectopic ACTH production is predominantly caused by occult carcinoid tumors, most frequently in the ___

A

lung, but also in thymus or pancreas.

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173
Q

Screening tests for Cushings syndrome

A
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174
Q

Next step after having positive screening test for Cushing syndrome

A

Get ACTH level

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175
Q

Cutoff ACTH value for distinguishing ACTH dependent from independent Cushing

A
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176
Q

Next step after confirming ACTH INdependent Cushings

A

UNenhanced CT of the adrenals

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177
Q

Next step after confirming ACTH dependent Cushings

A
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178
Q

For ACTH-dependent cortisol excess, ______ is the investigation of choice

A

magnetic resonance image (MRI) of the pituitary
but it may not show an abnormality in up to 40% of cases because of small tumors below the sensitivity of detection

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179
Q

most common cause of mineralocorticoid excess is

A

primary aldosteronism

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180
Q

The clinical hallmark of mineralocorticoid excess is

A

hypokalemic hypertension

181
Q

Diagnostic screening for mineralocorticoid excess is not currently recommended for all patients with hypertension but should be restricted to those who

A

exhibit hypertension associated with drug resistance
hypokalemia
an adrenal mass
or onset of disease before the age of 40 years

182
Q

How long should you hold MR antagonists before doing ARR?

A

4 weeks

183
Q

What is a positive ARR

A

ARR screening is positive if the ratio is >750 pmol/L per ng/mL per hour, with a concurrently high normal or increased aldosterone

184
Q

What are the confirmatory tests for mineralocorticoid excess

A

The most straightforward is the saline infusion test, which involves the IV administration of 2 L of physiologic saline over a 4-h period.

Failure of aldosterone to suppress <140 pmol/L (5 ng/dL) is indicative of autonomous mineralocorticoid excess.

Alternative tests are the oral sodium loading test (300 mmol NaCl/d for 3 days) or the fludrocortisone suppression test (0.1 mg q6h with 30 mmol NaCl q8h for 4 days);

185
Q

Next step when Primary aldosteronism is confirmed but CT of adrenals is normal and with family of early onset hypertension

A

Screen for glucocorticoid remediable aldosteronism; if positive, start Dexa 0.125-0.5 mg/day

186
Q

What age should adrenal vein sampling be done in px with primary aldosteronism and unilateral adrenal mass?

A

> 40

187
Q

Screening test for incidentaloma

A
188
Q

CT scan features of an incidentaloma that makes it likely malignant

A

Tumor >= 4cm and >=20 HU

189
Q

Patients with confirmed ACC and successful removal of the primary tumor should receive adjuvant treatment with ______, particularly in patients with a high risk of recurrence as determined by tumor size >8 cm, histopathologic signs of vascular invasion, capsule invasion or violation, and a Ki67 proliferation index ≥10%

A

mitotane (o,p’DDD)

Adjuvant mitotane should be continued for at least 2 years, if side effects are tolerated. Regular monitoring of plasma mitotane levels is mandatory (therapeutic range 14–20 mg/L; neurotoxic complications more frequent at >20 mg/L).

Mitotane is usually started at 500 mg tid, with stepwise increases to a maximum dose of 2000 mg tid in days (high-dose saturation) or weeks (low-dose saturation) as tolerated.

190
Q

Most common cause of adrenal insufficiency

A

Hypothalamic-pituitary origin of disease

191
Q

Most common cause of primary adrenal insufficiency

A

autoimmune adrenalitis

192
Q

Electrolyte abnormalities present in primary adrenal insufficiency

A

adrenal insufficiency and is found in 80% of patients at presentation. Hyperkalemia is present in 40% of patients at initial diagnosis.

193
Q

Confirmatory test for adrenal insufficiency

A

The diagnosis of adrenal insufficiency is established by the short cosyntropin test

The cutoff for failure is usually defined at cortisol levels of <450–500 nmol/L (16–18 μg/dL) sampled 30–60 min after ACTH stimulation;

** same lang ang screening and confirmatory for adrenal insufficiency

194
Q

Next step when adrenal insufficiency is confirmed

A

Once adrenal insufficiency is confirmed, measurement of plasma ACTH, renin and aldosterone is the next step

195
Q

Treatment for acute adrenal insufficiency

A

Acute adrenal insufficiency requires immediate initiation of rehydration, usually carried out by saline infusion at initial rates of 1 L/h with continuous cardiac monitoring.

Glucocorticoid replacement should be initiated by bolus injection of 100 mg hydrocortisone, followed by the administration of 200 mg hydrocortisone over 24 h, preferably by continuous infusion or alternatively by bolus IV or IM injections.

Mineralocorticoid replacement can be initiated once the daily hydrocortisone dose has been reduced to <50 mg because at higher doses hydrocortisone provides sufficient stimulation of MRs.

196
Q

At what level of hydrocortisone requirement can you start the patient with acute adrenal insufficiency with mineralocorticoid replacement?

A

Mineralocorticoid replacement can be initiated once the daily hydrocortisone dose has been reduced to <50 mg because at higher doses hydrocortisone provides sufficient stimulation of MRs.

Mineralocorticoid replacement in primary adrenal insufficiency should be initiated at a dose of 100–150 μg fludrocortisone.

197
Q

Supraphysiologic glucocorticoid treatment with doses equivalent to _____ hydrocortisone or more will affect bone metabolism, and these patients should undergo regular bone mineral density evaluation

A

30 mg

198
Q

How is adequacy of treatment with mineralocorticoid replacement in px with acute adrenal insufficiency be measured

A

The adequacy of treatment can be evaluated by measuring blood pressure, sitting and standing, to detect a postural drop indicative of hypovolemia.

In addition, serum sodium, potassium, and plasma renin should be measured regularly. Renin levels should be kept in the upper normal reference range

199
Q

Next diagnostic step when primary adrenal insufficiency is confirmed

A

Adrenal autoantibodies

200
Q

Next diagnostic step when secondary adrenal insufficiency is confirmed

A

MRI of the pituitary

201
Q

the most common syndromic cause of obesity

A

Prader-Willi syndrome (PWS)

202
Q

Cancers associated with obesity

A

The largest effects are on colorectal, kidney, and pancreatic cancer, adenocarcinoma of the esophagus, and, in women, endometrial carcinoma

203
Q

For obese patietns it is recommended to initiate treatment with a calorie deficit of _____ compared with the patient’s habitual diet

A

500–750 kcal/d

Alternatively, a diet of 1200–1500 kcal/d for women and 1500–1800 kcal/d for men (adjusted for the individual’s body weight) can be prescribed

204
Q

How is very low calorie diet defined?

A

The primary purpose of a VLCD is to promote a rapid and significant (13- to 23-kg) short-term weight loss over a 3- to 6-month period. The proprietary formulas designed for this purpose typically supply ≤800 kcal, 50–80 g of protein, and 100% of the recommended daily intake for vitamins and minerals

205
Q

When is surgery indicated in obese patients?

A
206
Q

MOA of Lorcaserin for weight loss

A

5-HT2C receptor agonist

207
Q

Orlistat is a synthetic hydrogenated derivative of a naturally occurring lipase inhibitor, lipostatin, that is produced by the mold

A

Streptomyces toxytricini.

208
Q

Definition of moderate and severe obesity

A

severe obesity (BMI ≥40 kg/m2 ) or for those with moderate obesity (BMI ≥35 kg/m2 )

209
Q

the most commonly undertaken and most accepted bypass procedure for obesity

A

Roux-en-Y

210
Q

Criteria for diagnosing DM

A
211
Q

How frequent should a person diagnsed with GDM be worked up for DM

A

ADA recommends that women with a history of GDM undergo lifelong screening for the development of diabetes or prediabetes at least every 3 years

212
Q

Criteria for screening for T2DM

A
213
Q

useful marker of insulin secretion and allows discrimination of endogenous and exogenous sources of insulin in the evaluation of hypoglycemia

A

C peptide

214
Q

Glucose levels > ____ mmol/L or ____ mg/dK stimulate insulin synthesis

A

3.9 mmol/L (70 mg/dL)

215
Q

The major susceptibility gene for type 1 DM is located in the HLA region on chromosome ___ .

A

6

216
Q

Most prominent gene that is a variant of the _____that has been associated with both type 2 DM and IGT in several populations

A

transcription factor 7-like 2 gene

217
Q

The ADA suggests that metformin be considered in individuals with both IFG and IGT who are at very high risk for progression to diabetes (age <__ years, BMI ≥__ kg/m2, and women with a history of GDM)

A

60 yrs
BMI >=35

218
Q

When should you screen for distal symmetric polyneuropathy in patients with DM?

A

The ADA recommends annual screening for distal symmetric polyneuropathy beginning with the initial diagnosis of diabetes and annual screening for autonomic neuropathy 5 years after diagnosis of type 1 DM and at the time of diagnosis of type 2 DM. This testing is aimed at detecting loss of protective sensation (LOPS) caused by diabetic neuropathy

mnemonic: T2DM–> 2day mo na itest

219
Q

Is nephropathy considered micro or macrovascular complication of DM?

A

microvascular

220
Q

Recommended BP for px with T2DM

A

The American Diabetes Association (ADA) recommends blood pressure control <130/80 mmHg for individuals with high cardiovascular risk and <140/90 mmHg for individuals with lower cardiovascular risk.

221
Q

hallmark of proliferative diabetic retinopathy

A

The appearance of neovascularization in response to retinal hypoxemia is the hallmark of proliferative diabetic retinopathy

222
Q

When should you screen for albuminuria for px with T2DM

A

commence 5 years after the onset of type 1 DM and at the time of diagnosis of type 2 DM

basically same timeline with dx dystal symmetric neuropathy

223
Q

The ADA suggests a protein intake of _____ in individuals with diabetic kidney disease.

A

0.8 mg/kg of body weight/day

224
Q

In px with DM, Nephrology consultation should be considered when the estimated GFR is <____ or with atypical features such as hematuria, rapidly declining renal function, or proteinuria > 3 g/day.

Referral for transplant evaluation should be made when the GFR approaches _____

A

30 mL/min per 1.743 m2

20 mL/min per 1.73 m2

225
Q

Most commonly involved CN in DM neuropathy

A

CN III

226
Q

The most prominent GI symptoms for DM neuropathy are

A

delayed gastric emptying (gastroparesis) and altered small- and large-bowel motility (constipation or diarrhea).

227
Q

treatment for DM cystopathy

A

Diabetic cystopathy should be treated with scheduled voiding or self-catheterization.

228
Q

Class of DM drugs that cannot be used for CHF

A

TZD

229
Q

A possible increased risk of lower limb amputation and Fournier’sgangrene has been reported with what type of OHAS

A

SGLT-2 inhibitor therapy.

230
Q

most common pattern of dyslipidemia in DM

A

The most common pattern of dyslipidemia is hypertriglyceridemia and reduced HDL cholesterol levels.

231
Q

Statin of choice in px with renal dse

A

Atorvastatin

232
Q

Providers should consider screening for asymptomatic PAD in individuals >50 years of age who have diabetes and other risk factors using _____

A

ankle-brachial index testing

233
Q

The most common skin manifestations of DM are ____ and ___and are usually relieved by skin moisturizers.

A

xerosis and pruritus

234
Q

What constitutes the Whipples triad of hypoglycemia?

A

Whipple’s triad: (1) symptoms consistent with hypoglycemia, (2) a low plasma glucose concentration measured with a precise method, and (3) relief of symptoms after the plasma glucose level is raised.

235
Q

When hypoglycemia is prolonged beyond ~___, cortisol and growth hormone also support glucose production and restrict glucose utilization to a limited amount (both mechanisms are reduced by ~80% compared to epinephrine).

A

~4h

Thus, cortisol and growth hormone play no role in defense against acute hypoglycemia.

236
Q

What is the primary secondary and third defense against hypoglycemia

A
237
Q

Critical diagnostic findings in insulinoma

A

Critical diagnostic findings are a plasma insulin concentration ≥3 μU/mL (≥18 pmol/L), a plasma C-peptide concentration ≥0.6 ng/ mL (≥0.2 nmol/L), and a plasma proinsulin concentration ≥5.0 pmol/L when the plasma glucose concentration is <55 mg/dL (<3.0 mmol/L) with symptoms of hypoglycemia.

A low plasma β-hydroxybutyrate concentration (≤2.7 mmol/L) and an increment in plasma glucose level of >25 mg/dL (>1.4 mmol/L) after IV administration of glucagon (1.0 mg) indicate increased insulin (or IGF) actions

238
Q

Treatment for insulinoma

A

Surgical resection of a solitary insulinoma is generally curative.

Diazoxide, which inhibits insulin secretion, or octreotide can be used to treat hypoglycemia in patients with unresectable tumors

everolimus, an mTOR inhibitor, has also been successful in combination with the above approaches

239
Q

Treatment for hypoglycemia

A

If the patient is able and willing, oral treatment with glucose tablets or glucose-containing fluids, candy, or food is appropriate. A reasonable initial dose is 15–20 g of glucose. If the patient is unable or unwilling (because of neuroglycopenia) to take carbohydrates orally, parenteral therapy is necessary. IV administration of glucose (25 g) should be followed by a glucose infusion guided by serial plasma glucose measurements. If IV therapy is not practical, SC or IM glucagon (1.0 mg in adults) can be used, particularly in patients with T1DM.

oral glucose –> IV glucose –> SC/IM glucagon

240
Q

Symptoms of diabetes usually resolve when the plasma glucose is < ______, and thus most DM treatment focuses on achieving the second and third goals.

A

<11.1 mmol/L (200 mg/dL)

241
Q

What are the treatment goals for DM?

A
242
Q

To avoid exercise-related hyper- or hypoglycemia, individuals with type 1 DM should
(1) monitor blood glucose before, during, and after exercise
(2) delay exercise if blood glucose is ______ and ketones are present
(3) if the blood glucose is ____ , ingest carbohydrate before exercising
(4) monitor glucose during exercise and ingest carbohydrate as needed to prevent hypoglycemia
(5) decrease insulin doses (based on previous experience) before and after exercise and inject insulin into a nonexercising area
(6) learn individual glucose responses to different types of exercise.

A

(2) >14 mmol/L (250 mg/ dL)
(3) <5.0 mmol/L (90 mg/dL)

In individuals with type 2 DM, exercise-related hypoglycemia is less common but can occur in individuals taking either insulin or insulin secretagogues.

243
Q

Frequency of SMBG monitoring in px with T1DM or T2DM

A

> 3x/day

244
Q

In patients achieving their glycemic goal, the ADA recommends measurement of the HbA1c at least _____

A

twice per year.

245
Q

Longest acting insulin

A

Degludec

246
Q

Short-acting insulin analogues should be injected just before (______) and regular insulin (____) prior to a meal.

A

<10 min

30–45 min

247
Q

Highest Hba1c reduction

A

Biguanides and sulfonylureas

248
Q

OHAS associated with pancreatitis

A

GLP 1 agonists

249
Q

OHAS associated with inc risk of hyperkalemia

A

SGLT 2 inh

250
Q

OHAS associated with elevated LFT

A

a glucosidase inhibitor

251
Q

OHAS associated with Angioedema/urticarial and immune-mediated dermatologic effects

A

DPP4 inhibitor

252
Q

OHAS associated with CHF

A

Thiozolidinediones

** also contraindicated in hepatic insuffiency

253
Q

OHAS associated with Vit B12 deficiency

A

Biguanides

254
Q

OHAS that can cause weight gain

A

TZD and Insulin secretagogues

255
Q

Contraindications to alpha glucosidase inhibitor

A

These agents should not be used in individuals with inflammatory bowel disease, gastroparesis, or a serum creatinine >177 μmol/L (2 mg/dL)

256
Q

Effect of TZD on lipid profile

A

Rosiglitazone raises low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides slightly. (Lipid profile rose sa rosi-glitazone)

Pioglitazone raises HDL to a greater degree and LDL a lesser degree but lowers triglycerides

257
Q

SGLT 2 inhibitor assoc with inc risk of bladder CA

A

dapagliflozin

258
Q

Individuals who require >____ per day of long-acting insulin should be considered for combination therapy with metformin a GLP-1 receptor agonist, or a thiazolidinedione as these can reduce insulin requirements in some individuals with type 2 DM.

A

1 unit/kg

259
Q

How do you differentiate DKA vs HHS vs euglycemic DKA

A

See table

260
Q

Formula for corrected Na

A

(1.6-mmol/L [1.6-meq] reduction in serum sodium for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose)

261
Q

Why do you shift fluid to 0.45 saline in DKA

A

The change to 0.45% saline or using lactated Ringer’s helps to reduce the trend toward hyperchloremia later in the course of DKA

262
Q

When should long acting insulin be administered in tx patients with DKA?

A

Long-acting insulin, in combination with SC short-acting insulin, should be administered as soon as the patient resumes eating, because this facilitates transition to an outpatient insulin regimen and reduces length of hospital stay.

It is crucial to continue the insulin infusion or insulin SC until adequate insulin levels are achieved by administering long-acting insulin by the SC route. Even relatively brief periods of inadequate insulin administration in this transition phase may result in DKA relapse

263
Q

In euglycemic DKA associated with SGLT2 inhibitors, the pharmacologic effect may persist for____ days following discontinuation of SGLT2 inhibitor therapy as evidenced by ongoing glucosuria despite normoglycemia (glucose <180 mg/dL), during which time relapse of ketoacidosis is common if nutritional intake has not advanced (e.g., in the postoperative setting).

A

10–14

264
Q

Hyperglycemia usually improves at a rate of ______ per h as a result of insulin-mediated glucose disposal, reduced hepatic glucose release, and rehydration.

A

4.2–5.6 mmol/L (50–100 mg/dL)

265
Q

When the plasma glucose reaches ______ , glucose should be added to the 0.45% saline infusion to maintain the plasma glucose in the 8.3–11.1 mmol/L (150–200 mg/dL) range, and the insulin infusion should be continued at a lower rate to inhibit ketogenesis

A

11.1– 13.9 mmol/L (200–250 mg/dL)

More rapid correction of the serum glucose can precipitate the development of cerebral edema

266
Q

When may bicarbonate be given in DKA?

A

in the presence of severe acidosis (arterial pH <7.0), sodium bicarbonate (50 mmol [meq/L] in 200 mL of sterile water with 10 meq/L KCl per h) may be administered for the first 2 h until the pH is >7.0

267
Q

In DKA, If the serum phosphate is <_____, then phosphate supplement should be considered and the serum calcium monitored

A

0.32 mmol/L (1 mg/dL)

268
Q

Glycemic goals in inpx according to ADA

A

.The ADA suggests the following glycemic goals for hospitalized patients:
(1) in critically or non–critically ill patients: glucose of 7.8–10.0 mmol/L or 140–180 mg/dL;
(2) in selected patients: glucose of 6.1–7.8 mmol/L or 110–140 mg/dL with avoidance of hypoglycemia;
(3) the target range in the perioperative period should be 80–180 mg/dL (4.4–10.0 mmol/L)

269
Q

Insulin infusion is the preferred method for managing patients with type 1 DM over a prolonged (several hours) perioperative period or when serious concurrent illness is present (______u/h of regular insulin)

A

0.5–1.0 units

270
Q

If new-onset hyperglycemia remains during chronic treatment with supraphysiologic doses of glucocorticoid (>___ mg of prednisone or equivalent), the DM may be called “steroid-induced diabetes.”

A

5

271
Q

Current recommendations advise screening for glucose intolerance between weeks ____ of pregnancy in women not known to have diabetes

A

24 and 28

272
Q

What constitutes the harmonizing definition of metabolic syndrome?

A
273
Q

The most accepted and unifying hypothesis
to describe the pathophysiology of the metabolic syndrome

A

insulin resistance

274
Q

what in the lipid profile is an excellent marker of insulin resistance

A

hyperTAG

The other major lipoprotein disturbance in the metabolic syndrome is a reduction in HDL cholesterol.

275
Q

How much in % does fibrate decrease TAG

A

30-45%

276
Q

How much in % does nicotinic acid decrease TAG

A

20-35%

277
Q

only currently available drug with predictable
HDL cholesterol–raising properties

A

Nicotinic acid

nicotinic acid can increase HDL cholesterol by up to 30% above baseline

278
Q

Formula for corrected Calcium

A

An algorithm to correct for protein changes adjusts the total serum calcium (in mg/dL) upward by 0.8 times the deficit in serum albumin (g/dL) or by 0.5 times the deficit in serum immunoglobulin (in g/dL).

279
Q

Effect of aluminum hydroxide on Phosphate absorption

A

Decreased

280
Q

Effect of dec ph in calcium absorption

A

inc

281
Q

when should be phosphate measured?

A

basal, fatsing state due to wide variation throughout the day

282
Q

Dent’s disease is an X-linked recessive disorder caused by inactivating mutations in ____ , a chloride transporter expressed in endosomes of the proximal tubule;

A

CLCN5

features include hypercalciuria, hypophosphatemia, and recurrent kidney stones

283
Q

Respiratory failure and cardiac dysfunction, which are reversible with phosphate treatment, may occur at serum phosphate levels of ____

A

0.5–0.8 mmol/L (1.5–2.5 mg/dL).

284
Q

What is the rate of phosphate infusion in patients with hypophosphatemia?

A

See table

Hypocalcemia, if present, should be corrected before administering IV phosphate

285
Q

Hyperphosphatemia, defined in adults as a fasting serum phosphate concentration >____, usually results from impaired glomerular filtration, hypoparathyroidism, excessive delivery of phosphate into the ECF (from bone, gut, or parenteral phosphate therapy), or a combination of these factors

A

1.8 mmol/L (5.5 mg/dL)

same with K

286
Q

What is the treatment for hyperphosphatemia?

A

> Volume expansion may enhance renal phosphate clearance.
Aluminum hydroxide antacids or sevelamer may be helpful in chelating and limiting absorption of offending phosphate salts present in the intestine.
Hemodialysis is the most effective therapeutic strategy and should be considered early in the course of severe hyperphosphatemia, especially in the setting of renal failure and symptomatic hypocalcemia

287
Q

Hypomagnesemia usually signifies substantial depletion of body magnesium stores (___mmol/kg)

A

0.5–1

288
Q

What is the disadvantage of giving IV MgSO4 over MgCl2 in correcting for hypomagnesemia

A

MgSO4 may be given IV instead of MgCl2 , although the sulfate anions may bind calcium in serum and urine and aggravate hypocalcemia

289
Q

How is hypomagnesemia treated?

A

Mild, asymptomatic hypomagnesemia may be treated with oral magnesium salts (MgCl2 , MgO, Mg[OH]2 ) in divided doses totaling 20–30 mmol/d (40–60 meq/d).

More severe hypomagnesemia should be treated parenterally, preferably with IV MgCl2 , which can be administered safely as a continuous infusion of 50 mmol/d (100 meq Mg2+/d) if renal function is normal.

If GFR is reduced, the infusion rate should be lowered by 50–75%.

290
Q

How frequent should you repeat serum magnesium monitoring while correcting for hypomagnesemia

A

Serum magnesium should be monitored at intervals of 12–24 h during therapy, which may continue for several days because of impaired renal conservation of magnesium (only 50–70% of the daily IV magnesium dose is retained) and delayed repletion of intracellular deficits, which may be as high as 1–1.5 mmol/kg (2–3 meq/kg

291
Q

The most prominent clinical manifestations of hypermagnesemia are vasodilation and neuromuscular blockade, which may appear at serum magnesium concentrations >__ mmol/L (>_ meq/L; > _ mg/dL)

A

2 mmol/L (>4 meq/L; >4.8 mg/dL)

292
Q

How is hypermagnesemia treated?

A

Vigorous IV hydration should be attempted, if appropriate. Hemodialysis is effective and may be required in patients with significant renal insufficiency.

Calcium, administered IV in doses of 100–200 mg over 1–2 h, has been reported to provide temporary improvement in signs and symptoms of hypermagnesemia

293
Q

The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a ______

A

serum 25(OH)D level.

294
Q

The National Academy of Medicine has defined vitamin D sufficiency as a vitamin D level >____, although higher levels may be required to optimize intestinal calcium absorption in the elderly and those with underlying disease states, including obesity

A

50 nmol/L (>20 ng/mL)

295
Q

In patients who are vitamin D replete and are taking adequate calcium supplementation, the 24-h urinary calcium excretion should be in the range of ____ mg/24 h

A

100–250

Levels >250 mg/24 h predispose to nephrolithiasis and should lead to a reduction in vitamin D dosage and/or calciums supplementation

296
Q

Most common cause of hypercalcemia

A

hyperparathyroidism

If hypercalcemia has been manifest for >1 year, malignancy can usually be excluded as the caus

297
Q

Second most common cause of hypercalcemia

A

malignancy

298
Q

When the calcium level is >_____ calcification in kidneys, skin, vessels, lungs, heart, and stomach occurs, and renal insufficiency may develop, particularly if blood phosphate levels are normal or elevated due to impaired renal excretion.

Severe hypercalcemia, usually defined as ≥ _______can be a medical emergency; coma and cardiac arrest can occur

A

3.2 mmol/L (12.8 mg/dL)

3.7–4.5 mmol/L (14.8–18.0 mg/dL)

**factor is 4 in converting mmol to mg/dL

299
Q

The distinctive bone manifestation of hyperparathyroidism is ____

A

osteitis fibrosa cystica

300
Q

Indications for surgery in asymptomatic primary hyperparathyroidism

A
301
Q

What tests should be requested for monitoring primary hyperparathyroidism

A

Annually lahat except for skeletal (1-2 yrs)

302
Q

when does calcium go down after parathyroidectomy?

A

A decline in serum calcium occurs within 24 h after successful surgery;

usually, blood calcium falls to low-normal values for 3–5 days until the remaining parathyroid tissue resumes full hormone secretion

303
Q

What level of Calcium do you usually expect Chovstek’s and Trosseaus

A

Signs of hypocalcemia include symptoms such as muscle twitching, a general sense of anxiety, and positive Chvostek’s and Trousseau’s signs coupled with serum calcium consistently <2 mmol/L (8 mg/dL)

304
Q

What is the recommended rate of infusion when correcting for hypocalcemia?

A

An infusion of 0.5–2 mg/kg per hour or 30–100 mL/h of a 1-mg/mL solution usually suffices to relieve symptoms.

Usually, parenteral therapy is required for only a few days. If symptoms worsen or if parenteral calcium is needed for >2–3 days, therapy with a vitamin D analogue and/or oral calcium (2–4 g/d) should be started. It is cost-effective to use calcitriol (doses of 0.5–1 μg/d) because of the rapidity of onset of effect and prompt cessation of action when stopped, in comparison to other forms of vitamin D

305
Q

What is the effect of magnesium on PTH?

A

If magnesium deficiency is present, it can complicate the postoperative course since magnesium deficiency impairs the secretion of PTH

306
Q

responsible humoral agent in most solid tumors that cause hypercalcemia

A

PTHrP

307
Q

histolgy of solid tumor associated with hypercalcemia

A

Squamous cell tumors are most frequently associated with hypercalcemia, particularly tumors of the lung, kidney, head and neck, and urogenital tract.

308
Q

___- dependent reduction in 1,25(OH)2 D thus seems to be an important stimulus for the development of secondary hyperparathyroidism

A

FGF23

309
Q

The bone disease seen in patients with secondary hyperparathyroidism and CKD is termed ____ and affects primarily bone turnover

A

renal osteodystrophy

310
Q

How is hypocalcemia due to secondary hyperparathyroidism treated?

A

> includes reduction of excessive blood phosphate by restriction of dietary phosphate, the use of nonabsorbable phosphate binders, and careful, selective addition of calcitriol (0.25–2 μg/d) or related analogues.

> Calcium carbonate became preferred over aluminum containing antacids to prevent aluminum-induced bone disease. However, synthetic gels that also bind phosphate (such as sevelamer) are now widely used, with the advantage of avoiding not only aluminum retention but also excess calcium loading, which may contribute to cardiovascular calcifications.

> Intravenous calcitriol (or related analogues), administered as several pulses each week, helps control secondary hyperparathyroidism.

311
Q

Most common form of hyperparathyroidism

A

Asymptomatic

312
Q

Lab test that may help differentiate hyperpathyroidism with other causes of hypercalcemia

A

The immunoassay for PTH usually separates hyperparathyroidism from all other causes of hypercalcemia (exceptions are very rare reports of ectopic production of excess PTH by nonparathyroid tumors).

Patients with hyperparathyroidism have elevated PTH levels despite hypercalcemia, whereas patients with malignancy and the other causes of hypercalcemia (except for disorders mediated by PTH such as lithium-induced hypercalcemia) have levels of hormone below normal or undetectable

313
Q

How can 1,25(OH)2 D levels differetiate primary hyperparathyroidism from other disorders associated with hypercalcemia?

A

1,25(OH)2 D levels are elevated in many (but not all) patients with primary hyperparathyroidism. In other disorders associated with hypercalcemia, concentrations of 1,25(OH)2 D are low or, at the most, normal

Measurement of 1,25(OH)2 D is critically valuable in establishing the cause of hypercalcemia in sarcoidosis and certain lymphomas.

314
Q

What tx option for severe hypercalcemia may present with fever?

A

Pamidronate
P-eber

315
Q

What tx option for severe hypercalcemia has the highest antiresorptive properties?

A

Denosumab

316
Q

What tx option for severe hypercalcemia is associated with tachyphylaxis?

A

Calcitonin

317
Q

a monoclonal antibody that binds to RANK ligand (RANKL) and prevents it from binding to the receptor RANK on osteoclast precursors and mature osteoclasts.

A

Denosumab

318
Q

Duration of effec of calcitonin

A

Calcitonin, after 24 h of use, is no longer effective in lowering calcium

319
Q

The malignancies in which hypercalcemia responds to glucocorticoids include

A

multiple myeloma, leukemia, Hodgkin’s disease, other lymphomas, and carcinoma of the breast, at least early in the course of the diseases

319
Q

Approach to management of severe hypercalcemia

A

Severe hypercalcemia (≥3.7 mmol/L [15 mg/dL]) requires rapid correction. IV pamidronate or zoledronate or subcutaneous denosumab should be administered.

In addition, for the first 24–48 h, aggressive sodium-calcium diuresis with IV saline should be given and, following rehydration, large doses of furosemide or ethacrynic acid, but only if appropriate monitoring is available and cardiac and renal function are adequate

320
Q

Definition of osteoporosis

A

2.5 standard deviations (SDs) or more below the mean for young healthy adults of the same sex and race—also referred to as a T-score of –2.5.

Patients who present with hip or spine fractures by definition have osteoporosis and will require treatment for both the fractureitself and the underlying skeletal disorder

321
Q

How does vitamin d insufficiency cause osteoporosis?

A

Vitamin D insufficiency leads to compensatory secondary hyperparathyroidism and is an important risk factor for osteoporosis and fractures

322
Q

How does estrogen deficiency cause bone loss?

A

Estrogen deficiency causes bone loss by two distinct but interrelated mechanisms: (1) activation of new bone remodeling sites and (2) initiation or exaggeration of an imbalance between bone formation and resorption, in favor of the latter

Loss of estrogen increases production of RANKL and reduces production of osteoprotegerin, increasing osteoclast formation and recruitment

323
Q

What are the drugs associated with osteoporosis?

A

See table

Glucocorticoids are the most common cause of medication-induced osteoporosis

324
Q

What are the indications for BMD testing?

A
325
Q

Indications for vertebral testing

A
326
Q

When osteoporosis is found associated with symptoms of rash, multiple allergies, diarrhea, or flushing, mastocytosis should be considered and excluded by using ______

A

24-h urine histamine collection or serum tryptase

326
Q

Biochemical markers of bone metabolism

A
327
Q

Adequate calcium intake per age group

A
328
Q

SERM that protects the uterus and breast from effects of estrogen and makes the use of progestin unnecessary

A

Bazedoxifene

329
Q

Tamoxifen is protective against breast CA but increases the risk for this type of CA

A

uterine

unlike raloxifene

330
Q

Contraindication of alendronate

A

contraindicated in patients who have stricture or inadequate emptying of the esophagus

331
Q

Adverse events associated with bisphosphonate

A

All bisphosphonates have been associated with some musculoskeletal and joint pains of unclear etiology, which are occasionally severe. There is potential for renal toxicity, and bisphosphonates are contraindicated in those with an estimated glomerular filtration rate <30–35 mL/min. Hypocalcemia can occur.

Also associated with osteonecrosis of the jaw and atypical femoral fracture

332
Q

What treatment for osteoporosis when discontinued is associated with rebound increase in bone turnover and bone loss

A

When denosumab is discontinued, there is a rebound increase in bone turnover and an apparent acceleration of bone loss. This likely reflects the maturation of osteoclast precursors that have accumulated in marrow when the drug was administered and can become mature bone resorbing cells once the drug is withdrawn

333
Q

a humanized antibody that blocks the osteocyte production of sclerostin, resulting in an increase in bone formation and decline in bone resorption

A

romosozumab

334
Q

a cathepsin K inhibitor, inhibits the osteoclast collagenase enzyme, preventing bone resorption but not affecting osteoclast viability

A

odanacatib

335
Q

Currently ______ measured on a fasting serum sample in the morning is the preferred marker of bone resorption, and ____ or ____ the is the preferred marker for formation

A

collagen C-telopeptide

osteocalcin or propeptide of type 1 collagen (P1NP)

336
Q

All patients on long-term (>___ months) glucocorticoids should have measurement of bone mass at both the spine and the hip using DXA

A

3

If only one skeletal site can be measured, it is best to assess the spine in individuals <60 years and the hip in those >60 years.

337
Q

Which of the following is more characteristic of an ACTH-secreting pituitary tumor as compared to an ectopic ACTH secretion?
A. Rapid in onset
B. More common in males than females
C. Serum potassium is < 3.3 ug/L in less than 10 percent of cases
D. Cortisol > 5ug/dL after high dose dexamethasone suppression testing

A

C. Serum potassium is < 3.3 ug/L in less than 10 percent of cases

338
Q

Which of the following organisms cause chronic thyroiditis?
A. Aspergillus
B. Mycobacteria
C. Strongyloides
D. Viral

A

C. Strongyloides

339
Q

What is the putative trigger to develop Type 1 DM in genetically susceptible individuals?
A. Coxsackie virus
B. Parvovirus
C. HIV
D. HPV

A

A. Coxsackie virus

340
Q

A 35/M was previously diagnosed by his primary care physician with diabetes 5 years ago. He was initially started on insulin but was eventually shifted to metformin once his sugar was controlled. On physical exam, his BMI is 20 kg/m2 and does not exhibit acanthosis nigricans. He, however, complains of alopecia. CBG taken was 350 mg/dl but stat ketones were negative. On work-up, islet antibodies were positive. What is the most likely diagnosis for this patient?
A. Ketosis-prone type 2 diabetes mellitus
B. Latent autoimmune diabetes of the adult
C. Maturity-onset diabetes of the young
D. Fulminant diabetes

A

B. Latent autoimmune diabetes of the adult

341
Q

A 38/F came into your clinic concerned about having diabetes. She has a strong family history of the disease and her father progressed to dialysis-requiring renal failure because of it. Her BMI is 28 kg/m2. She was otherwise asymptomatic and physical examination was unremarkable. When is it appropriate to screen diabetes and repeat the test if results are normal?
A. Now then every year thereafter
B. Now then every three years
C. Age 40 then every year thereafter
D. Age 40 then every three years

A

A. Now then every year thereafter

342
Q

What lipid lowering drug has been shown to reduce the progression of retinopathy without reducing cardiovascular events?
A. Statins
B. Fenofibrate
C. Niacin
D. Bile acid resin

A

B. Fenofibrate

343
Q

The body’s behavioral defense against hypoglycemia is effective at what glycemic threshold?
A. 80-85 mg/dL
B. 65-70 mg/dL
C. 50-55 mg/dL
D. <50 mg/dL

A

C. 50-55 mg/dL

344
Q

Which of the following patients with subclinical hypothyroidism will benefit from levothyroxine?
A. 45 year old woman with palpitations
B. 50 year old man, asymptomatic, TSH of 15 mIU/L
C. 55 year old perimenopausal woman
D. 60 year old man, admitted for pneumonia

A

B. 50 year old man, asymptomatic, TSH of 15 mIU/L

since TSH >10

345
Q

A 19-year-old college student comes to the clinic reporting infrequent palpitations. He reports no other symptoms. He had thyroid tests done revealing the following: TSH 0.35 Uiu/ml (N 0.4-6.0), FT4 1.5 ng/dL (N 0.8-2.0), FT3 5.6 pmol/L (N 4.0-7.4). PE, including neck exam, is unremarkable. What is the diagnosis?
A. Primary thyrotoxicosis
B. Subacute thyroiditis
C. Subclinical hyperthyroidism
D. Subclinical hypothyroidism

A

C. Subclinical hyperthyroidism

346
Q

A 22-year-old woman presents with tremors, palpitations, diffusely enlarged thyroid gland and characteristic eye stare. Tests show low TSH and elevated FT3 and FT4. She is started on once-daily methimazole. 2 weeks later, she calls you to report fever and a sore throat. What will be your advice?
A. Discontinue the drug and have a CBC done
B. Hold the drug until the fever subsides
C. Substitute the methimazole with propylthiouracil
D. Take paracetamol and reassure the patient

A

A. Discontinue the drug and have a CBC done

347
Q

A 33-year-old consults in the clinic for a palpable thyroid nodule. She denies any hypo-/ hyperthyroid symptoms. On ultrasound, the nodule appears fluid-filled, with smooth, sharp borders. What is the most likely diagnosis?
A. Classic papillary carcinoma
B. Colloid nodule
C. Hurthle cell adenoma
D. Thyroid metastasis

A

B. Colloid nodule

348
Q

A 42-year-old comes in for a follow-up visit. She has been diagnosed with papillary thyroid cancer, initially presenting with a palpable thyroid nodule. She has undergone total thyroidectomy, with a tumor size of 1.5 cm. There are no signs of regional and distal metastases. What is the next step in this patient’s management?
A. Field radiation therapy
B. Multi-drug chemotherapy
C. Radioiodine treatment
D. TSH suppression therapy

A

D. TSH suppression therapy

349
Q

A 30-year-old woman came in due to 5 year history of gradually enlarging anterior neck mass. Biopsy reveals papillary thyroid carcinoma. A total thyroidectomy is done but there is residual thyroid tissue due to the encasement of internal carotid area. What will be the TSH goal of this patient?
A. <0.1 mIU/L
B. 0.1-0.5 mIU/L
C. 0.5-1 mIU/L
D. 0.5-2 mIU/L

A

A. <0.1 mIU/L

350
Q

Which of the following is characteristic of primary adrenal insufficiency?
A. High ACTH, high renin, low aldosterone
B. High ACTH, low renin, high aldosterone
C. Low ACTH, high renin, low aldosterone
D. Low ACTH, low renin, high aldosterone

A

A. High ACTH, high renin, low aldosterone

351
Q

A 46-year-old man is referred to you for a consideration of pheochromocytoma, after presenting with headaches, palpitations and anxiety. Except for hypertension, his medical history is unremarkable. Medications are lisinopril and amlodipine. On PE, BP is 170/90 mmHg, and HR is 90/min. The remainder of the PE is unrevealing. Plasma free metanephrines are 3.5x elevated. What is the most appropriate next step in the management?
A. Discontinue antihypertensives and repeat biochemical testing
B. Perform clonidine suppression test
C. Perform contrast-enhanced adrenal CT scan
D. Start propranolol for additional BP control and relief of palpitations

A

C. Perform contrast-enhanced adrenal CT scan

352
Q

Aside from symptomatic relief of menopause, which of the following is a definite benefit from the use of postmenopausal hormonal therapy?
A. Decrease in risk of dementia in older women
B. Decrease in risk of endometrial cancer
C. Increase in bone mineral density
D. Increase in risk of gallbladder disease

A

C. Increase in bone mineral density

353
Q

A 58-year old consults for vaginal dryness, hot flashes and sleep disturbances. She is menopause since 3 years prior. Medical history is pertinent for controlled type 2 diabetes diagnosed 7 years prior, diabetic kidney disease (eGFR 56 mL/min/1.73m2 ), non-alcoholic fatty liver disease (NAFLD), glaucoma and depressive disorder. Medications include once-daily metformin, silymarin, fluoxetine and timolol eyedrops. She asks about hormonal therapy, but is wary due to her multiple co-morbid illnesses. Which of the following is a contraindication in this patient’s case?
A. Concomitant antidepressant use
B. History of glaucoma
C. Liver disease
D. Low eGFR

A

C. Liver disease

Others: unexplained vaginal bleeding, VTE, thrombophilia

354
Q

A 45-year-old woman is referred to you for “abnormal FBS.” She has no known co-morbidities, and a routine fasting sugar is 122 mg/dL. BMI is 36. Which of the following medications will offer the greatest weight loss?
A. Insulin
B. Metformin
C. Orlistat
D. Pioglitazone

A

C. Orlistat

Weight loss 9-10%/yr

355
Q

Patients with dka would present with high or low triglycerides?

A

high

356
Q

Which of the following risk factors has the highest relative risk for the occurrence of diabetes mellitus (DM)? (UNITE CPG)
A. Conditions associated with insulin resistance (e.g. acanthosis nigricans)
B. Previous history of gestational DM
C. Previous history of increased fasting glucose (IFG)
D. Previous history of impaired glucose tolerance (IGT)

A

C. Previous history of increased fasting glucose (IFG)

357
Q

medications approved for use in the management of chronic painful diabetic neuropathy

A

Duloxetine and Pregabalin

358
Q

Which of the following fulfills criteria for metabolic syndrome according to the Harmonizing Definition Criteria?
A. Filipino female, with BP of 130/80 mmHg
B. Filipino female, with HDL of 45 mg/dL
C. Filipino male, with waist circumference of 84 cm
D. Filipino male, with fasting blood sugar of 92 mg/dL

A

B. Filipino female, with HDL of 45 mg/dL

HDL<50 in F

359
Q

Definition of osteopenia

A

-1 to -2.5

360
Q

In which of the following situations will you recommend bone mineral density testing?
A. 20-year old man, smoker, with family history of fragility fracture
B. 30-year old woman with lupus, on prednisone 10mg/day for the last 6 months
C. 50-year old man with back pain and a lumbosacral x-ray showing bone spurs
D. 60-year old woman, formerly a marathon runner

A

B. 30-year old woman with lupus, on prednisone 10mg/day for the last 6 months

prednisone >5 mg/day for >3 mos

361
Q

During pregnancy, propylthiouracil should be limited to the first trimester. Subsequently, maternal anti-thyroid therapy should be converted to methimazole at a ratio of:
a. 5-10 mg of propylthiouracil to 1 mg of methimazole
b. 15–20 mg of propylthiouracil to 1 mg of methimazole
c. 25-30 mg of propylthiouracil to 1 mg of methimazole
d. 30-40 mg of propylthiouracil to 1 mg of methimazole

A

b. 15–20 mg of propylthiouracil to 1 mg of methimazole

362
Q

Which of the following characteristics about ACTH-secreting pituitary tumors best differentiate it from ectopic ACTH secretion?
a. 24 hour urine free cortisol is elevated
b. Cortisol is <5 ug/dL after high-dose dexamethasone suppression
c. Associated with pigmentation and rapid onset of clinical features
d. Basal inferior petrosal : peripheral vein ACTH ratio is <2

A

b. Cortisol is <5 ug/dL after high-dose dexamethasone suppression

24 hr urine free cortisol is elevated in both

High dose Dexa suppression test will be able to inhibit cortisol production in ACTH-dependent pituitary tumors via the feedback mechanism but has NO EFFECT on ECTOPIC ACTH sources

Rapid onset of symptoms and pigmentation are associated with ECTOPIC ACTH secretion

Basal inferior petrosal : peripheral vein ACTH ratio of <2 is consistent with ECTOPIC ACTH secretion

363
Q

Which of the following statements is true regarding diagnostic workup for adrenal incidentalomas?
a. MRI with GAD is the procedure of choice for imaging the adrenal glands.
b. FNA or CT-guided biopsy of an adrenal mass is rarely indicated.
c. Tumor density can reliably differentiate adrenal adenomas from carcinomas
d. Tumors >4 cm are more likely malignant with a 90% specificity

A

b. FNA or CT-guided biopsy of an adrenal mass is rarely indicated.

364
Q

Which of the following features present in primary adrenal insufficiency best distinguish it from secondary adrenal insufficiency?
a. Alabaster-colored skin
b. Hyponatremia
c. Hyperreninemia
d. Low blood pressure

A

Hyperreninemia

PRIMARY ADRENAL INSUFFICIENCY
Characterized by the loss of both glucocorticoid and mineralocorticoid secretion

A distinguishing feature of primary adrenal insufficiency is hyperpigmentation, which is caused by excess ACTH stimulation of
melanocytes.

Hyponatremia can be present in both mineralocorticoid deficiency and in secondary adrenal insufficiency due to diminished inhibition of ADH release by cortisol.

Increased plasma renin will confirm presence of mineralocorticoid deficiency

Low BP and postural hypotension can be present in both

365
Q

Which of the following statements most accurately reflect frequently used insulin regimens in Type 1 DM
a. In general, Type 1 DM patients require 1-2 units/kg per day of insulin.
b. A common insulin-to-carbohydrate ratio is 1 unit per 15 g of carbohydrate.
c. Insulin is given as multiple doses with 70% given as basal insulin.
d. Supplemental insulin is given at 2 units of insulin for every 50 mg/dL over glucose target.

A

b. A common insulin-to-carbohydrate ratio is 1 unit per 15 g of carbohydrate.

a. In general, Type 1 DM patients require 1-2 units/kg per day of insulin. In general, individuals with type 1 DM require 0.3-0.7 units/kg per day

c. Insulin is given as multiple doses with 70% given as basal insulin. –> 50%

d. Supplemental insulin is given at 2 units of insulin for every 50 mg/dL over glucose target. –> 1-2u for every 30-60 over target

366
Q

A 70/F with T2DM on metformin complains of frequent nausea, diarrhea and anorexia. Since she is not able to eat properly, she has intermittent episodes of light headedness and blurring of vision. Her current HBA1c is 8.5. Which of the following glucose-lowering agents is best suited for her in place of metformin?
a. Dapagliflozin
b. Miglitol
c. Repaglinide
d. Glimepiride

A

a. Dapagliflozin

367
Q

Which of the following T2DM patients will benefit the most in the initiation of insulin therapy?
a. 40/M with waist circumference of 95 cm
b. 45/F with HbA1c of 8.0 on metformin monotherapy
c. 50/M with FBS of 190 mg/dL not yet on any meds
d. 55/F with tuberculosis-related cachexia

A

d. 55/F with tuberculosis-related cachexia

Insulin is the safest and most effective option in such cases to achieve glycemic control and prevent further catabolic effects of hyperglycemia.

Insulin should be considered as part of the initial therapy in type 2 DM, particularly in:
* lean individuals
* those with severe weight loss
* in individuals with underlying renal or hepatic disease that precludes oral glucose-lowering agents
* In individuals who are hospitalized or acutely ill.

368
Q

A 50/M with T2DM was rushed in the ER due to severe abdominal pain and vomiting. Blood glucose was 300 mg/dL with an arterial pH of 7.2 and a serum bicarbonate of 12 mEq/L. Serum creatine was 250 mmol/L, sodium was 122, chloride was 79 and potassium was 3.0 mEq/L. Which of the following management measures is the most appropriate for the patient’s condition?

a. Administer short-acting regular insulin IV (0.1 units/kg) bolus then 0.1 units/kg/hr by infusion.
b. Give 150 mEqs sodium bicarbonate bolus then give additional 250 mEqs by infusion over 24 hours.
c. Measure electrolytes and anion gap every 4 hours for first 24 hours.
d. Run 2-3 L of 0.45% saline at 10-20 mL/kg/hr over the first 1-3 hours.

A

c. Measure electrolytes and anion gap every 4 hours for first 24 hours.

a. Administer short-acting regular insulin IV (0.1 units/kg) bolus then 0.1 units/kg/hr by infusion. - Hook to kcl first

b. Give 150 mEqs sodium bicarbonate bolus then give additional 250 mEqs by infusion over 24 hours.- not indicated since pH 7.2

d. Run 2-3 L of 0.45% saline at 10-20 mL/kg/hr over the first 1-3 hours.- should be PNSS since Na is only 122

369
Q

A 56/M with T2DM was admitted in the ICU due to acute respiratory failure from hospital acquired pneumonia. His CBGs have been ranging from 200 – 300 mg/dL. Which of the following glycemic-lowering agents is most appropriate for him?

a. Insulin glulisine as subcutaneous boluses
b. Regular insulin as intravenous infusion
c. Insulin apidra as intravenous boluses
d. Insulin glargine as single subcutaneous bolus

A

b. Regular insulin as intravenous infusion

IV regular insulin is the standard of care for critically ill patients because:
It provides rapid onset and precise control of blood glucose levels.
It allows for easy titration and adjustment based on frequent glucose monitoring, which is essential in ICU settings.
It is recommended in situations like sepsis, acute illness, or respiratory failure where glycemic variability is high.

370
Q

A 45/M T2DM patient complained of frequent light headedness, diaphoresis and palpitations. His CBGs ranges from 45-80 mg/dL/ His workup revealed a 1.0 cm pancreatic head mass on abdominal CT scan. Which of the following pathophysiologic features best explain his symptoms in correlation with his disease?
a. Failure of insulin secretion to fall during hypoglycemia
b. Overproduction of an incomplete form of insulin growth factor II
c. Impaired gluconeogenesis and low gluconeogenic precursors
d. Combined deficiency of glucagon and epinephrine

A

a. Failure of insulin secretion to fall during hypoglycemia

The patient’s symptoms of frequent lightheadedness, diaphoresis, palpitations, and low CBG levels (45–80 mg/dL), along with the finding of a 1.0 cm pancreatic head mass, suggest an insulinoma.

371
Q

What is the drug of choice for a diabetic 30/F presenting with a triglyceride level of 600 mg/dL despite active lifestyle management?
a. Atorvastatin
b. Cholestyramine
c. Ezetemibe
d. Omega-3 FA

A

d. Omega-3 FA

Omega-3 fatty acids are highly effective for lowering triglycerides, especially in severe cases.

Statins are primarily used for lowering LDL cholesterol and reducing cardiovascular risk. While they have a modest triglyceride-lowering effect (10–30%), they are not sufficient for severe hypertriglyceridemia (≥500 mg/dL).

Bile acid sequestrants lower LDL cholesterol but can raise triglyceride levels, especially in patients with baseline hypertriglyceridemia.

372
Q

Prophylactic radiation therapy may be indicated to prevent the development of what syndrome after adrenalectomy in the setting of residual corticotrope adenoma?
a. Albright syndrome
b. Kallmann syndrome
c. Nelson syndrome
d. Wolfram syndrome

A

c. Nelson syndrome

NELSON’S SYNDROME A disorder characterized by rapid pituitary tumor enlargement and increased pigmentation secondary to high ACTH levels. Prophylactic radiation therapy may be indicated to prevent the development of Nelson’s syndrome after adrenalectomy.

373
Q

A 30/M patient presents in the ICU with progressive decrease in sensorium. He underwent cranial surgery for head trauma 2 days prior. Pertinent workup revealed a serum sodium of 168 mmol/L. Average 24 hour urine output for the past 2 days was 4000 mL. Which of the following findings will best point to his likely diagnosis?
a. Urine osmolarity of <300 mosm/L
b. Plasma AVP <1 pg/mL
c. No pituitary bright spot on MRI
d. Plasma osmolarity of >300 mosm/L

A

c. No pituitary bright spot on MRI

Acute hypernatremia and increased volume of urine in the setting of post-cranial surgery is highly suggestive of post-op pituitary diabetes insipidus

Urine osmolarity of <300 mosm/L is present in pituitary DI, primary polydipsia and nephrogenic DI

Plasma AVP <1 pg/mL is present in both primary polydipsia and pituitary DI

The pituitary bright spot is almost always absent or abnormally small in patients with pituitary DI Plasma osmolarity of >300 can be present in both DI and non-DI etiologies

374
Q

Which of the following is a specific feature of Cushing’s syndrome?
a. Buffalo hump
b. Proximal myopathy
c. Facial plethora
d. Hirsutism

A

b. Proximal myopathy

A diagnosis of Cushing’s should be considered when several clinical features are found in the same patient, in particular when more specific features are found. These include fragility of the skin, with easy bruising broad (>1 cm), purplish striae signs of proximal myopathy, which becomes most obvious when trying to stand up from a chair without the use of hands or when climbing stairs

375
Q

A 35/M presents with consistent home BPs of 160-170/100-110 despite compliance with telmisartan. Pertinent labs revealed a serum potassium of 3.0 mEq/L. Which of the following is the most practical strategy to observe in preparation for further workup for the cause of his hypertension?
a. Order for plasma renin and aldosterone levels right away
b. Stop telmisartan at least 2 weeks prior to ARR measurement
c. Stop telmisartan and shift to carvedilol 4 weeks prior to ARR measurement
d. Continue telmisartan and correct hypokalemia prior to ARR measurement

A

d. Continue telmisartan and correct hypokalemia prior to ARR measurement

The accepted screening test is concurrent measurement of plasma renin and aldosterone with subsequent calculation of the aldosterone-renin ratio (ARR)

Serum potassium should be normalized prior to testing Stopping antihypertensive medication can be cumbersome, particularly in patients with severe hypertension. For practical purposes, in the first instance the patient can remain on the usual antihypertensive medications, with the exception that MR antagonists need to be ceased at least 4 weeks prior to ARR measurement.

Carvedilol can falsely increase ARR

376
Q

Which of the following monogenic forms of DM will respond well to sulfonylurea treatment?
a. MODY 1
b. MODY 2
c. MODY 3
d. MODY 4

A

c. MODY 3

MONOGENIC FORMS OF DM MODY 1, MODY 3, and MODY 5 are caused by mutations in hepatocyte nuclear transcription factor (HNF) 4a, HNF-1a, and HNF-1B, respectively.

Individuals with an HNF-1a mutation (MODY 3) have a progressive decline in glycemic control but may respond to sulfonylureas.

Individuals with MODY 2, the result of mutations in the glucokinase gene, have mild-to-moderate, but stable hyperglycemia that does not respond to oral hypoglycemic agents

MODY 4 is a rare variant caused by mutations in pancreatic and duodenal homeobox 1, a transcription factor that regulates pancreatic development and insulin gene transcription

377
Q

Which of the following screening procedures is part of the guidelines for comprehensive diabetes care for all individuals with DM?

a. Lipid profile testing every 6 months
b. Urine albumin testing every 4 months
c. Blood pressure assessment every 3 months
d. Foot examination by the patient monthly

A

c. Blood pressure assessment every 3 months

Lipids annually

Diabetes-related kidney disease testing annually Blood pressure assessment quarterly

Foot examination
1-2 times/year by provider
Daily by patient

378
Q

Which of the following statements is true regarding the properties of glycated hemoglobin?
a. It detects glycemic variability like self-monitoring of blood glucose
b. Glycemic level in the preceding month contributes about 70% to the HbA1c value.
c. Recent intercurrent illnesses can impact HbA1c.
d. Nocturnal hyperglycemia will be reflected in the HbA1c.

A

d. Nocturnal hyperglycemia will be reflected in the HbA1c.

ASSESSMENT OF LONG TERM GLYCEMIC CONTROL
Measurement of glycated hemoglobin (HbA1c) is the standard method for assessing long-term glycemic control.

Glycemic level in the preceding month contributes about 50% to the HbA1c value

As the primary predictor of long-term complications of DM, the HbA1c should mirror, to a certain extent, the short-term measurements of SMBG

These two measurements are complementary in that recent intercurrent illnesses may impact the SMBG measurements but not the HbA1c

Likewise, postprandial and nocturnal hyperglycemia may not be detected by the SMBG of fasting and preprandial capillary plasma glucose but will be reflected in the HbA1c

The HbA1c is an “average” and thus does not detect glycemic variability in the way SMBG and CGM can.

379
Q

Which of the following statements is true regarding the properties of the different classes of glucose-lowering agents?
a. SGLT2 inhibitors are more effective than biguanides in lowering HbA1c
b. DPP-IV inhibitors begin to lower the plasma glucose immediately
c. GLP-1 receptor agonists directly cause hypoglycemia d. Sulfonylureas exhibit longer glycemic control than thiazolidinediones

A

b. DPP-IV inhibitors begin to lower the plasma glucose immediately

Insulin secretagogues, biguanides, GLP-1 receptor agonists, and thiazolidinediones improve glycemic control to a similar degree (1–2% reduction in HbA 1c) and are more effective than a-glucosidase inhibitors, DPP-IV inhibitors, and SGLT2 inhibitors

Assuming a similar degree of glycemic improvement, the clinical advantage of one class of drugs is not clear; any therapy that improves glycemic control is likely beneficial.

Insulin secretagogues, GLP-1 receptor agonists, DPP-IV inhibitors, a-glucosidase inhibitors, and SGLT2 inhibitors begin to lower the plasma glucose immediately, whereas the glucose-lowering effects of the biguanides and thiazolidinediones are delayed by weeks .

Not all agents are effective in all individuals with type 2 DM.

Biguanides, a-glucosidase inhibitors, GLP-1 receptor agonists, DPP-IV inhibitors, thiazolidinediones, and SGLT2 inhibitors do not directly cause hypoglycemia

Most individuals will eventually require treatment with more than one class of oral glucose-lowering agents or insulin, reflecting the progressive nature of type 2 DM

Durability of glycemic control is slightly less for sulfonylureas compared to metformin or thiazolidinediones

380
Q

A 70/F with CKD Stage 4 from DM kidney disease came in for her follow-up. She fears that she might also become blind due to her diabetes just like what happened to her father before. Which among her lab findings/characteristics is the strongest predictor for her developing DM retinopathy?
a. Diagnosed DM since 50 years of age
b. Uncontrolled SBP at 150-160 mmHg
c. Urine albumin/crea ratio of 1000 mg/g
d. 1st degree relative with history of DM retinopathy

A

a. Diagnosed DM since 50 years of age

Duration of DM and degree of glycemic control are the BEST PREDICTORS of the development of retinopathy.

Nonproliferative retinopathy is found in many individuals who have had DM for >20 years.
Hypertension, nephropathy and dyslipidemia are also risk factors.

Although there is genetic susceptibility for retinopathy, it confers less influence than either duration of DM or degree of glycemic control.

381
Q

Which of the following statements is true regarding pharmacotherapy for treating DM nephropathy?
a. ACE inhibitors are superior over ARBs in terms of albuminuria reduction.
b. There is no benefit in starting ACE-inhibitors prior to onset of albuminuria.
c. Combination of ACE-inhibitors and ARBs can be used for greater albuminuria reduction.
d. Dihydropyridine CCBs can be used if there are contraindications to ACE-inhibitors or ARBs.

A

b. There is no benefit in starting ACE-inhibitors prior to onset of albuminuria.

Either ACE inhibitors or ARBs should be used to reduce the albuminuria and the associated decline in GFR that accompanies it in individuals with type 1 or type 2 DM.

Most experts believe that the two classes of drugs are equivalent in patient with diabetes.

ARBs can be used as an alternative in patients who develop ACE inhibitor–associated cough or angioedema.

After initiation of therapy, some increase the dose and monitor the urinary albumin.

There is no benefit of intervention prior to onset of albuminuria or using a combination of an ACE inhibitor and an ARB.

If use of either ACE inhibitors or ARBs is not possible or the blood pressure is not controlled, then, diuretics, calcium channel blockers (nondihydropyridine class), or beta blockers should be used.

381
Q

Which of the following statements is true regarding HMG-CoA Reductase Inhibitors?

a. Transaminase elevation of 3x the normal levels in the absence of symptoms does not warrant discontinuation of the drug.
b. They have a modest HDL-raising effect (5-10%) that is generally dose-dependent.
c. Serum CK levels need to be monitored routinely in patients taking these agents to monitor for myopathy.
d. Doubling of the current dose produces a ~15% further reduction in plasma LDL levels.

A

a. Transaminase elevation of 3x the normal levels in the absence of symptoms does not warrant discontinuation of the drug.

the magnitude of LDL lowering associated with statin treatment varies widely among individuals, but once a patient is on a statin, the doubling of the statin dose produces an ~6% further reduction in the level of plasma LDL-C

Statins also reduce plasma TGs in a dose-dependent fashion, which is roughly proportional to their LDL-C–lowering effects

Statins have a modest HDL-raising effect (5–10%) that is not generally dose-dependent.

Serum CK levels need not be monitored on a routine basis in patients taking statins, because an elevated CK in the absence of symptoms does not predict the development of myopathy and does not necessarily suggest the need for discontinuing the drug .

Substantial (greater than three times the upper limit of normal) elevation in transaminases is relatively rare, and mild-to-moderate (one to three times normal) elevation in transaminases in the absence of symptoms need not mandate discontinuing the medication

382
Q

Which of the following is the most important component of weight loss management in metabolic syndrome?

a. Behavior modification
b. Caloric restriction
c. Increased physical activity
d. Pharmacotherapy

A

b. Caloric restriction

In general, recommendations for weight loss include a combination of caloric restriction, increased physical activity, and behavior modification.

Caloric restriction is the most important component, whereas increases in physical activity are important for maintenance of weight loss.

383
Q

A 60/F was admitted for severe hip and lower back pain after falling from her bed. Physical exam revealed proximal myopathy. Pertinent diagnostic findings include an ionized calcium of 0.7 mmol/L (2.81 mg/dL), serum 25(OH)D of 10 ng/mL and osteopenia and fracture on the pelvic bone. Which of the following findings is expected to be seen on further workup?
a. Normal levels of 1,25(OH)2D
b. Decreased levels of PTH
c. Normal levels of urine calcium
d. Increased levels of phosphorus

A

a. Normal levels of 1,25(OH)2D

The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level.

The National Academy of Medicine has defined vitamin D sufficiency as a vitamin D level >50 nmol/L (>20 ng/mL)

Vitamin D deficiency leads to impaired intestinal absorption of calcium, resulting in decreased serum total and ionized calcium values. This hypocalcemia results in secondary hyperparathyroidism .

In addition to increasing bone resorption, PTH decreases urinary calcium excretion while promoting phosphaturia. This results in hypophosphatemia .

Since PTH is a major stimulus for the renal 25(OH)D 1a-hydroxylase, there is increased synthesis of the active hormone, 1,25(OH)2D.

Paradoxically, levels of this hormone are often normal in severe vitamin D deficiency.

Therefore, measurements of 1,25(OH)2D are not accurate reflections of vitamin D stores and should not be used to diagnose vitamin D deficiency in patients with normal renal function

384
Q

A 65/M with squamous cell lung CA is seen at the ER lethargic and dyspneic. BP was 140/80 and PE revealed engorged neck veins and diffuse crackles all over. Pertinent lab results showed a serum calcium of 15 mg/dL and creatinine of 450 mmol/L. Which of the following is the best strategy to quickly lower his hypercalcemia?
a. Fast drip with 1L plain saline over 2-3 hours
b. Fast drip with 1L plain saline over 2-3 hours plus furosemide 40 mg IV bolus
c. Start Zolendronate 4 mg IV infusion over 15 minutes
d. Start Calcitonin 200 IU nasal spray, 1 spray per nostril

A

d. Start Calcitonin 200 IU nasal spray, 1 spray per nostril

Patient has Hypercalcemia of Malignancy (from Lung CA). His PE indicates that he has pulmonary congestion

Although hydration is the initial choice of treatment for hypercalcemia, it is contraindicated for this patient.

Hydration + forced diuresis is likewise contraindicated

Zolendronate cannot be used due to elevated creatinine.

Calcitonin is the best strategy for rapid correction of hypercalcemia, followed by hemodialysis for this patient.

385
Q

Which thyroidal illness presents with a histopathologic picture of patchy inflammatory inflammation with disruption of thyroid follicles, presence of multinucleated giant cells and eventual progression to granuloma formation? (HPIM 20th ed. C377 P2708)

a. Acute thyroiditis
b. de Quervain’s thyroiditis
c. Atrophic thyroiditis
d. Riedel’s thyroiditis

A

b. de Quervain’s thyroiditis

AKA granulomatous thyroiditis

386
Q

Which true of factors that alter thyroid function in pregnancy?
a. Rise in TSH that persists into the middle of pregnancy.
b. Estrogen-induced decrease in TBG during the first trimester.
c. Increased thyroid hormone metabolism by the placenta.
d. Decreased urinary iodide excretion.

A

c. Increased thyroid hormone metabolism by the placenta.

Inc TBG and urinary iodine excretion in pregnancy

387
Q

A 45/M came in due to uncontrolled hypertension. He is currently on 3 antihypertensive medications and a diuretic. On probing, you note that he frequently has palpitations, headache and profuse sweating. Which of the following laboratory tests is consistent with the likely diagnosis?

a. Anemia
b. Hyponatremia
c. Hyperglycemia
d. Hypocalcemia

A

c. Hyperglycemia

Catecholamines (especially epinephrine) stimulate glycogenolysis and gluconeogenesis, leading to transient hyperglycemia.

This is a common finding in pheochromocytoma and can sometimes mimic diabetes or impaired glucose tolerance.

388
Q

A 40 year old previously healthy male consults the clinic for decrease in libido. He also complains of headache, loss of muscle mass and decrease in libido. He denies seizures, asthenia, or any unexplained weight changes. On PE, vital signs are stable but there is note of bilateral visual field cuts on confrontation test. There is also note of milky discharge from both nipples upon pinching but with no tenderness or warmth. Further work up shows: Prolactin levels: 400 ng/ml (NV <20 ng/ml) IGF-1: 100 ng/ml (NV 48-292) TSH: 3.2 uIU/ml (NV 0.3-4.0) FT4: 15 pM (NV 11.5-23) 8am serum cortisol: 12 ug/dl (NV 10-20) Cranial MRI: 3.2 cm sellar mass abutting the optic chiasm with hypoenhancement on gadolinium contrast. What is the next best step?
A. Recommend serial MRI and prolactin determination
B. Start bromocriptine
C. Start octreotide
D. Refer to NSS for transphenoidal excision

A

B. Start bromocriptine

Still the first line is dopamine agonists

Surgery is indicated if:
The tumor is resistant to medical therapy.
There is acute visual loss or other signs of neurological compromise that cannot wait for medical therapy to take effect.

389
Q

A 27 year old male referred you for palpitations of 2 months duration associated with unexplained weight loss, shortness of breath, easy fatigability, heat intolerance and excessive sweating. On examination, patient is noted to be mildly anxious. HR 120s bpm regular RR 24 cpm BP 130/90 mmHg. There is no note of lid lag or exophthalmos. There is a palpable nontender anterior neck nodule on the right with no bruit. There are fine finger tremors and DTRs are ++. Initial work up shows TSH 0.002 mIU/L (N: 0.5-4.0) FT4 30 pmol/L (N: 9-23). Which is the next best test to order?
A. FT3
B. Anti TPO and Anti Thyroglobulin
C. TRAb and TSI
D. Thyroid scan

A

D. Thyroid scan

390
Q

A 40-year old woman with PCOS, came in for a wellness check-up. She is currently asymptomatic. Latest labs showed FBS of 121mg/dl HDL 51mg/dl, LDL 98mg/dl, triglycerides 155mg/dl. Her regular BP is at 130/80, without medications. BMI is 26. What is the next best step?
A. Request for a 75-gram OGTT
B. Request for a repeat FBS
C. Do a point-of-care glycosylated hemoglobin
D. Start metformin therapy

A

A. Request for a 75-gram OGTT

The patient has polycystic ovary syndrome (PCOS), which is associated with insulin resistance and an increased risk of type 2 diabetes mellitus (T2DM). Her fasting blood sugar (FBS) of 121 mg/dL falls into the range of impaired fasting glucose (IFG) (100–125 mg/dL). To confirm the diagnosis of prediabetes or diabetes, further testing is necessary.

391
Q

A 62-year-old woman is admitted to the hospital because of disorientation and dehydration. She is presently managed at the Oncology clinic for stage IIIB squamous cell carcinoma of the lung. Labs done on admission: serum calcium level 17.9 mg/dL (NV 8.6 – 10.3mg/dL), phosphate of 1.8 mg/dL (normal 2.5-4.3 mg/dL) intact PTH of 0.3 pg/mL (normal 10–65 pg/mL). Parathyroid hormone–related peptide (PTHrP) screening was positive. Over the first 24 hours, the patient received 4 L of pNSS with furosemide diuresis. Repeat labs the following day show a decrease of calcium to 14 mg/dl. Patient is now more oriented but is complaining of fatigue and general weakness. What is the next best treatment approach?
A. Continue therapy with large-volume fluid administration and forced diuresis with furosemide.
B. Initiate therapy with hydrocortisone
C. Initiate therapy with calcitonin
D. Initiate therapy with zolendronate.

A

D. Initiate therapy with zolendronate

Bisphosphonates, such as zoledronate, are first-line treatments for hypercalcemia of malignancy. They inhibit osteoclast-mediated bone resorption and provide sustained calcium reduction over several days to weeks.

392
Q

A 51year old female, perimenopausal but otherwise healthy golfer complained of dull heavy low back pains. No significant past medical history. Systemic findings are unremarkable with stable vital signs. BMI is 20kg/m2. Lumbosacral spine xray was suggestive of osteoporosis. Bone densitometry DXA scan revealed a T-score of -2.7 at spinal area. Other labs showed crea of 0.7 mg/dl, iCa 1.33 mg/dl (NV 1.0-1.35), Vit D 38 ng/mL (NV >30), ALT 19. What is the next best step?
a. Request for intact PTH
b. Request for 75g OGTT and HbA1c
c. Request for TSH
d. Start Calcium and Vitamin D supplementation

A

c. Request for TSH

393
Q

A 56/M with lung cancer was referred for a 2 month history of progressive skin hyperpigmentation, unexplained weight gain, and generalized muscle weakness. On history, he was also recently diagnosed with type 2 DM and hypertension. Family history is unremarkable. Vital signs: BP 150/100 HR 70 bpm RR 22cpm afebrile. There is note of rounding of the face with purplish abdominal striae and central obesity and bipedal edema. Laboratory results of work up were as follows:
Crea 0.9 mg/dl (nv 0.5-1.2) Na 140 mmol/L (nv 135-145) K 3.0 mmol/L (nv 3.5-5.1)
FBS 154 mg/dl HbA1c 8.2% ACTH 321 pg/mL (nv 10-60) 24H UC cortisol 134 mcg/24H (nv 4-40)

Dexamethasone suppression test results: using 0.5mg dexamethasone q6, 8am cortisol 20 ug/dl using 2mg dexamethasone q6, 8am cortisol 18 ug/dl

What is the next best step?
a. Order pituitary MRI
b. Order chest and abdomen CT scan
c. Check IGF 1, TSH, FT4, prolactin levels
d. Perform inferior petrosal venous ACTH sampling

A

b. Order chest and abdomen CT scan

Most likely ectopic source of ACTH since no suppression on high dose dexa
Hypokalemia <3.3 also more common in ectopic source

394
Q

A 29/F G1P0 PU 8 weeks AOG was referred for 75g OGTT results as follows:
FBS 88 mg/dl
1H 235 mg/dl
2H 212 mg/dl

What is your diagnosis?

a. Type 2 Diabetes Mellitus
b. Gestational Diabetes Mellitus
c. Impaired Glucose Tolerance
d. Stress Induced hyperglycemia

A

a. Type 2 Diabetes Mellitus

395
Q

A 45-year-old patient undergoes an oral glucose tolerance test (OGTT) and has a 2-hour plasma glucose level of 8.5 mmol/L (153 mg/dL). The patient has _____.
A. Normal glucose tolerance
B. Impaired fasting glucose (IFG)
C. Impaired glucose tolerance (IGT)
D. Diabetes mellitus (DM)

A

B. Impaired fasting glucose (IFG)

396
Q

A 35-year-old female requested for an executive check-up where her HbA1C is 6.3%. She should be advised to have screening for DM every_____ year/s.
A. 1
B. 3
C. 4
D. 5

A

A. 1

The patient in this case has pre-diabetes (IGT). Individuals with IFG, IGT, or an HbA1c of 5.7–6.4% should be monitored annually to determine if diagnostic criteria for diabetes are present. The ADA suggests that metformin be considered in individuals with both IFG and IGT who are at very high risk for progression to diabetes (age <60 years, BMI ≥35 kg/m2, and women with a history of GDM).

397
Q

A 50-year-old Diabetic Female, weighing 50kgs with history of MI a month ago came in for follow up. Her current T2DM medications include Insulin GlargineU300 25U SC OD, Linagliptin, and Dapagliflozin. Repeat labs: FBS 12 umol/L, HDL 1 umol/L, TG 2.5 umol/L. The BEST next step in the management is to add ________.
A. Acarbose
B. Gliclazide
C. Pioglitazone
D. Semaglutide

A

D. Semaglutide

Pioglitazone and GLP1 agonists may be added to metformin if still uncontrolled

Semaglutide has been shown to decrease CV events.
Pioglitazone is contraindicated since the patient had a recent MI and may precipitate heart failure.

398
Q

ET, 70/F, was brought to the ER for slurring of speech and decrease in sensorium. CBG was 29 mg/dL. She regained consciousness after 1 vial of D50-50 was given. Repeat CBG was 72 mg/dL. She was a known hypertensive on Olmesartan, was started on Gliclazide for DM, Atorvastatin for Dyslipidemia, and Cefalexin and Ambroxol for productive cough 4 days ago. Aside from Gliclazide, which among her medications may have contributed to the hypoglycemia?
A. Ambroxol
B. Atorvastatin
C. Cefalexin
D. Olmesartan

A

D. Olmesartan

Many other drugs have been associated with hypoglycemia. These include commonly used drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists, β-adrenergic receptor antagonists, quinolone antibiotics, indomethacin, quinine, and sulfonamides

399
Q

Which of the following malignancies RARELY cause hypercalcemia?
A. Small cell lung CA
B. Squamous cell lung CA
C. Multiple myeloma
D. Leukemia

A

A. Small cell lung CA

SCCA-most common malignancy cause of hypercalcemia

400
Q

A 50-year-old obese female with type 2 DM inadequately controlled on metformin, pioglitazone and Insulin glargine 30U SC at bedtime. She complained of nausea, vomiting, and diarrhea. Afraid of hypoglycemia, discontinued Insulin. After 4 days, she develops lethargy and is brought to the emergency room. On examination, she is afebrile and unresponsive to verbal command. Blood pressure is 84/52. Skin turgor is poor and mucous membranes dry. Neurological examination does not point to any focal deficits. Laboratory results are as follows: Na 126 K 4 Cl 95 HCO3 22 Glucose 1100 BUN 84 Crea 3.0. Patient was initially hydrated with 0.9% NSS and Insulin IV bolus was given followed by Insulin Drip, what is the next step in the management?
A. Continue Insulin Drip, and hydrate using 0.9% NSS
B. Continue Insulin Drip, and hydrate using 0.45% Saline Solution
C. Give Insulin IV boluses, and hydrate using 0.9% NSS
D. Give Insulin IV boluses, and hydrate using 0.45%
Saline Solution

A

B. Continue Insulin Drip, and hydrate using 0.45% Saline Solution

Once hemodynamically stable, PNSS should be shifted to 0.45 to reduce hyperchloremic acidosis

401
Q

.A 40-year-old Female came in for her 1st executive check-up, Weight 80 Kgs, Height 6 feet. Vital signs showed BP 140/80mmHg, HR 95, RR 19. Laboratory Tests Showed: FBS 7.5 umol/L (135 mg/dL), HDL 0.44 umol/L (17 mg/dL), TG 2 umol/L (77 mg/dL). What is the BEST management for this case?
A. Advice weight loss
B. Start Losartan
C. Start Insulin
D. Start Atorvastatin

A

A. Advice weight loss

402
Q

Which of the following marker provides the BEST assessment for cardiovascular risk among patients taking statin?
A. ApoB
B. HDL-C
C. LDL-C
D. Lp(a)

A

A. ApoB

There is increasing evidence that measurement of plasma ApoB levels may provide a better assessment of cardiovascular risk than the LDL-C level, and even the non-HDL-C level, and is recommended by some experts. While this has not yet become standard clinical practice, the data supporting the use of ApoB as a risk marker and guide to therapeutic intervention are quite strong. There is also increasing interest in Lp(a), an independent ASCVD risk factor that is highly heritable and may be helpful in risk stratification.

403
Q

A 28-year-old female with symptoms of weight loss, palpitations, and heat intolerance consulted at IM OPD
Clinic. On physical examination, she has a diffusely enlarged thyroid gland and exophthalmos. Which of the following initial laboratory tests would be most appropriate to confirm the diagnosis?
A. Thyroid peroxidase antibodies
B. Serum thyroglobulin
C. TSH and free T4
D. Reverse T3

A

C. TSH and free T4

If with features of graves, no need for TPO ab
Needed only in the hypothyroidism algorithm

404
Q

A 25-year-old male sought consult at the IM outpatient department because of galactorrhea. He is a known hypertensive with occasional headache and palpitations, maintained on Verapamil for the past 4 years. He is currently taking Omeprazole for his GERD. Physical examination was unremarkable. What is the likely cause of his elevated prolactin level?
A. Prolactinoma
B. Intake of verapamil
C. Hypertension
D. Current use of Omeprazole

A

B. Intake of verapamil

Drug-induced inhibition or disruption of dopaminergic receptor function is a common cause of hyperprolactinemia. Verapamil blocks dopamine release leading to hyperprolactinemia.

405
Q

A 36-year-old male was referred from urology department for evaluation of polyuria, nocturia and polydipsia for 8 months. On PE, weight of 69 kg, height of 64 inches, BP 110/70, HR 85, RR 15 and the rest of his PE is normal. His urine output was 4500 ml for the past 24hrs. Laboratory studies revealed creatinine 0.6 mg/dL (NV 0.7-1.3 mg/dL), Na 145 mmol/L (NV 135-145 mmol/L), K 4 mmol/L (NV 3.5-5.0 mmol/L), RBS 95 mg/dL, urine osmolality 240 mOsm/L. What is your next step to determine the etiology of the patient’s condition?
A. Basal plasma AVP
B. Brain MRI
C. Kidney and urinary bladder ultrasonography
D. Fluid deprivation test

A

A. Basal plasma AVP

406
Q

A 22-year-old female with no known comorbids was admitted due to easy fatigability and tiredness which started 2 months ago. Initial VS: BP 90/60 HR 52 RR 16 temp 37.2. On PE: diffuse alopecia and non-pitting edema on the lower extremities. Thyroid gland is diffusely enlarged, irregular and firm in consistency. At ER, she had a decrease in sensorium and generalized seizures. TSH is elevated with low T4 and T3. What will be the BEST management?
A. Give levothyroxine as single IV bolus
B. Start oral methimazole immediately
C. Avoid hydrocortisone
D. External warming

A

A. Give levothyroxine as single IV bolus

Given the clinical vignette, the patient seems to have myxedema coma. Clinical manifestations include reduced level of consciousness, sometimes associated with seizures, as well as the other features of hypothyroidism. LT4 can initially be administered as a single IV bolus of 200–400 μg, which serves as a loading dose, followed by a daily oral dose of 1.6 μg/kg per day, reduced by 25% if administered IV.

407
Q

A 65-year-old male hypertensive and diabetic was admitted due to diarrhea. At the ER, BP 160/90 HR 120 RR 16 temp 39.5. He was agitated. Thyroid glands were firm and enlarged but non nodular. CBC showed WBC count with shift to the left. CXR revealed cardiomegaly. 12 LECG Atrial Fibrillation. What is your primary impression?
A. Myxedema Coma
B. Apathetic thyrotoxicosis
C. Thyroid Storm
D. Euthyroid Hyperthyroxinemia

A

C. Thyroid Storm

Thyrotoxic crisis, or thyroid storm, is rare and presents as a life-threatening exacerbation of hyperthyroidism, accompanied by fever, delirium, seizures, coma, vomiting, diarrhea, and jaundice. Thyrotoxic crisis is usually precipitated by acute illness (e.g., stroke, infection, trauma, DKA), surgery (especially on the thyroid), or radioiodine treatment of a patient with partially treated or untreated hyperthyroidism.

B - A condition in the elderly where features of thyrotoxicosis may be subtle or masked, and patients may present mainly with fatigue and weight loss.

D - Caused by the inhibition of T4 to T3 conversion due to Amiodarone intake

408
Q

A 55-year-old postmenopausal came in for evaluation due to recurrent back pain. Bone density scan (DXA) scan revealed a T-score is <-1.0. Which of the following statements is correct for her condition?
A. She has osteoporosis.
B. She has normal bone density for her age.
C. She has <50% risk of fracture.
D. She has increased risk of osteoporosis

A

D. She has increased risk of osteoporosis

409
Q

Which of the following would you consider vertebral testing?
A. A 65-year-old female with a femoral neck T score of 1
B. A 69-year-old female bone mineral density T score at the hip of 1.5
C. A 49-year-old male with low trauma fracture
D. A 60-year-old postmenopausal female with height loss of 0.9 inches

A

D. A 60-year-old postmenopausal female with height loss of 0.9 inches

410
Q

.A 56-year-old male with adrenocortical carcinoma (ACC) underwent successful removal of primary tumor. What is your next step in management?
A. He needs adjuvant radiation.
B. He needs adjuvant mitotane.
C. He needs glucocorticoid replacement.
D. He needs adjuvant cisplatin

A

B. He needs adjuvant mitotane.

Patients with confirmed ACC and successful removal of the primary tumor should receive adjuvant treatment with mitotane, particularly in patients with a high risk of recurrence as determined by tumor size >8 cm, histopathologic signs of vascular invasion, capsule invasion or violation, and a Ki67 proliferation index ≥10%. Adjuvant mitotane should be continued for at least 2 years, if side effects are tolerated.

411
Q

A 24-year-old female consulted due to amenorrhea. PE revealed central adiposity, abdominal striae and diastolic hypertension. She had a negative pregnancy test. Laboratory tests result revealed Na 140 (NV 135-145 mmol/L), K 2.9 mmol/L (NV 3.5-5.0 mmol/L). The 24-hour urinary free cortisol excretion is 300 mcg/24hrs (NV 10-100 mcg/24hrs). ACTH is 10 pg/mL (NV 10-60 pg/ml). What is your next BEST step?
A. Enhanced Adrenal CT scan
B. Unenhanced Adrenal CT scan
C. Low dose dexamethasone test
D. High dose dexamethasone test

A

D. High dose dexamethasone test

To further differentiate if acth dependent or not since ACTH not >15 or <5

412
Q

A 29-year-old male consulted due to hypokalemia. Vital signs BP 120/100 HR 89 RR 14 temp 36.9. PE revealed central adiposity and abdominal striae. Midnight salivary cortisol 1.1 mcg/dL (NV 0.25-0.31 mcg/dL). Plasma ACTH was 10 pg/mL (NV 10-60 pg/ml). His dexamethasone test revealed 60% cortisol suppression after every 6 hours of 2mg dexamethasone for 2 days.
What is the BEST treatment?
A. Unilateral adrenalectomy
B. Bilateral adrenalectomy
C. Transphenoidal pituitary surgery
D. Observe and repeat CT scan after 6 months

A

C. Transphenoidal pituitary surgery

POSITIVE if:
● Low dose DEX test (Plasma cortisol >50 nmol/L after 0.5 mg DEX q6h for 2 days or a single dose of 8 mg overnight)
● High dose DEX test (Cortisol suppression >50% after q6h 2 mg DEX for 2 days)

413
Q

55/M with Type 2 DM, hypertension, obstructive sleep apnea, dyslipidemia consults for weight management. His computed BMI is 33. Guidelines from the AHA/ACC/TOS recommend initiating diet therapy of
A. A total calorie requirement (TCR) of 1200-1500 kcal/day to achieve goal weight loss of 1-2 kg/week
B. A TCR of 1500-1800 kcal/day to achieve goal weight loss of 1-2 kg/week
C. A calorie deficit of at least 800 kcal/day compared to patient’s usual diet to achieve goal weight loss of 1-2 lbs/week
D. A calorie deficit of at least 500 kcal/day compared to patient’s usual diet to achieve goal weight of 1-2 lbs/week

A

D. A calorie deficit of at least 500 kcal/day compared to patient’s usual diet to achieve goal weight of 1-2 lbs/week

A calorie deficit of 500–750 kcal/day is recommended to achieve a weight loss of approximately 1–2 pounds (0.45–0.9 kg) per week.

1,500–1,800 kcal/day for men or individuals with higher calorie needs.

414
Q

True of the pathogenesis and mechanism of hypercalcemia of malignancy:
A. Small cell lung cancer which most frequently metastasize to the bone, promote bone resorption through local bone destruction and lead to hypercalcemia
B. Renal tumors secrete parathyroid hormone related peptide which cause increase bone resorption and lead to hypercalcemia, hypophosphatemia even in the absence of bone mets
C. Direct bone marrow invasion of leukemia and lymphoma ironically rarely cause hypercalcemia of malignancy
D. The most common mechanism of hypercalcemia in malignancy is due to direct bone marrow invasion of malignant cells which produce lymphokines and cytokines that promote bone destruction

A

B. Renal tumors secrete parathyroid hormone related peptide which cause increase bone resorption and lead to hypercalcemia, hypophosphatemia even in the absence of bone mets

415
Q

44/F with early menopause for bilateral salpingooophorectomy was noted to have a BMD T score of - 2.6 at the lumbar and -2.8 at the femoral sites. Which of the following is true in the management of this patient?
A. The recommended daily allowance for supplemental Vitamin D is 1000 to 2000 IU to maintain 25 OHD >30 ng/ml
B. The recommended daily allowance for supplemental calcium is 1000 to 1200 mg calcium
C. Calcium supplements of 1200 mg can be given in a single dose
D. Weight bearing exercises prevent bone loss and improves bone mass

A

A. The recommended daily allowance for supplemental Vitamin D is 1000 to 2000 IU to maintain 25 OHD >30 ng/ml

If not at risk of osteporosis - only need >20 ng/mL but since with risk since menopause , need to maintain >30

416
Q

19/M with history of childhood GH deficiency is referred to your clinic by his pediatrician for continuity of care. He has been undergoing GH replacement therapy since he was 7 years old for GH deficiency. On examination, patient was noted to have normal body habitus with appropriate height for age. Vital signs were stable. Retesting his GH reserves using the Insulin tolerance test shows that at 60 min after IV insulin infusion started, his serum glucose dropped to 36mg/dl with GH level of 5.1 ug/L. What is your best advise?
A. Adjust his recombinant GH therapy to adult dose
B. Discontinue recombinant GH therapy and monitor patient
C. Test for anterior pituitary sufficiency for FSH/LH, ACTH and TSH
D. Start oral prednisone and levothyroxine replacement therapy

A

B. Discontinue recombinant GH therapy and monitor patient

A peak GH level ≥5 µg/L during hypoglycemia (glucose <40 mg/dL) indicates sufficient GH reserve in adults, ruling out GH deficiency.

417
Q

43/M s/p transphenoidal excision of ACTH-secreting adenoma is referred to you for recurrent early morning hypoglycemia. He has been complaining of progressive easy fatigability, generalized body weakness, anorexia and nausea. Work up showed 8 AM plasma cortisol 2.2 mcg/dL (NV 5-25) Plasma ACTH 6 pg/mL (NV 10-60) What is the best treatment?
A. Start prednisone 5mg BID
B. Starting dose of prednisone replacement preferably should generally not exceed 20 mg daily, divided into 2-3 doses
C. Starting dose of hydrocortisone replacement preferably should generally not exceed 20mg daily, divided into 2-3 doses
D. Start hydrocortisone at 25mg BID

A

C. Starting dose of hydrocortisone replacement preferably should generally not exceed 20mg daily, divided into 2-3 doses

Hydrocortisone is preferred over prednisone for adrenal insufficiency because: It has a shorter half-life, better mimicking the natural diurnal rhythm of cortisol secretion. It is easier to titrate to physiologic doses.

418
Q

Islet cell autoantibodies (ICA) are best described as:
A. A composite of a single antibody directed at pancreatic islet.
B. Having a direct role in beta cell death.
C. Occurring as 2 or more autoantibodies in 80% of T1DM after a 15-year follow-up.
D. Presenting in less than 10% of new onset T1DM.

A

C. Occurring as 2 or more autoantibodies in 80% of T1DM after a 15-year follow-up.

419
Q

The pathophysiologic feature of Type 2 diabetes mellitus includes which of the following?
A. Abnormal lipid metabolism
B. Decreased hepatic glucose synthesis
C. Localized low-grade tissue inflammation
D. All of the above are correct.

A

A. Abnormal lipid metabolism

inc hepatic glucose synthesis

Systemic low grade inflammation

420
Q

The proposed mechanism for the decline in insulin secretory capacity observed in Type 2 DM is attributed to which of the following?
A. Acute hyperglycemia from insulin resistance
B. Decreased circulating free fatty acid levels
C. Presence of amyloid fibrillar deposits
D. Reduction in the quantity of islet-associated macrophages

A

C. Presence of amyloid fibrillar deposits

421
Q

Thiazolinediones are associated with which of the following agent-specific disadvantages?
A. Flatulence
B. Higher risk for fractures
C. Hypoglycemia
D. Pancreatitis

A

B. Higher risk for fractures

They decrease bone mineral density by promoting adipocyte differentiation at the expense of osteoblastogenesis, leading to reduced bone formation.

Same with canagliflozin

422
Q

Which one of the following antidiabetic agents acts in a glucose-dependent manner?
A. Acarbose
B. Gliclazide
C. Metformin
D. Sitagliptin

A

D. Sitagliptin

Dpp4 inhibitors –> incretin

423
Q

GG, a 60-year old patient with Type 2 DM presents with persistently elevated fasting glucose levels. For most of the day, her blood glucose levels fall within the range of 160-180 mg/dl. Before sleeping, her glucose level was measured at 165 mg/dl. She did not eat anything after measurement. The following morning, her blood glucose was elevated at 225 mg/dl. You recognize this as possibly associated with increased hepatic glucose production during fasting states. Which of the following addresses this?
A. Canagliflozin 100 mg/tab, 1 tab once a day before breakfast
B. Gliclazide 80 mg/tab, 1 tab twice a day before breakfast and supper
C. Metformin 1000 mg/tab, 1 tab twice a day after breakfast and supper
D. Sitagliptin 100 mg/tab, 1 tab once a day before breakfast

A

C. Metformin 1000 mg/tab, 1 tab twice a day after breakfast and supper

Metformin is a first-line therapy for T2DM and works by reducing hepatic glucose production (primarily gluconeogenesis). It improves insulin sensitivity in the liver and peripheral tissues. By addressing excessive hepatic glucose output, metformin is particularly effective in reducing fasting blood glucose levels.

424
Q

Which of the following is associated with Aldosterone-producing Adrenal (Conn’s) Adenomas?
A. Accumulation of DOC due to mutations in CYP11B1 or CYP17A1
B. Autonomous aldosterone excess caused by somatic mutations in the potassium channel GIRK4, encoded by KCNJ5
C. Mutantg ENaC beta or gamma subunits, resulting in reduced degradation of ENaC, enhancing mineralocorticoid action
D. Mutations in HSD11B2 with consequent lack of renal activation of cortisol, and eventual excess activation of the MR

A

B. Autonomous aldosterone excess caused by somatic mutations in the potassium channel GIRK4, encoded by KCNJ5

424
Q

Which of the following causes of mineralocorticoid excess is caused by a chimaeric gene resulting
from crossover of promoter sequences between the CYP11B1 and CYP11B2 genes involved in gluco- and
mineralocorticoid synthesis, respectively?
A. Bilateral adrenal hyperplasia
B. Cushing’s syndrome
C. Glucocorticoid-remediable aldosteronism (GRA)
D. Glucocorticoid resistance

A

C. Glucocorticoid-remediable aldosteronism (GRA)

425
Q

Which of the following situations mandates screening for mineralocorticoid excess in the setting of hypertensions?
A. Bilateral adrenal masses
B. Cerebrovascular events at < 40 years of age
C. Hypokalemia < 3.0 mmol/L
D. Resistant hypertension to > 2 antihypertensive medications

A

B. Cerebrovascular events at < 40 years of age

426
Q

Which of the following agents impair osteoclastis activity in part by inducing apoptosis?
A. Alendronate
B. Calcitonin
C. Denosumab
D. Raloxifene

A

A. Alendronate

Alendronate, a bisphosphonate, impairs osteoclast activity primarily by inducing osteoclast apoptosis and inhibiting bone resorption

Calcitonin inhibits osteoclast activity by directly binding to calcitonin receptors on osteoclasts, leading to decreased bone resorption. However, it does not induce apoptosis

Denosumab is a monoclonal antibody that targets RANKL, preventing it from binding to its receptor (RANK) on osteoclast precursors. This inhibits the formation, function, and survival of osteoclasts but does not directly induce apoptosis.

Raloxifene is a selective estrogen receptor modulator (SERM) that mimics estrogen’s effects on bone by reducing bone resorption. It has no direct impact on osteoclast apoptosis.

427
Q

A 48-year-old male sought consult for his annual company check-up. He is asymptomatic. His mother is Diabetic and his father is Hypertensive. His body mass index is 25.3kg/m2. Patient had blood examination as part of his routine company check-up. Given his above clinical features, which of his laboratory findings can be considered as an additional risk factor that predisposes him to develop Type 2 DM?
a. Triglycerides= 2.77 mmol/L
b. 2H PG= 7.6 mmol/L
c. HbA1c= 5.6%
d. HDL= 0.80 mmol/L

A

d. HDL= 0.80 mmol/L

HDL 0.8 mmol/L x 38.67 (conversion factor) =30.9

TAG should be > 2.82

428
Q

A 22-year-old Type 1 Diabetic patient plans to engage in physical activity and attend regular gym sessions. What
should you prescribe him?
a. Ingest carbohydrate before exercising if blood glucose is 6mmol/L.
b. Delay exercise if blood glucose is 12mmol/L and ketones are present.
c. Monitor glucose during exercise and ingest carbohydrate to prevent hypoglycemia.
d. Increase insulin doses (based on previous experience) before and after exercise and inject
insulin into a non-exercising area.

A

c. Monitor glucose during exercise and ingest carbohydrate to prevent hypoglycemia.

429
Q

A 19-year-old female, known Diabetic with poor compliance to medication was rushed to the ER due to abdominal pain and vomiting. Upon assessment, the following findings were noted: Vital Signs: BP= 130/70, HR=105, RR=26 Temperature=37.6C Drowsy, in respiratory distress. Initial laboratory work-up showed: CBG= high ABG= uncompensated metabolic acidosis Serum Ketone= positive. Her condition can be explained by which mechanism?
a. Glucagon excess that increases the activity of pyruvate kinase.
b. Insulin deficiency which decreases the activity of phosphoenolpyruvate carboxykinase.
c. The combination of insulin deficiency and hyperglycemia reduces the hepatic level of fructose-2,6-bisphosphate.
d. Insulin deficiency enhances the levels of the GLUT4 glucose transporter, which impairs glucose uptake into skeletal muscle.

A

c. The combination of insulin deficiency and hyperglycemia reduces the hepatic level of fructose-2,6-bisphosphate.

430
Q

A 21-year-old male came to the ER due to nausea, vomiting, abdominal pain and generalized weakness. Vital signs were as follows: BP=110/70, HR=108 RR=28, Temperature= 38.9. Initial laboratory work-up showed: CBG= high ABG= uncompensated metabolic acidosis Plasma Ketone= positive Appropriate management of this case includes:
a. Replacement of potassium at 10meqs/hr if the potassium is <3.5mmol/L in the next 24 hours.
b. If the serum phosphate is <0.32mmol/L, then phosphate supplementation should be considered.
c. In case of severe acidosis (pH< 7.0), compute for the bicarbonate deficit and replace it in 12 to 24 hours until pH is 7.0.
d. When the plasma glucose reaches 300mg/dL, glucose should be added to the 0.45% saline infusion to maintain the plasma glucose in 250 mg/dL range, and the insulin infusion should be continued at a lower rate

A

b. If the serum phosphate is <0.32mmol/L, then phosphate supplementation should be considered.

Hypophosphatemia may result from increased glucose usage, but randomized clinical trials have not demonstrated that phosphate replacement is beneficial in DKA. If the serum phosphate is <0.32 mmol/L (1 mg/dL), then phosphate supplement should be considered and the serum calcium monitored

431
Q

A 48-year-old male, known Diabetic sought consult with the following lipid profile:
Triglycerides= 568mg/dL
HDL=28mg/dL
LDL= 64mg/dL
The patient is already on lifestyle modification for the past 6 months. Which medication can be prescribed to him to
reduce his risk of pancreatitis?
a. Bile acid sequestrants
b. Nicotinic acid
c. Fenofibrate
d. Statin

A

c. Fenofibrate

Fibrates are first-line therapy for patients with severe hypertriglyceridemia (TG >500 mg/dL) to prevent pancreatitis.

Niacin may cause insulin resistance

432
Q

A 34-year-old female consulted due to weight gain. Her waist circumference is 35 inches and her body mass
index is 30kg/m2. She has no other co-morbidities. Which of the following pulmonary abnormalities may be
associated with her condition?
a. decreased minute ventilation
b. increased chest wall compliance
c. decreased expiratory reserve volume
d. increased functional residual capacity

A

c. decreased expiratory reserve volume

433
Q

A 29-year-old male sought consult for coarse facial features and progressively enlarging hands and feet. He also complained of hyperhidrosis and arthralgia. He has bitemporal hemianopsia on visual field exam. His vital signs are stable. His initial laboratory work-up showed: Growth hormone: 56.9 ng/mL (normal: 0-5 ng/mL), taken when patient was fasting IGF-1: elevated Rest of pituitary hormone: normal Fasting blood sugar: 117 mg/dL Colonoscopy: no polyp or mass ECG: regular sinus rhythm, normal axis with left ventricular hypertrophy What should you do next?
a. Repeat IGF-1 on fasting and stimulated state
b. Request for pituitary, chest and abdominal CT-scan
c. Determine growth hormone level after 75 grams oral glucose load
d. No further work-up needed. Proceed with definitive treatment.

A

c. Determine growth hormone level after 75 grams oral glucose load

Age-matched serum IGF-1 levels are elevated in acromegaly. Consequently, an IGF-1 level provides a useful laboratory screening measure when clinical features raise the possibility of acromegaly.

The diagnosis of acromegaly is confirmed by demonstrating the failure of GH suppression to <0.4 μg/L within 1–2 h of an oral glucose load (75 g). When ultrasensitive GH assays are used, normal nadir GH levels are even lower (<0.05 μg/L).

434
Q

A 34-year-old male patient came in due to complaints of increase urinary frequency and volume, amounting to 90 mL/kg. He weighs 88 kilograms. His laboratory results are as follows:
24 hour Urine volume: almost 8500 cc
Urine osmolarity: 230 mosm/Liter
Urine specific gravity: 1.001
Basal plasma arginine vasopressin: 5pg/mL
Pituitary MRI result showed presence of bright spot.

Based on the above findings, which is the most likely diagnosis?

a. Pituitary Diabetes Insipidus
b. Nephrogenic Diabetes Insipidus
c. Primary Poyldipsia- Dipsogenic Type
d. Primary Polydipsia- Psychogenic Type

A

b. Nephrogenic Diabetes Insipidus

435
Q

Who among these patients are at increased risk for generalized osteoporosis?
a. L.Q., 38-year-old male with elevated TSH and low fT4
b. M.C., a 40-year-old female with low level of Prolactin
c. A.F, a 42-year-old male with low cortisol and ACTH
d. S.D., a 44-year-old female with HbA1c of 5.6% and FBS of 5.5mmol/L

A

c. A.F, a 42-year-old male with low cortisol and ACTH

Adrenal insufficiency is a well-recognized risk factor for generalized osteoporosis.

a. should be hyper not hypothyroidism
b. hyper not hypo prolactinemia

436
Q

A 35-year-old female was referred by her Ob-Gynecologist due to easy fatigability, menstrual irregularity and constipation. Part of her work-up revealed a normal TSH and low fT4 and fT3. Thyroid function tests were done twice and yielded same results. She has no known co-morbidities. She is not taking any medications. What should be the next step in managing this patient?
a. Evaluate pituitary function.
b. Facilitate a thyroid scan with uptake
c. Observe and repeat thyroid function tests after 3 months.
d. No further work-up needed. Start treatment with Levothyroxine.

A

a. Evaluate pituitary function.

The patient has low free T4 (fT4) and free T3 (fT3) with a normal TSH. This pattern suggests central (secondary or tertiary) hypothyroidism, which is caused by dysfunction at the level of the pituitary or hypothalamus

437
Q

. A 65-year-old female was rushed to the ER due to decreasing sensorium. She was previously diagnosed with unrecalled thyroid disease, non-compliant to medication and was lost to follow-up. She is bradycardic and hypothermic. She also has generalized edema. Work-up revealed elevated TSH and low fT4. Her Chest X-Ray revealed pneumonia on right lower lung field. What should be part of her management?
a. Hypotonic IV fluids should be preferred if available. b. Parenteral hydrocortisone (50mg every 6 h) should be administered.
c. An initial loading dose of 30-50 μg Liothyronine should be followed by 2.5–10 μg 8 hourly, with lower doses for those at cardiovascular risk.
d. Levothyroxine can initially be administered as a single IV bolus of 200–400 μg, which serves as a loading dose, followed by a daily oral dose of 1.6 μg/kg/d, increased by 25% if administered IV.

A

b. Parenteral hydrocortisone (50mg every 6 h) should be administered.

D also correct but steroids first due to decreased adrenal reserve

438
Q

A 32-year-old male consulted due to symptoms of thyrotoxicosis. There was no thyroid-related eye disease as well as thyromegaly. Thyroid function tests which were done twice showed normal TSH and elevated fT4 and fT3. What is his most likely diagnosis?
a. de Quervain’s thyroiditis
b. Sick Euthyroid Syndrome
c. Subclinical Hyperthyroidism
d. TSH-secreting Pituitary Adenoma

A

d. TSH-secreting Pituitary Adenoma

The patient presents with symptoms of thyrotoxicosis, normal TSH, and elevated free T4 (fT4) and free T3 (fT3). This pattern suggests inappropriate TSH secretion despite elevated thyroid hormones, which is most consistent with a TSH-secreting pituitary adenoma (TSHoma).

Subclinical is low TSH but normal TFTs hence not the answer

439
Q

A 34-year-old female consulted due to 4-week symptoms of palpitations, fever, hyperdefecation associated with painful thyroid gland radiating to the jaw. Eye examination did not show exophthalmos, retraction or lid lag. Neck examination did not reveal thyromegaly or mass or nodule. Thyroid function test results showed suppressed TSH and elevated fT4. Thyroid scan showed low radioactive iodine uptake. Which of the following is part of the appropriate management plan for this patient?
a. Aspirin 80mg/tablet may be given at a dose of 5-6 tablets every 4-6 hours.
b. Either PTU or Methimazole can be given during the thyrotoxic phase, but preferably Methimazole.
c. Levothyroxine replacement may be needed if the hypothyroid phase is prolonged, but doses should be 50–100 μg/day
d. If Aspirin or NSAID is not sufficient, Prednisone may be given at a dose of 3-4mg/kg/day for 8 to 12 weeks and must be tapered based on patient’s symptoms.

A

c. Levothyroxine replacement may be needed if the hypothyroid phase is prolonged, but doses should be 50–100 μg/day

Patient has subacute thyroiditis (de Quervain’s thyroiditis)

a. Aspirin 80mg/tablet may be given at a dose of 5-6 tablets every 4-6 hours. –> Relatively large doses of aspirin (e.g., 600 mg every 4–6 h) or nonsteroidal anti-inflammatory drugs (NSAIDs) are sufficient to control symptoms in many cases.
600 = 7-8 tabs

b. Either PTU or Methimazole can be given during the thyrotoxic phase, but preferably Methimazole. —->
Antithyroid drugs play no role in treatment of the thyrotoxic phase. LT4 replacement may be needed if the hypothyroid phase is prolonged, but doses should be low enough (50–100 μg daily) to allow TSH-mediated recovery.

d. If Aspirin or NSAID is not sufficient, Prednisone may be given at a dose of 3-4mg/kg/day for 8 to 12 weeks and must be tapered based on patient’s symptoms. –> 6-8 weeks

440
Q

A 36-year-old female came in due to palpable nodule on her neck. She was clinically euthyroid. There were no complaints of hoarseness, dysphagia or odynophagia. On neck palpation, an approximately 2.5 x 1.5 cm mass was palpated on her left thyroid gland. There was no palpable lymph node. TSH was suppressed. What should be the next best step in managing this patient?
a. Request for radionuclide scan
b. Start treatment with Methimazole
c. Refer to surgery and schedule for lobectomy
d. Do Fine Needle Aspiration Biopsy of the thyroid nodule

A

a. Request for radionuclide scan

441
Q

A 31-year-old male suspicious of Cushing’s syndrome had a non-suppressible low dose dexamethasone suppression test and an elevated 24-hour urine free cortisol levels. Serum ACTH was elevated. Pituitary Magnetic Resonance Imaging showed a pituitary mass, 1.2 cm x 0.9 cm x 0.8 cm. High dose dexamethasone suppression test was done and results showed non-suppressed level of cortisol. CRH test done showed non-stimulated levels of ACTH and cortisol. What should be the next plan of management?
a. Start Mitotane followed by Radiotherapy
b. Transphenoidal excision of pituitary mass
c. Perform inferior petrosal sinus sampling
d. Subject patient to adrenal gland protocol then treat with Ketoconazole

A

c. Perform inferior petrosal sinus sampling

Equivocal results in DDX 2

442
Q

A 32-year-old female consulted due to progressive weight gain, easy bruisability, proximal myopathy, purplish abdominal striae >1cm, impaired glucose tolerance and hypertension. There were no known co-morbidities. Patient denies use of steroids. Initial work-up revealed 4 times elevated urinary cortisol and elevated ACTH. Which of the following is the most likely diagnosis?
a. Macronodular Adrenal Hyperplasia
b. McCune-Albright Syndrome
c. Adrenocortical adenoma
d. Ectopic ACTH Syndrome

A

d. Ectopic ACTH Syndrome

The elevated urinary cortisol and ACTH levels point to an ACTH-dependent cause of hypercortisolism, with ectopic ACTH syndrome (EAS) being the most likely diagnosis based on the clinical and biochemical findings.

443
Q

A 44-year-old male was diagnosed with Primary Aldosteronism based on a positive Aldosterone-Renin Ratio and an elevated aldosterone levels on confirmatory test. On history, he claimed that most of the time, his blood pressure was 140-150/90mmHg and serum potassium was normal. There is no family history of early-onset hypertension or Primary Aldosteronism. Imaging revealed bilateral micronodular hyperplasia. What will be your next plan of action?
a. Schedule for Adrenal Vein Sampling
b. Do Fludrocortisone Suppression Test
c. Start treatment with Spironolactone
d. Refer to Urologist for Bilateral Adrenalectomya

A

c. Start treatment with Spironolactone

444
Q

A 43-year-old female came in due to generalized weakness, nausea, dizziness, vomiting and abdominal pain. Blood pressure was 90/60mmHg. Capillary blood glucose was 68mg/dL. She was suspected to have Adrenal Insufficiency hence she had cosyntropin test that revealed low level of cortisol. Further diagnostic exam showed low ACTH, normal renin and normal aldosterone. There was no history of previous steroid intake. How should you proceed with the diagnostic work-up?
a. Screen for autoantibodies
b. Facilitate Insulin Tolerance Test
c. Do CT-Scan of chest and abdomen
d. Perform MRI of the pituitary gland

A

d. Perform MRI of the pituitary gland