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Patho > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

T/F When carcinomas cannot be histologicially distinguished from adenomas, the only sure sign of malignancy is metastasis.

A

1

True; We see this, for example, with the parathyroid glands.

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1
Q

____________________________ syndrome refers to the unregulated secretion of hormones and hormone-like compounds from tumors

A
  1. Paraneoplastic
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2
Q

T/F The posterior pituitary hormones are prolactin and ACTH.

A
  1. False; ACTH and prloactin are anterior pituitary hormones. The posterior pituitary hormones are ADH and oxytocin.
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3
Q

T/F Neurohormones released by the posterior pituitary are not synthesized in the posterior pituitary.

A
  1. True; They are synthesized by neurons whose cell bodies lie in the hypothalamus.
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4
Q

T/F Neurohormones released by the anterior pituitary are not synthesized in the anterior pituitary.

A
  1. False; Anterior pituitary hormones are synthesized by ant. pituicytes (ant. pituitary cells) -under the regulation of hypothalamic releasing hormones.
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5
Q

T/F Continual stimulation of the adrenal medulla by ACTH would lead to hyperplasia of the adrenal medulla

A
  1. False; The adrenal medullary cells do not express ACTH receptors on their surfaces. They are thus oblivious to ACTH and would not respond to it at all.
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6
Q

T/F Continual stimulation of the adrenal cortex by ACTH would lead to adrenocortical hyperplasia

A
  1. True; ACTH does indeed stimulate the adrenal cortex- esp. the zona fasiculata that makes cortisol; Continual ACTH stimulation of the cortex would indeed lead to adrenocortical hyperplasia. There is a similar relationship between the follicular cells of the thyroid and TSH.
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7
Q

The [anterior/ posterior] pituitary is also known as the adenohypophysis.

A
  1. anterior; The anterior pituitary is a gland (‘adeno-‘) derived from the oral mucosa.
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8
Q

The [anterior / posterior] pituitary is also known as the neurohypophysis.

A
  1. posterior; The posterior pituitary is derived from the neural tissue (‘neuro-‘) of the hypothalamus.
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9
Q

The [anterior/ posterior] pituitary is derived from epithelial cells in the mouth region which migrate upward in the head.

A
  1. anterior
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10
Q

The connection between the hypothalamus and the [anterior/ posterior] pituitary gland is mainly a vascular one.

A
  1. anterior
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11
Q

The connection between the hypothalamus and the [anterior/ posterior] pituitary gland is mainly a neural one.

A
  1. posterior
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12
Q

The ________________________ is the stalk of the pituitary gland.

A
  1. infundibulum
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13
Q

___________________ is a control loop whereby the product or output of a system acts back on the system to repress or stop its own production.

A

14

Negative feedback, or feedback inhibition

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14
Q

The _________________________, a region of the brain, largely controls the secretion of hormones by the anterior pituitary.

A
  1. hypothalamus
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15
Q

A(n) ___________________ hormone regulates the hormonal functioning of a distant endocrine gland.

A
  1. tropic
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16
Q

____________ is the hypothalamic hormones that controls the release of TSH by the anterior pituitary.

A
  1. TRH, or Thyrotropin Releasing Hormone
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17
Q

_________________ is the hypothalamic hormones that controls the release of FSH and LH by the anterior pituitary.

A
  1. GnRH, or Gonadotropin Releasing Hormone
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18
Q

______________ is the hypothalamic hormones that controls the release of ACTH by the anterior pituitary.

A
  1. CRH, or Corticotropin Releasing Hormone
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19
Q

T/F Laron dwarfism is easily treated in children by administration of growth hormone.

A
  1. False; Recall that Laron hormone is due to insensitivity of the growth hormone receptor. Therefore, supplying exogenous growth hormone will do little to overcome that deficiency. But growth hormone is tropic in that it elecits the release of
    somatomedin (mostly from liver cells), and it is somatomedin that actually stimulates growth in stature. Thus administration of somatomedin, not growth hormone, will bypass the receptor deficiencies of Laron dwarfism and cause growth of long bones.
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20
Q

________________________ refers to the deficient secretion of one or more of the hormones secreted by the pituitary.

A
  1. Hypopituitarism
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21
Q

______________________ refers to total failure of pituitary function; no pituitary hormones are being secreted.

A
  1. Panhypopituitarism
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22
Q

____________________, or ischemic necrosis of the pituitary, usually is caused by hypotension secondary to postpartum hemorrhage.

A
  1. Sheehan syndrome
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23
Q

In children, ___________________ results from the inadequate secretion of growth hormone.

A
  1. pituitary dwarfism
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24
Q

____________________ refers to a condition marked by short statue due to extreme insensitivity of the growth hormone receptor to growth hormone.

A
  1. Laron dwarfism
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25
Q

Which ONE of the following is not a classic symptom of panhypopituitarism?

A. General weakness
B. Heat intolerance
C. Poor appetite
D. Weight loss
E. Hypotension
F. Amenorrhea and impotence
G. In men, loss of muscle mass, and facial and pubic hair
H. Pallor
I. (None. All of the above are typical symptoms of panhypopituitarism)
A

B. Panhypopituitarism produces cold intolerance. The loss of TSH also causes low serum T3 and T4. Since these control the metabolic rate, in their absence, a person does not produce much body heat and feels chilled all the time. In other words, they cannot tolerate chilly temperatures because they are not producing enough internal heat. Note that the lack of T3 and T4 also account for the general weakness, poor appetite, weight loss, and hypotension (remember that T3 and T4 increase sympathetic influence, so in their absence…).

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26
Q

T/F Pituitary adenomas are about three times more common in women than in men.

A
  1. False; Pituitary adenomas are actually most common in middle-aged men.
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27
Q

T/F Although the pituitary gland is composed of several populations of pituicytes, each secreting their own set or sets of hormones, a functional pituitary adenoma usually only secretes one hormone.

A
  1. True; for example, a prolactinoma arises from the lactotropic pituicytes and only secretes prolactin.
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28
Q

T/F In pre-pubertal patients, somatotropic adenomas result in pituitary dwarfism.

A
  1. False; A somatotropic adenoma would secrete high levels of growth hormone and thus cause gigantism, not dwarfism.
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29
Q

T/F In post-pubertal patients, somatotropic adenomas result in acromegaly.

A
  1. True; Remember that with high levels of growth hormone, the growth extends to the soft organs as well, such that cardiomegaly is common.
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30
Q

[Lactotropic/ Somatotropic / Thyrotropic / Corticotropic] adenomas secrete prolactin.

A
  1. Lactotropic, otherwise known as a prolactinoma.
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31
Q

[Lactotropic/ Somatotropic / Thyrotropic / Corticotropic] adenomas secrete ACTH.

A
  1. Corticotropic
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32
Q

Cushing [disease/ syndrome ] refers to hypercortisolism produced by a corticotropic adenoma of the pituitary.

A
  1. Cushing disease. The name is specifically reserved to the hypercortisolism due to a prolactinoma; all other types of hypercortisolism are refered to as Cushing syndrome.
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33
Q

_____________________ are benign neoplasms of the anterior lobe of the pituitary and are often associated with excess secretion of pituitary hormones and evidence of corresponding
endocrine hyperfunction.

A
  1. Pituitary adenomas
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34
Q

A _____________________ is a common name for a lactotropic adenoma.

A
  1. prolactinoma
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35
Q

________________, a dopamine analog, can suppress the secretion of prolactin from a prolactinoma.

A
  1. Bromocriptine; Recall that PIF- prolactin inhibitory factor- is dopamine, and bromocriptine is a dopamine analog (agonist).
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36
Q

Which ONE of the following is not a typical mass effect produced by pituitary adenomas?

A. Bitemporal hemianopsia
B. Oculomotor palsy
C. Bell palsy
D. Severe headache
E. Hypothalamic dysfunction
F. (None. All of the above are typical symptoms resulting from the mass effects of a pituitary adenoma)
A
  1. C. Bell palsy, which is probably caused by viral inflammation of the facial nerve.
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37
Q

Which ONE of the following is not a typical symptom of a prolactinoma?

A. Amenorrhea
B. Dysfunctional uterine bleeding
C. Galactorrhea
D. Infertility
E. Impotence
F. (None. All of the above are typical symptoms of a prolactinoma)
A
  1. B. These symptoms of a prolactinoma are easily explained. Galactorrhea results in a woman from the high prolactin levels. Recall that prolactin inhibits the release of LH and FSH by inhibiting the hypothalamic release of GnRH. This results in infertility, amenorrhea, and impotence. DUB is due to high unopposed estrogen levels, a situation we would not see with low FSH and LH.
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38
Q

T/F The treatment for diabetes insipidus may include ADH replacement therapy.

A
  1. True; Of course this would be of most benefit to patients with central diabetes insipidus.
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39
Q

A key feature of SIADH is sodium retention and the inability to concentrate the urine.

A
  1. False; It’s backwards- the situation described is for diabetes insipidus. In SIADH a patient hypersecretes ADH, so the condition is characterized by the inability to dilute the urine, and sodium loss (natriuresis) resulting in hyponatremia. Also, be careful on the exam- I might flip this question, so it DOES describe SIADH.
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40
Q

T/F A common cause of SIADH is a paraneoplastic small cell carcinoma of the lungs.

A
  1. True
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41
Q

T/F The clinical picture of SIADH is dominated by hyponatremia, cerebral edema, and CNS dysfunctions such as headache and vomiting; severe cases may lead to convulsions and coma.

A
  1. True
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42
Q

In [central/ nephrogenic] diabetes insipidus, the posterior pituitary secretes insufficient ADH.

A
  1. Central
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43
Q

In [central/ nephrogenic] diabetes insipidus, the kidney tubules show insufficient response to circulating ADH.

A
  1. nephrogenic
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44
Q

______________________ is a posterior pituitary disorder characterized by the inability to concentrate the urine, with resulting polyuria and polydipsea; the biochemical basis is an insufficient ADH activity.

A
  1. Diabetes insipidus
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45
Q

_________________ is a disorder characterized by excessive release ADH from the posterior pituitary gland or another source.

A
  1. SIADH, or syndrome of inappropriate ADH secretion
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46
Q

Which ONE of the following is not a common treatment option for SIADH?

A. Long-term fluid restriction
B. IV saline
C. Demeclocycline or tolvaptan
D. (None of the above, i.e., they are all common treatments for SIADH)

A
  1. D. Of course, treating any underlying illness would also be part of the treatment plan.
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47
Q

Which ONE of the following is NOT a typical symptom/finding of diabetes insipidus?

A. Intense thirst
B. Copious urine output
C. Renal calculi
D. Lack of sugar in the urine
E. (None. All of the above are typical symptoms of diabetes insipidus)
A
  1. No renal calculi.
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48
Q

[Iodine / Calcium/ Vitamin D/ Iron / Sulfur / Zinc ] is a chemical element found in the thyroid hormones T3 and T4.

A
  1. Iodine
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49
Q

The ____________________________ cells of the thyroid gland are responsible for the production of the thyroid hormones T3 and T4.

A
  1. follicular; parafollicular cells produce calcitonin.
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50
Q

____________________ from the anterior pituitary stimulates follicular activity in the thyroid and the release of T3 and T4 hormones.

A
  1. TSH; And TSH in turn is regulated by TRH from the hypothalamus.
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51
Q

Which ONE of the following statements is NOT TRUE regarding the thyroid hormones T3 & T4?

A. T3 & T4 are catecholamines
B. T3 & T4 are derived from two molecules of tyrosine
C. T3 & T4 contain three or four iodine molecules
D. T3 & T4 are stored in colloid attached to thyroglobulin
E. T3 has about 10 times more biological activity than T4
F. T4 is converted to T3 in the peripheral tissues (mainly liver) of the body
G. (None. All of the above are true regarding T3 and T4)

A
  1. A. Like T3 and T4, catecholamines are also formed from the amino acid tyrosine. However, T3 and T4 are not catecholamines- they do not possess the catechol group.
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52
Q

Which ONE of the following conditions is most likely to lead to a goiter?

A. Secondary hypothyroidism due to failure of the hypothalamus or pituitary gland.
B. Primary hyperthyroidism due to a small but hypersecreting thyroid tumor
C. Secondary hyperthyroidism due to a small but hypersecreting pituitary tumor

A
  1. C. In case A, the hypothalamus/pituitary is misbehaving, so that TSH levels will be low. In B, high levels of thyroid hormones will suppress TSH production, so again, TSH levels will be low. In any case, remember my rule-goiters are likely to develop when TSH or TSH-like stimulation is excessive.
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53
Q

T/F Goiters can develop in a setting of hypopituitarism secondary to hypothalamic or anterior pituitary failure.

A

56A
False
With hypothalamic or anterior pituitary failure, TSH levels will be low. Hence, no goiter.

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54
Q

T/F Thyroid cancer can lead to the production of a goiter.

A

56B
True
A tumor can enlarge the thyroid and thus cause a goiter.

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55
Q

T/F Goiters will not develop in the absence of TSH overstimulation.

A

56C
False
While TSH overstimulation is a major cause of goiters, there are other ways they can develop in the absence of elevated TSH levels. Neoplasia and TSI antibodies immediately come to mind.

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56
Q

T/F Lack of dietary iodine may lead hypothyroidism but does not lead to goiter formation.

A

56D
False
Lack of dietary iodine is a MAJOR cause of goiters worldwide.

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57
Q

T/F Goiters can develop in a setting of hypopituitarism via primary failure of the thyroid itself.

A

56E
True
Thyroid failure means low T3 and T4 levels, which in turn means high TSH levels and thyroidal overstimulation. Hence, primary thyroid failure can indeed lead to goiter formation.

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58
Q

T/F Goiters can develop in the setting of hyperthyroidism via a functional pituitary adenoma.

A

56F
True
If the tumor is a thyrotropic adenoma (which secretes TSH) then yes, a goiter may develop.

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59
Q

T/F Goiters can develop in the setting of hyperthyroidism via antibody stimulation of the thyroidal follicular cells.

A

56G
True
This is precisely the case in Graves disease.

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60
Q

T/F Patients with nontoxic goiter are usually euthyroid.

A

57

True

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61
Q

T/F For reasons that are unclear, in nontoxic goiter the capacity of the thyroid to produce thyroid hormones is impaired.

A

58

True

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62
Q

_______________________ refers to an enlargement of the thyroid that is not
associated with functional, inflammatory, or neoplastic alterations

A

59
Nontoxic goiter; ‘Nontoxic’ means that patients are neither hypothyroid nor hyperthyroid- they are euthyroid. These goiters are not associated with functional disturbances (such as pituitary hypo- or hyper-secretion, there is no evidence of thyroiditis (inflammation), and there is not sign of a thyroid tumor.

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63
Q

T/F Typically, in cases of nontoxic goiter, the ability of the thyroid gland to produce thyroid hormones is impaired, and patients thus develop hypothyroidism.

A

60A
False
With nontoxic goiters, the ability of the thyroid gland to produce hormone is impaired, but the body compensates (increased thyroid stimulation via TSH) so that a patient usually maintains normal T3 and T4 levels.

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64
Q

T/F Diffuse nontoxic goiters are the early stage of the disease and are most common during pregnancy and in adolescent patients.

A

60B

True

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65
Q

T/F Diffuse nontoxic goiters often show nodularity.

A

60C
False
If they showed nodularity, they would be multinodular nontoxic goiters.

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66
Q

T/F Endemic nontoxic goiters occur in a defined region of the world- usually an area that is iodine deficient or an area where people consume large quentities of crops that inhibit thyroid hormone synthesis (e.g., crucifers).

A

60D
True
Of course, lack of dietary iodine is the MAJOR cause of endemic goiters worldwide.

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67
Q

T/F In diffuse nontoxic goiters, the entire thyroid is enlarged, its follicles hyperplastic and hypertrophic.

A

60E
True
Thyroid failure means low T3 and T4 levels, which in turn means high TSH levels and thyroidal overstimulation. Hence, primary thyroid failure can indeed lead to goiter formation.

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68
Q

T/F (Diffuse nontoxic) Sporadic goiters are idiopathic.

A

60F
True
Also, sporadic goiters are more common in women than men, for unknown reasons.

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69
Q

T/F Multinodular nontoxic goiters represent the early stage of the disease and are more common in adolescent patients.

A

60G

False

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70
Q

T/F Multinodular nontoxic goiters can evolve into hyperthyroidism.

A

60H
True
These are called toxic multinodular goiters; their hyperthyroidism differs from Graves disease in that toxic multinodular goiters do not produce the infiltrative ophthalmopathy (exophthalmos).

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71
Q

T/F Some multinodular goiters progress to cancer.

A

60I
True
The frequency of this progression is low (~5%) but not zero.

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72
Q

T/F Nontoxic goiters may cause dysphagia, dyspnea, jugular compression, hoarseness.

A

60J

True

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73
Q

T/F Exophthalmia is seen in all types of hyperthyroidism.

A

61
False; It is pathognomonic for Graves disease, and is not seen in other types of hyperthyroidism such as toxic multinodular goiter.

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74
Q

T/F Goiters do not develop in untreated Graves disease.

A

62

False; In fact, goiters are quite common in untreated Graves disease.

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75
Q

T/F Ironically, the hyperthyroidism of untreated Graves disease may evolve into thyroid failure and hypothyroidism.

A

63
True; Presumably the constant stimulation and hyperthyroidism overwhelms the gland; it fails and the person lapses into hypothyroidism.

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76
Q

T/F In Graves disease, high T3/T4 levels are accompanied by low TSH levels.

A

64

True; And important diagnostic results.

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77
Q

T/F In Graves disease, radioactive iodine uptake tests show decreased uptake of iodine by the thyroid gland.

A

65

False; In graves disease, the thyroid is overactive- it’s going to take up lots of iodine!

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78
Q

T/F A typical course of treatment for Graves disease is (1) administer adrenergic antagonists to alleviate the heightened sympathetic effects, followed by (2) administration of antithyroidal drugs to inhibit T3/T4 release.

A

66

True

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79
Q

_________________ is a hypermetabolic state caused by elevated circulating levels of free T3 and T4; hyperthyroidism is the most common cause of this condition.

A

67

Thyrotoxicosis

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80
Q

__________________ is caused by excessive thyroid activity.

A

68

Hyperthyroidism

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81
Q

_____________ is an autoimmune disorder caused by antibodies that agonistically bind to the surface TSH receptors of the thyroid follicular cells, stimulating them.

A

69

Graves disease, the most common cause of hyperthyroidism

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82
Q

Circulating antibodies called _______________, or TSIs, are the root cause of Graves disease.

A

70

thyroid stimulation immunoglobins

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83
Q

____________ is a common antithyroid drug commonly used to treat the hyperthyroidism of Graves disease.

A

71

Either propylthiouracil or methimazole work here.

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84
Q

Which ONE of the following is NOT a typical symptom of the hyperthyroidism of Graves disease?

A. Tachycardia and cardiac palpitations
B. Diarrhea
C. Pallor and cold, clammy skin
D. Exophthalmos
E. Weight loss and increased appetite
F. Restlessness, nervousness, anxiety, and sweating
G. (None. All of the above are typical symptoms of hyperthyroidism)

A

71

C. Cold, clammy, pallid skin is typical of hypothyroidism.

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85
Q

T/F In thyrotoxic patients, the skin tends to be cool, dry, and pallid due to decreased peripheral blood flow and vasoconstriction.

A

72A
False
This is backwards. Remember that high circulating levels of T3/T4 activates the sympathetic nervous system. Sympathetic effect on the skin is vasodilation (to increase heat loss), resulting in warm, soft, moist, and flushed skin.

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86
Q

T/F In thyrotoxic patients, cold intolerance is common.

A

72B
False
Again, backwards. These patients are producing lots of internal heat, so they have heat intolerance (and would probably welcome cool air around them).

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87
Q

T/F In thyrotoxic patients, tachycardia and palpitations are common.

A

72C
True
Think sympathetic effects on the body- fast heart beat and palpitations are examples.

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88
Q

T/F In thyrotoxic patients, cardiomegaly and cardiac arrhythmias may develop, and these may lead to congestive heart failure and death.

A

72D
True
Another cardiac complication is thyrotoxic cardiomyopathy.

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89
Q

T/F Thyrotoxic effects on the nervous system include nervousness, insomnia, and inability to concentrate

A

72E
True
Again, think sympathetic effects on the body

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90
Q

T/F Constipation is common in thyrotoxic patients

A

72F
False
Usually the opposite is seen- increased peristalsis resulting in diarrhea.

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91
Q

T/F In thyrotoxic patients, distal muscle weakness but increased muscle mass are common.

A

72G
False
Again, backwards. In thyrotoxicosis we see proximal muscle weakness and decreased muscle mass.

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92
Q

T/F High T3/T4 levels activates osteoclasts, leading to osteoporosis and hypercalcemia.

A

72H
True
One effect of the osteoporosis is increased rate of bone fracture.

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93
Q

T/F Untreated infantile hypothyroidism results in permanent mental retardation known as cretinism.

A

73

True

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94
Q

T/F Depending on cause, myxedema can usually be reversed with iodine supplements or thyroid hormone replacement therapy.

A

74

True

95
Q

T/F The mental retardation of cretinism will usually disappear once the underlying hypothyroidism is successfully treated.

A

75

False; The underlying hypothyroidism may disappear on treatment, but any mental impairments will be permanent.

96
Q

T/F In primary hypothyroidism, circulating T3 and T4 levels are low but serum TSH levels are high.

A

76

True

97
Q

T/F In secondary hypothyroidism, circulating T3 and T4 levels are low but serum TSH levels are high.

A

77
False; The fact that this is secondary hypothyroidism means that the pituitary (or hypothalamus) has the problem, and TSH levels are consequently low.

98
Q

[Primary/ Secondary] hypothyroidism occurs as a result of hypothalamic or pituitary disease.

A

78
Secondary; Remember, if the problem is in the gland itself, it’s primary. If the problem affects the gland but is not in the gland itself, it is secondary.

99
Q

[Congenital/ Acquired / Autoimmune ] hypothyroidism is also known as cretinism.

A

79

Congenital

100
Q

One cause of [congenital/ acquired / autoimmune ] hypothyroidism is total thyroidectomy.

A

80
Acquired; This should be a give-away. Thyroidectomy is a post-partum procedure- children aren’t born with it, so it is not a congenital condition, and antibodies and immune cells are not involved so it is not an autoimmune condition. This happens to you during your life, i.e., it is acquired.

101
Q

______________________ arises from a functional failure of the thyroid and its inability to meet the body’s demands for T3 and T4.

A

81

Primary hypothyroidism

102
Q

__________________ is the most common cause of autoimmune hypothyroidism.

A

82

Hashimoto thyroiditis

103
Q

In ________________, proteoglycans accumulate in the extracellular matrix and bind water; the skin appears dull, puffy, and yellowed, with sparse hair and periorbital puffiness.

A

83

myxedema

104
Q

Which ONE of the following is NOT a typical symptom of hypothyroidism?

A. Sleepiness
B. Reduced stamina and endurance
C. Lack of mental alertness
D. Decreased motility in the intestine (=constipation)
E. Bradycardia
F. Weak, stiff, achy skeletal muscles
G. Brittle hair
H. (None. All of the above are typical symptoms of hypothyroidism)
A

84

H.

105
Q

T/F Hypothyroidism: The skin is cool, pale, and puffy.

A

85A
True
This peculiar form of edema is termed myxedema.

106
Q

T/F Hypothyroidism: The skin is quite moist due to increased sweating.

A

85B
False
Decreased sympathetic activity decreases sweat and sebaceous gland activities, so the skin is not moist but dry.

107
Q

T/F Hypothyroidism: Skin lesions heal slowly.

A

85C
True
This is due to decreased peripheral circulation (poor blood flow to the skin).

108
Q

T/F Hypothyroidism: Hoarseness is common.

A

85D
True
Due to increased deposition of glycosaminoglycans in and around the larynx.

109
Q

T/F Hypothyroidism: Heart rate and stroke volume are increased.

A

85E
False
Backwards; the decreased sympathetic activity lowers heart rate and stroke volume, so that cardiac output is reduced. Exercise intolerance is common

110
Q

T/F Hypothyroidism: Lethargy and somnolence may develop, and slowed mentation causes memory loss.

A

85F
True
This is due, at least in part, to thelowered cardiac output- the brain is hypoxic.

111
Q

T/F Hypothyroidism: Reproductive effects of hypothyroidism include anovulation, menstrual irregularities, erectile dysfunction, and oligospermia.

A

85G
True
Loss of libido is another effect.

112
Q

T/F Hypothyroidism: Diarrhea

A

85H
False
Hypothyroidism slows the GI tract, so decreased motility results in constipation and stool impaction.

113
Q

T/F Hypothyroidism: In children, untreated hypothyroidism may cause dwarfism.

A

85I
True
The so-called ‘thyroid dwarfism.’ This is due to the fact that thyroid hormones are required for growth hormone to fully manifest.

114
Q

T/F Hypothyroidism: Brittle hair

A

85J

True

115
Q

T/F Mild cases of Hashimoto thyroiditis often require no treatment, and moderate cases are often treated with thyroid hormone replacement therapy.

A

86

True; Surgery is only required when there are compression effects on surrounding tissues

116
Q

T/F Hashimoto thyroiditis and Graves disease are the two most common immunologically mediated disorders of the thyroid.

A

87

True

117
Q

T/F Hashimoto thyroiditis results in gradual thyroid failure due to autoimmune destruction of the thyroid gland.

A

88

True

118
Q

T/F Microscopic examination of a thyroid with Hashimoto thyroiditis reveals extensive infiltration of the parenchyma by lymphocytes and plasma cells; germinal centers are common.

A

89

True

119
Q

T/F In Hashimoto thyroiditis, the thyroid follicles are enlarged and hypertrophic due to the elevated TSH levels.

A

90
False; In Hashimoto thyroiditis, the follicles are being destroyed by the immune system, and thus are atrophic (not enlarged). The gland itself may be enlarged, not by follicular hypertrophy, but by the accompanying inflammation and fibrosis.

120
Q

T/F The most common initial presentation of Hashimoto thyroiditis is a painless goiter in a middle-aged woman.

A

91

True; Usually there are signs of hypothyroidism as well.

121
Q

T/F Unlike Graves disease, goiters are not seen in Hashimoto thyroiditis.

A

92
False; Goiters can develop in Hashimoto thyroiditis through a combination of TSH stimulation, immune cell infiltration and inflammation, and fibrosis.

122
Q

___________________ is a term that encompasses a heterogeneous group of inflammatory disorders of the thyroid gland, including those that are caused by autoimmune mechanisms or by infectious agents.

A

93

Thyroiditis; Note the phrase ‘inflammatory disorders of the thyroid’, cuing you onto the fact that this a thyroidisis.

123
Q

___________ is characterized by the presence of circulating antibodies to thyroid antigens and features of cell-mediated immunity to thyroid tissue.

A
  1. Hashimoto thyroiditis
124
Q

___________________ refers to a situation sometimes seen in Hashimoto thyroiditis where the longer-term hypothyroidism is preceded by a transient thyrotoxicosis due to massive disruption of thyroid follicles.

A

95

Hashitoxicosis

125
Q

T/F Most (at least 90%) patients with subacute thyroiditis return to normal thyroid function without medical treatment.

A

96

True

126
Q

T/F Subacute thyroiditis is best treated with thyroid hormone replacement therapy.

A

97

False; In most cases, patients with subacute thyroiditis require no specific medical treatment.

127
Q

__________________ thyroiditis is a self-limited thyroid condition associated with a triphasic clinical course of hyperthyroidism, hypothyroidism, and return to euthyroidism.

A

98
Subacute thyroiditis; This definition applies to all the variants of this disorder- de Quervain, painfull, and postpartum subacute thyroiditis.

128
Q

Which ONE of the following best describes the typical clinical course of subacute thyroiditis?

A. Hyperthyroidism, followed by hypothyroidism, and then a return to euthyroidism
B. Hyperthyroidism, followed by euthyroidism, and then persistent hypothyroidism
C. Hypothyroidism, followed by hyperthyroidism, and then a return to euthyroidism
D. Hypothyroidism, followed by euthyroidism, and then persistent hyperthyroidism
E. (None of the above describe the typical clinical course of subacute thyroiditis)

A

99
A. We’ve seen this pattern before. Initial destruction of thyroidal follicles releases massive amounts of preformed T3 and T4, and hyperthyroidism ensues. When the hormone stores are exhausted, hypothyroidism appears. Eventually, the
thyroid recovers, and euthyroidism returns.

129
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis is a self-limited thyroid condition associated with a triphasic clinical course of hyperthyroidism, hypothyroidism, and return to euthyroidism.

A

100A

General

130
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis is an infrequent, self-limited disorder of the thyroid characterized by granulomatous inflammation and caused by viral infection.

A

100B

de Quervian thyroiditis

131
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

The initial presenting symptom of this thyroiditis is typically an exquisitely tender (i.e., painful) thyroid gland.

A

100C

de Quervian thyroiditis

132
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis is characterized by lymphocytic infiltration and mild enlargement of the thyroid but without thyroid pain.

A

100D

Painless thyroiditis

133
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis is the most common cause of thyroid pain.

A

100E

de Quervian thyroiditis

134
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis is a rare disorder of unknown etiology characterized by extensive fibrosis involving the
thyroid and contiguous neck structures.

A

100F

Riedel thyroiditis

135
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis usually requires no medical treatment at all

A

100G

de Quervian thyroiditis

136
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

Although most patients with this thyroiditis become euthyroid within a year, about a third of patients will progress to frank hypothyroidism within a 10 year period

A

100H

painless thyroiditis

137
Q

T/F Subacute thyroiditis:
General, de Quervian thyroiditis, painless thyroiditis, or Riedel thyroiditis?

This thyroiditis involves heavy fibrosis in the neck region and is treated with some combination of corticosteroids, tamoxifen, and/or surgery

A

100I

Riedel thyroiditis

138
Q

T/F On gross examination, follicular adenoma presents as numerous nodules that project from the surface of the thyroid.

A
  1. False; This description is precisely that of a multinodular goiter. Follicular adenomas present as a solitary nodule that projects from the surface of the thyroid. In fact, this is how you tell the two apart- single nodule, follicular adenoma; multiple nodules, multinodular goiter.
139
Q

T/F Most thyroid cancers are medullary carcinomas of the parafollicular cells.

A

102

False; The most common type of thyroid cancer is papillary carcinoma; this is a follicular cancer.

140
Q

T/F Papillary carcinomas typically invade the lymphatics and spread to the nearby cervical lymph nodes.

A

103
True; Papillary carcinomas do not usually spread to more distant sites because they do not invade the blood vessels for hematogenous spread.

141
Q

T/F Medullary carcinomas typically invade the blood vessles; they often spread to the lungs, bones, and liver.

A

104

True

142
Q

T/F Medullary and follicular carcinomas account for the majority of thyroid cancers associated with previous exposure to ionizing radiation (e.g., radioactivity)..

A

105
False; This ‘honor’ goes to papillary carcinomas. There was an increase in papillary carcinomas after Chernobyl, and will undoubtedly be another increase in Japan after the Fukushima incident.

143
Q

T/F In papillary thyroid carcinoma, the presence of metastases to the cervical lymph nodes at the time of surgery does not change the prognosis.

A

106

True

144
Q

T/F Papillary thyroid carcinoma has a poor prognosis; less than 20% of patients survive 5 years post diagnosis.

A

107

False; PTC has an excellent prognosis, with a 10 year survival rate of over 95%.

145
Q

__________________ refers to a benign neoplasm of the thyroid that exhibits follicular differentiation.

A

108

Follicular adenoma

146
Q

___________________ is the most common tumor of the thyroid gland.

A

109

Follicular adenoma

147
Q

Which ONE of the following does NOT pertain to papillary thyroid carcinoma?

A. A painless palpable nodule in an otherwise normal gland.
B. A nodule with enlarged cervical lymph nodes.
C. Cervical lymphadenopathy in the absence of a palpable thyroid nodule.
D. Tumors larger than 0.5 cm can be detected as cold areas in a thyroid scintiscan.
E. (None, i.e., all of the above pertain to papillary thyroid carcinoma)

A

110

E. They’re all true of papillary thyroid carcinoma.

148
Q

T/F The parathyroid glands release parathyroid hormone (PTH), the most important hormone in lowering serum calcium levels.

A

111

False; PTH raises serum calcium levels.

149
Q

Most individuals have [1/ 2 / 3 / 4 / 6 / 8 / 10] parathyroid glands, located on the posterior aspect of the thyroid gland.

A

112
Four is the typical number, though someindividuals are known to have up to 8 parathyroid glands located anywhere in the neck or upper chest.

150
Q

Which ONE of the following is not a recognized mode of action of parathyroid hormone (PTH) in raising serum calcium levels?

A. PTH causes bone cells to absorb the bony matrix & release calcium into blood
B. PTH causes the kidneys to reabsorb more Ca++, thus reclaiming calcium from the urine and returning it to the plasma.
C. Via vitamin D, PTH increases absorption of Ca++ by the intestinal mucosa
D. PTH causes the tissues of the body to take up less calcium from the plasma, thereby helping to keep plasma levels high.
E. PTH stimulates the conversion of relatively inactive vitamin D to its more active form, calcitriol.
F. (None. All of the above are recognized modes of action of PTH.)

A

113

D. PTH is not known to affect calcium uptake by body tissues..

151
Q

T/F Patients with all forms of hypoparathyroidism are successfully treated with vitamin D and calcium supplementation.

A

114

True

152
Q

T/F The hallmark of hypoparathyroidism is tetany, due to the accompanying hypocalcemia.

A

115

True

153
Q

T/F Pseudohypoparathyroidism presents with hypocalcemia, such that tetany and cramping are common.

A
  1. True; Recall that a lowered blood calcium level decreases the threshold of neurons and muscle cells, so that they are excited and depolarize (i.e., fire a nerve signal) more easily. This translates into highly excitable- irritable- nerves and spastic muscles.
154
Q

[Surgery / Autoimmune phenomena / Parathyroid agenesis / Genetic mutations] is/are themost common cause of hypoparathyroidism.

A

117

Surgery- they took out the parathyroids!

155
Q

[Hypercalcemia/ Hypocalcemia] is the consistent result of hypoparathyroidism.

A

118

Hypocalcemia

156
Q

[Hyperparathyroidism / Hypoparathyroidism / Pseudohypoparathyroidism / Turner syndrome] can often be recognized clinically by the presence of shortened metacarpals, the so-called knuckle-knuckle-dimple-dimple sign.

A

119

Pseudohypoparathyroidism; remember that knuckle-knuckle-dimple-knuckle is a sign of Turner syndrome.

157
Q

____________________ results from decreased secretion of parathyroid hormone (PTH) or from decreased end-organ sensitivity to PTH.

A

120

Hypoparathyroidism

158
Q

_________________ reflects target organ insensitivity to PTH, and designates a group of hereditary conditions characterized by hypocalcemia.

A

121
Pseudohypoparathyroidism; In other words, pseudohypoparathyroidism is due to PTH insensitivity in the target organ- the cells can’t ‘see’ PTH that is present.

159
Q

Which ONE of the following is NOT a typical symptom/sign of hypoparathyroidism?

A. Paresthesias
B. Renal calculi
C. Tetany
D. Cataracts
E. Parkinsonian-like movement disorders due to calcification of the basal nuclei
F. Anxiety, depression, confusion
G. Increased intracranial pressure
H. (None; all of the above are typical symptoms/signs of hypoparathyroidism)
A

122
B. Incidentally, the paradoxical association of hypocalcemia with intracranial calcification may be due to increased phosphate levels, resulting in tissue deposits with locally produced calcium.

160
Q

T/F Secondary hyperparathyroidism occurs in the context of chronic hypocalcemia.

A

123

True; Usually this is due to kidney disease, but other factors- such as hypovitaminosis D- can cause it as well.

161
Q

T/F Hyperparathyroidism is a rare disorder most common in young to middle-aged men.

A

124
False, false, false; Hyperparathyroidism is one of the most common endocrine disorders, occurring four times more often in women that men and typically occurring inolder adults (older 50 years of age).

162
Q

T/F By far, the most common cause of hyperparathyroidism is a parathyroid carcinoma.

A

125

False; The most common cause is a parathyroid adenoma. In fact, parathyroid carcinoma is downright rare.

163
Q

T/F Hyperparathyroidism results in hypercalcemia.

A

126

True; Remember, PTH raises blood calcium levels, so oversecretion of PTH….

164
Q

T/F Classically, parathyroid adenoma involves all four glands, while parathyroid hyperplasia is almost always solitary .

A

127
False; This is backwards. Hyperplasia usually hits all four glands (or at least two or three) while parathyroid adenoma is solitary (as is carcinoma)..

165
Q

T/F Some cases of secondary hyperparathyroidism respond to dietary vitamin D supplementation.

A

128

True; If hypovitaminosis was the underlying cause of th secondary hypoparathyroidism.

166
Q

__________________ refers to the syndrome caused by excessive secretion of PTH by a parathyroid adenoma, primary hyperplasia of all the parathyroids, or parathyroid carcinoma..

A

129

Primary hyperparathyroidism

167
Q

_________________ is caused by any condition that gives rise to chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands; it is encountered mainly in patients with chronic renal failure

A

130
Secondary hyperparathyroidism; Notice that low calcium levels stimulate the parathyroid glands just like TSH stimulates the thyroids.

168
Q

T/F Primary hyperparathyroidism:

Eroded bone matrix and osteoporosis

A

131A
True
‘Painful bones’; PTH activates osteoclasts.

169
Q

T/F Primary hyperparathyroidism:

Kidney stones and nephrocalcinosis

A

131B
True
‘Renal stones’

170
Q

T/F Primary hyperparathyroidism:

Metastatic calcification in body tissues

A

131C
True
Recall that metastatic calcification is due to high circulating levels of calcium.

171
Q

T/F Primary hyperparathyroidism:

Tetany

A

131D
False
Muscle spasms are more likely to occur with hypocalcemia.

172
Q

T/F Primary hyperparathyroidism:

Hypotension

A

131E

False

173
Q

T/F Primary hyperparathyroidism:

Pancreatitis, cholelithiasis, constipation

A

131F
True
‘Abdominal groans’

174
Q

T/F Primary hyperparathyroidism:

“Painful bones, renal stones, abdominal groans, and psychic moans”

A

131G

True

175
Q

T/F Primary hyperparathyroidism:

Depression, lethargy, and eventually seizures

A

131H
True
‘Psychic moans’.

176
Q

T/F Primary hyperparathyroidism:

Hyperactivity

A

131I
False
Weakness and fatigue are the norm, not hyperactivity.

177
Q

T/F All steroid hormones are cholesterol derivatives.

A

132

True; If it ain’t derived from cholesterol, it can’t be a steroid. Period.

178
Q

T/F DHEA is the most important of the mineralocorticoids.

A

133

False; DHEA is a gonadocorticoid; the most important mineralocorticoid is aldosterone.

179
Q

Aldosterone is the most important of the [mineralocorticoids/ glucocorticoids/ gonadocorticoids].

A

134

mineralocorticoids

180
Q

[Mineralocorticoids/ Glucocorticoids/ Gonadocorticoids / Corticosteroids] are the primary steroid hormones made and released by adrenal cortex.

A

135

Corticosteroids

181
Q

The [mineralocorticoids / glucocorticoids/ gonadocorticoids ] are the corticosteroids that help regulate electrolyte balance.

A

136

mineralocorticoids

182
Q

The adrenal _______________ is the innermost part of the adrenal gland; it releases the sympathetic hormones epinephrine and norepinephrine.

A

137

medulla

183
Q

The adrenal ______________ is the outermost part of the adrenal gland; it releases the adrenal steroid hormones.

A

138

cortex

184
Q

Which of the following (may be more than one) does not trigger (i.e., stimulate) the renin-angiotensin-aldosterone system?

A. Decreased plasma sodium
B. Decreased red blood cell count (increased hypoxia)
C. Decreased plasma volume
D. Decreased plasma calcium
E. Decreased arterial blood pressure
F. Increased water retention
G. (None; all of the above stimulate the renin-angiotensin-aldosterone system)

A

139
B, D, F
B) The kidneys monitor oxygen carrying capacity of the blood, and release erythropoietin when it drops too low.
D) The parathyroid glands monitor plasma calcium levels and release PTH when it drops too low..
F) The hypothalamus monitors the hydration state of the blood and increases or decreases the secretion of ADH accordingly..

185
Q

Which ONE of the following is not an effect of angiotensin II? Angiotensin II…

A. …causes vasoconstriction of arteries.
B. …acts on the hypothalamic thirst center to increase the sensation of thirst.
C. …increases ADH secretion by the posterior pituitary, causing the kidneys to reabsorb more water.
D. … increases aldosterone secretion by the adrenal cortex, causing the kidneys to reabsorb more sodium.
E. (None. All of the above are effects of angiotensin II)

A

140

E. (None. All of the above are effects of angiotensin II)

186
Q

Which ONE of the following is NOT an action of glucocorticoids like cortisol?

A. Glucocorticoids stimulate gluconeogenesis in liver cells.
B. Glucocorticoids promote glucose sparing.
C. Glucocorticoids lower blood glucose levels
D. Glucocorticoids promote protein and lipid breakdown
E. Glucocorticoids, at pharmacologic levels, suppress the immune system.
F. (None of the above, i.e., they are all true about glucocorticoids like cortisol)

A

141
C. As our stress hormones, glucocorticoids don’t lower glucose levels- just the opposite, they raise them. The body is in a stressful situation, and glucocorticoids ensure that body cells at least have enough fuel- glucose- to deal with the stress.

187
Q

T/F Pituitary disorders are the most common cause of secondary hyperaldosteronism.

A

143
False; Recall that the renin-angiotensin-aldosterone system is not controlled by the pituitary but by plasma sodium and blood volume/pressure. Thus, pituitary disoders do not directly cause secondary hyperaldosteronism.

188
Q

T/F Seventy percent of cases of Conn syndrome are due to a hypersecreting tumor of the adrenal medulla.

A

144
False; Most instances of Conn tumor are due to a hypersecreting tumor of adrenal cortex. Medullary tumors would be pheochromocytomas.

189
Q

T/F Aldosterone secretion is regulated by the pituitary hormone ACTH.

A

145
145. False; Under normal circumstances, ACTH has little to do with aldosterone secretion, which is regulated by the renin-angiotensin-aldosterone system.

190
Q

T/F In contrast to Conn syndrome, secondary hyperaldosteronism is associated with hyperreninemia due to excessive activation of the renin-angiotensin-aldosterone system.

A

146
True; This forms a handy lab test to distinguish between primary and secondary hyperaldosteronism. Aldosterone and renin levels elevated- secondary hyperaldosteronism. Aldosterone elevated, renin normal- Conn syndrome.

191
Q

T/F Hyperaldosteronism leads to enhanced activity of the Na+-K+ pumps in the kidney tubules, and usually results in hyponatremia and hyperkalemia.

A

147
False; This is almost correct, except the direction of the pumps. Sodium is pumped back INTO the body (from the urine), and potassium is pumped OUT of the body (into the urine). Thus hyperaldosteronism leads to hypernatremia and hypokalemia.

192
Q

T/F Conn syndrome is often treated by administration of aldosterone.

A

148
False; Conn syndrome is primary hyperaldosteronism. Instead of treating it with aldosterone, you would treat it with an aldosterone antagonist, such as spironolactone.

193
Q

[Primary/ Secondary] hyperaldosteronism is usually caused by conditions that reduce blood flow to the kidneys and thus excessive activation of the renin-angiotensin-aldosterone system.

A

149

Secondary

194
Q

In primary hyperaldosteronism, the renin-angiotensin-aldosterone system will be [suppressed / activated ] and plasma renin activity will be [ increased / decreased ].

A

150
RAA is suppressed and renin activity is decreased. This should make sense. If the purpose of the RAA system is to increase secretion of aldosterone, but aldosterone levels are already elevated, it makes sense that the RAA system would then be inhibited- ‘We don’t need no more stinkin’ aldosterone!’ Similarly, if renin activates the RAA system, but the RAA system is suppressed, then it makes sense that renin secretion will also be suppressed. ‘We don’t need no renin, either!’

195
Q

Primary hyperaldosteronism is also known as ________________.

A

151

Conn syndrome

196
Q

_____________ is the most common manifestation of primary hyperaldosteronism.

A

152

Hypertension, blood pressure elevation

197
Q

Which ONE of the following is NOT a common symptom associated with
hyperaldosteronism?

A. HYPERTENSION
B. Hypernatremia
C. Hypokalemia
D. Muscle weakness
E. Hypercalcemia
F. Fatigue
G. Polyuria and polydipsia
H. Metabolic alkalosis
I. If hypokalemia, then paresthesias and even frank tetany
J. (None; all of the above are symptoms consistent with hyperaldosteronism)
A

153

Hypercalcemia; aldosterone affects sodium and potassium, not calcium.

198
Q

T/F The typical treatment for hypercortisolism is resection of a hypersecreting tumor, or cessation of glucocorticoid administration, whichever is appropriate.

A

154

True

199
Q

Cushing [disease/ syndrome] refers to hypercortisolism due to a pituitary corticotropic adenoma.

A

155

Disease; all other causes of hypercortisolism is refered to as Cushing syndrome.

200
Q

___________________ refers to elevated blood sugar levels as a result of hypercortisolism.

A

156

Adrenal diabetes

201
Q

Which ONE of the following is the most common cause of Cushing syndrome?

A. Pituitary corticotropic adenoma (ACTH hypersecretion)
B. Exogenous glucocorticoids such as prednisone
C. Functional adrenocorticotropic tumors
D. Paraneoplasty; functional extrapituitary tumors that hypersecrete ACTH
H. (None; the most common cause of Cushing syndrome is not listed above)

A

157
B; Amongst all causes, the most common cause is ingestion or absorption of glucocorticoid drugs. Amongst just the endogenous causes, the most common is a pituitary corticotropic adenoma.

202
Q

Which of the following is NOT a typical manifestation of Cushing syndrome?

A. “Buffalo hump” in the lower neck/upper back region
B. “Moon face”
C. Low resistance to infections
D. Cutaneous striae, dermal atrophy
E. Menstrual irregularities
F. Hypoglycemia, oliguria
G. (None; all of the above are typical manifestations of Cushing syndrome).

A

158
F. Because of the diabetogenic effect of cortisol, Cushing syndrome cause hyperglycema, from which come glycosuria, polyuria, and polydipsia. The low resistance to infections is due to the fact the high levels of glucocorticoids suppresses the immune system.

203
Q

T/F The most common cause of adrenogenital syndrome in adult women is an androgen-producing tumor.

A

159

True

204
Q

T/F In neonates, adrenogenital syndrome is typically caused by mutation of one of the enzymes involved in steroid metabolism.

A

160
True; This is known as congenital adrenal hyperplasia. The hyperplasia is due to a chain of events, starting with low cortisol levels, which then cause high ACTH levels, which in turn stimulates the adrenal glands and results in hyperplasia.

205
Q

__________________ is a condition in which hypersecretion of adrenal sex steroids (androgens) leads to masculinization in girls and precocious pseudopuberty in boys.

A

161

Adrenogenital syndrome

206
Q

In _______________ adrenogenital syndrome (or congenital adrenal hyperplasia), a total lack of 21-hydroxylase activity results in no synthesis of either cortisol or aldosterone; such an individual cannot retain their sodium.

A

162

Salt-wasting; this manifestation of adrenogenital syndrome kills babies (dehydration, electrolyte imbalances).

207
Q

________________ adrenogenital syndrome (AS) (or congenital adrenal hyperplasia), the most common type of AS, is due to partial deficiency of 21-hydroxylase activity; such indiviuals can still make cortisol and aldosterone, though at lower levels than normal.

A

163

Late-onset; this form of AS may be asymptomatic, or may present as hirsutism and menstrual irregularities.

208
Q

Adrenogenital syndrome causes ___________________ in boys.

A

164

Precocious pseudopuberty

209
Q

Adrenogenital syndrome causes ___________________ in girls.

A

165

Virilization

210
Q

Which ONE of the following statements best describes the steroid deficiency or deficiencies accompanying a total lack of 21 hydroxylase activity?

A. Cortisol and aldosterone
B. Cortisol only
C. Cortisol and progesterone
D. Progesterone and estrogens
E. Testosterone and estrogen
F. Progesterone, estrogen, and testosterone
G. All corticosteroids
H. (None. Corticosteroid synthesis is not affected by a lack of 21 hydroxylase)
A

166
A. Cortisol and aldosterone. Examine the steroid biosynthesis chart on or about Slide 161. Recall that many mutations can alter 21 hydroxylase activity. If a patient has NO hydroxylase activity, then they will have extreme hypocortisolism with salt wasting (lack of aldosterone)- a very serious medical condition. On the other hand, some hydroxylase mutations will abolish cortisol synthesis but leave adequate aldosterone sythesis. Such individuals will experience hypocortisolism without the salt-wasting. In either case, lack of cortisol (with or without lack of aldosterone) shunts adrenal resources into gonadocorticoid synthesis, resulting in adrenogenital syndrome.

211
Q

Which ONE of the following is not a symptom/sign consistent with late-onset congenital adrenal hyperplasia?

A. 21 hydroxylase deficiency
B. Delayed menarche
C. Oligomenorrhea
D. Hirsutism
E. Truncal obesity and moon face
F. (None. All of the above are consistent with congenital adrenal hyperplasia)
A

167
E. Recall that in CAH, cortisol levels are down, whereas truncal obesity and moon face are seen in hypercortisolism. Thus they would not be present in CAH. Also, while several other enzyme deficiencies could be the cause of CAH (such as 11
hydroxylase), a 21 hydroxylase is by far the most common enzyme that is lacking.

212
Q

Unless antibiotic therapy is instituted immediately, Waterhouse-Friderichsen Syndrome may kill within hours to a few days.

A

168

True

213
Q

Addison disease progresses quickly, and when about 50% of the adrenal cortex (of both glands) is lost, it becomes clinically apparent.

A

169
False; This is a chronic disease, which takes a chronic, slowly progressive course. About 90% of the adrenal cortex needs to be lost before this disorder becomes clinically apparent.

214
Q

Both primary and secondary adrenocortical insufficiency usually result in hyperpigmentation.

A

170
False; The hyperpigmentation comes from the link between high ACTH and high MSH and POMC levels. Except that in secondary adrenocortical insufficiency ACTH levels are depressed, so that SAI would not lead to hyperpigmentation.

215
Q

Another distinction between primary (PAI) and secondary (SAI) adrenocortical insufficiency is that aldosterone levels are depressed in the former (PAI) but (near) normal in the latter (SAI).

A

171
True; Recall that PAI is due to adrenocortical destruction, while SAI is due to low ACTH levels. Recall also that ACTH largely controls cortisol, and to a lesser extent, gonadocorticoid levels, while the renin-angiotensin-aldosterone system controls aldosterone levels. In PAI, where the adrenal cortex is being destroyed, ALL corticosteroid levels will be down, whereas in in SAI, the low ACTH will depress cortisol and gonadocorticoid levels but leave aldosterone levels relatively untouched.

216
Q

__________________, or primary acute adrenocortical insufficiency, is acute,
bilateral, hemorrhagic infarction of the adrenal cortex, most commonly secondary to meningococcal or pseudomonal septicemia.

A

172
Waterhouse-Friderichsen syndrome; this may not become symptomatic until 90% of the adrenals are destroyed, and even today it still kills many of its victims.

217
Q

_______________, or primary chronic adrenocortical insufficiency, is marked by progressive destruction of the adrenal cortex, usually by autoimmune phenomena.

A

173
Addison disease; Although autoimmune adrenalitis is the most common cause of Addison disease, any process that slowly destroys the adrenal cortex, such as infection, can cause this disorder.

218
Q

Which ONE of the following is NOT a symptom consistent with Waterhouse-Friderichsen syndrome.

A. Rapidly progressing hypotension
B. Shock
C. Disseminated intravascular coagulopathy
D. Widespread purpura
E. (None; all of the above are symptoms of Waterhouse-Friderichsen syndrome)

A

174

E. This is a very serious syndrome, and without immediate antibiotic therapy it may kill within hours or a few days.

219
Q

Which ONE of the following is NOT a symptom commonly associated with Addison disease?

A. GI disturbances such as diarrhea and nausea
B. Weakness and easy fatigability
C. Hyperpigmentation
D. Hypernatremia and hypokalemia
E. Hypovolemia and hypotension
F. Poor resistance to stress
G. Cardiac conduction problems
H. (None of the above, i.e., they are all true about the symptoms of Addison disease)
A

175
D. Remember that aldosterone conserves sodium at the expense of potassium. In adrenocortical insufficiency, aldosterone levels are deficient, which will thus result in hyponatremia and hyperkalemia.

Notes:

(b) Probably due to the electrolyte disturbances, such as low sodium and high potassium.
(c) Due to the MSH, ACTH, and POMC connection.
(d) Due to the low aldosterone levels.
(e) Again due to the low aldosterone levels.
(f) Due to the low cortisol levels.
(g) Due to the electrolyte imbalances.

220
Q

Which ONE of the following is a valid distinction between primary (PAI) vs secondary (SAI) adrenocortical insufficiency?

A. In PAI cortisol levels are elevated while in SAI cortisol levels are depressed.
B. In PAI and SAI, ACTH levels are depressed.
C. Exogenously administered ACTH would raise cortisol levels in SAI but not in PAI
D. Exogenously administered cortisol would raise ACTH levels in PAI but not in SAI
E. Lowered blood sodium levels would activate the renin-angiotensin-aldosterone system and ultimately raise aldosterone levels in PAI
F. ACTH has no effect on the adrenals in either PAI or SAI.
G. (None. None of the above statements are a valid distinction between PAI and SAI)

A

176
C. For the explanations given below, keep in mind that PAI is slow destruction of the adrenal cortex, and ACTH cannot stimulate a cortex that has been lost. SAI, on the other hand, is a problem with the pituitary secretion of ACTH; the adrenals are healthy but are not receiving enough ACTH.

Notes:

(a) We are talking adrenocortical insufficiency- cortisol levels are depressed in both PAI and SAI.
(b) ACTH levels are depressed in SAI, but elevated in PAI (the pituitary is trying in vain to stimulate adrenals that are mostly destroyed).
(c) Remember again that the problem is low ACTH in SAI, so giving ACTH would raise cortisol levels. On the other hand, adrenal destruction has occurred in PAI, so raising ACTH levels won’t accomplish diddly-squat.
(d) In either case, cortisol has a negative feedback effect on ACTH, so raising cortisol levels by injection would only serve to lower ACTH levels.
(e) This might seem true at first, since low sodium is a trigger for the RAA system. But again, we are talking primary adrenocortical insufficiency here, and angiotensin II cannot squeeze aldosterone out of destroyed adrenals anymore than you can squeeze water out of a hard rock (I think that analogy works here).
(f) ACTH would raise cortisol levels in SAI.

221
Q

T/F The sine qua non of a pheochromocytoma is the elevated levels of epinephrine and norepinephrine.

A

177
True; Remember that sine qua non means, ‘(That) without which there is no other’, meaning you will not have a pheochromocytoma of any size without elevated E/NE levels.

222
Q

T/F Most pheochromocytomas are benign.

A

178

True; About 90% actually

223
Q

A ____________________ is a hyperfunctional tumor of the chromaffin cells of the adrenal medulla.

A

179

pheochromocytoma

224
Q

Which ONE of the following is NOT a symptom consistent with a tumor of the chromaffin cells of the adrenal medulla?

A. Hyperglycemia
B. Increased metabolic rate
C. Rapid heart beat and palpitations
D. Hypertension
E. Intense nervousness
F. Anhidrosis
G. (None of the above, i.e., they are all true about chromaffin cell tumors of the adrenal medulla)
A

180
F. All except anhidrosis are simply symptoms of increased sympathetic activity. Sweating is a sympathetic phenomenon, so anhidrosis- lack of sweating- would not be consistent with the heightened sympathetic activity of these tumors.

225
Q

T/F Type II diabetes mellitus responds well to a lifetime of insulin injections.

A

181
False; insulin levels may very well be normal in NIDDM; the problem is that target cells cannot respond properly to insulin, so injecting more insulin will not help. To be more precise, it may help initially, by flooding the body with so much insulin that it overcomes the hyporesponsiveness, but eventually the target cells stop responding to these high insulin levels, at which point further insulin injections will be of little help.

226
Q

T/F Glucagon targets the liver, muscles, and adipose tissue.

A

182

False; Glucagon targets the liver; insulin would target all these organs, and more.

227
Q

T/F In the endocrine pancreas, alpha cells secrete insulin and beta cells secrete glucagon.

A

183

False; It’s the other way around.

228
Q

Normally, [hypoglycemia/ hyperglycemia] results from hypersecretion of insulin.

A

184

hypoglycemia; remember that glucose brings the blood sugar- and other fuels- down in concentration.

229
Q

____________ and ____________ are the two primary mechanisms by which the high blood sugar of diabetes mellitus damages tissues around the body.

A

185

Nonenzymatic glycosylation and osmotic damage

230
Q

______________, some of which are strong organic acids, are created when fats are metabolized without adequate levels of carbohydrates.

A

186
Ketones, or ketone bodies. Acetone and acetoacetic acid are two examples. These are commonly created in diabetes mellitus, where adequate sugar (carbohydrate) is not imported into cells.

231
Q

Which ONE of the following is not a common symptom of hypoglycemia?

A. Tremulousness, weakness
B. Headache and confusion
C. Hunger, nervousness
D. Decreased sweating and bradycardia
E. Slurred speech
F. (None; all of the above are symptoms consistent with hypoglycemia)
A

187
D. The symptoms of hypoglycemia listed in this question are either due to reflexive activation of sympathetic nervous system caused by the hypoglycemia or to insufficient glucose to the brain. Decreased sweating and bradycardia are not
sympathetic effects- increased sweating and tachycardia are. Thus D is the incorrect answer.

232
Q

Which ONE of the following is NOT a symptom of diabetes mellitus?

A. Polyuria and dehydration
B. Polydipsea
C. Electrolyte imbalances
D. Polyphagia
E. Appearance of ketone bodies in the blood
F. Lipidemia
G. (None, i.e., all of the above are symptoms of diabetes mellitus)

A

188

G. (None, i.e., all of the above are symptoms of diabetes mellitus)

233
Q

Which ONE of the following is NOT TRUE of Type I diabetes mellitus (IDDM)?

A. IDDM is the less common form of diabetes mellitus
B. IDDM appears to be an autoimmune disease and is characterized by loss of insulin-secreting beta cells in the pancreas
C. Blood insulin levels are typically quite low in IDDM individuals
D. IDDM can be managed with life-long insulin injections
E. IDDM is also known as juvenile onset diabetes
F. IDDM is only found in juveniles
G. (None, i.e., all of the above are true of Type I diabetes mellitus)

A

189

F. Altho IDDM has a predilection for younger individuals, it can (and does) appear at any age, even in the elderly.

234
Q

Which ONE of the following is NOT TRUE of Type II diabetes mellitus (NIDDM)?

A. NIDDM is the more common form of diabetes mellitus
B. The insulin hyporesponsiveness of NIDDM extends to all cells in the body; all cells are essentially starved for glucose
C. NIDDM may involve problems with the insulin receptors themselves, or perhaps with intracellular processes occurring after receptor activation
D. Because of insulin hyporesponsiveness, target cells cannot respond properlyto insulin and internalize glucose
E. NIDDM involves insulin resistance: target cells do not respond adequately to insulin
F. In NIDDM, target cells are effectively starved for glucose even tho blood levels of glucose are high
G. NIDDM responds well to dietary restriction and exercise
H. (None, i.e., all of the above are true of Type II diabetes mellitus)

A

190
B. Remember that insulin only affects the up-regulation of the GLUT4 glucose transporter; cells (such as brain cells) that use other GLUT transporters will not respond to insulin under any circumstances. This makes sense, since brain cells need constant access to glucose, and could not tolerate having access at some times (high insulin) and not at other times (low insulin) to blood glucose.

Patho (6 decks)

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