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NYCC Visceral Pathology > Lab 5 Endocrine > Flashcards

Lab 5 Endocrine Flashcards

1
Q

Name the 6 hormones of the ant. pituitary.

A

Prolactin, GH, ACTH, TSH, FSH + LH

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2
Q

What is the target organ and major function of Prolactin?

A

Breast - milk formation

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3
Q

What is the target organ and major function of GH?

A

Bone + Soft Tiss. to secrete IGF which stimulates growth

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4
Q

What is the target organ and major function of ACTH?

A

Adrenal Cortex - production + release of cortisol

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5
Q

What is the function of Cortisol/Corticosteroids?

A

glucose metabolism; salt + H20 metabolism

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6
Q

What is the target organ and major function of TSH?

A

Thyroid - produce T3 and T4 = metabolic rate

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7
Q

What is the target organ and major function of FSH/LH in females?

A

Ovary (Corpus Luteum) - production and release of progesterone + estrogen = ovum formation

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8
Q

What is the target organ and major function of FSH/LH in males?

A

Testes - production and release of testosterone = testis sperm formation

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9
Q

How does the post. pituitary differ from the ant.?

A

STORES and releases ADH + Oxytocin (does NOT produce hormones)

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10
Q

Explain/draw the hypothalamic-pituitary-target organ axis for GH.

A

Hypothalamus: GHRH –> Ant. Pituiatry: GH –> Bone + Soft tiss —> IGF —> growth –> (-) feedback to Hypothalamus + Ant. pituitary

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11
Q

Explain/draw the hypothalamic-pituitary-target organ axis for ACTH.

A

Hypothalamus: CRH –> Ant. Pituiatry: ACTH –> Adrenal Cortex: cortisol –> (-) feedback to Hypothalamus + Ant. pituitary

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12
Q

Explain/draw the hypothalamic-pituitary-target organ axis for FSH/LH.

A

Hypothalamus: GnRH –> Ant. Pituiatry: FSH/LH –> Ovary/Testes: estrogen, progesterone, testosterone –> (-) feedback to Hypothalamus + Ant. pituitary

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13
Q

Explain/draw the hypothalamic-pituitary-target organ axis for TSH.

A

Hypothalamus: TRH –> Ant. Pituiatry: TSH –> Thyroid: TH (T3/4) –> (-) feedback to Hypothalamus + Ant. pituitary

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14
Q

What structure is found in the superio-lateral aspects of the sphenoid sinus?

A

Optic CN II

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15
Q

What consequences of a large pituitary macroadenoma are seen on an MRI?

A

macroadenoma extends into sphenoidal sinus; compression of both Optic CNs

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16
Q

describe what is meant by Microadenoma.

A

not visible/measurable

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17
Q

describe what is meant by Macroadenoma.

A

visible/measurement may be given; may exert mass or stalk effects; may compress optic chiasm resulting in severe HA, bitemporal hemianopsia, loss of central vision

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18
Q

describe what is meant by stalk effect (in example of null cell tumor)

A

hormone signaling affected = increase Prolactin (normally inhibited), decrease 5 hormones (ACTH, FSH/LH, GH, TSH)

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19
Q

describe what is meant by mass effect (in example of null cell tumor)

A

hormone release affected = decrease all 6 hormones (prolactin, ACTH, FSH/LH, TSH, GH)

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20
Q

how do gigantism and acromegaly differ?

A

gigantism - childhood before GP closure, proportionate large stature

acromegaly - skeletaly mature, normal stature, unproportionate soft tissue structures: elongated face, prominent brow ridge, markedly thickened hands, hyperplasia of ears, nose, lips.

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21
Q

how are gigantism and acromegaly assessed using laboratory tests?

A

IGF-1 (will be increased)

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22
Q

what are the complications of gigantism versus acromegaly?

A

gigantism - early arthritis, cardiovascular compromise

acromegaly - visceromegaly, diastema, hypertension, HAs

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23
Q

define Diastema

A

gappening of teeth

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24
Q

how is Hypertension a complication in acromegaly?

A

BV thickening

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25
Q

What hormone is involved in gigantism and acromegaly?

A

GH

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26
Q

What hormone is involved in Cushing’s syndrome?

A

ACTH - Cortisol

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27
Q

what are the manifestations of Cushing’s syndrome?

A

moon face, buffalo hump, purple striae, hirsutism

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28
Q

define Hirsutism.

A

excess growth of coarse, dark hair in females where men typically have it

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29
Q

Why does an individual with Cushing’s syndrome present with purple striae? what is purple striae?

A

Cortisol inhibits lymphocytes, macrophages, fibroblasts = dermal fragility + increased body mass; dermal tears w/ bleeding

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30
Q

Why does an individual with Cushing’s syndrome present with Hirsutism?

A

^adrenocortical hormones (aldosterone + sex hormones) = ^androgen = facial hair patterns

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31
Q

define a toxic goiter.

A

thyroid enlargement w/ increased TH

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32
Q

define a non-toxic goiter.

A

thyroid enlargement w/o increased TH

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33
Q

What hormone is involved in Grave’s disease?

A

TSH

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34
Q

Histologically, Grave’s disease displays follicles lined by ____ cells, and colloid that is ____.

A

hyperplastic, tall columnar; pink and scalloped

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35
Q

in Grave’s disease, the __ of thyrocytes (increase/decrease); and colloid (increases/decreases)

A

quantity; increase; decrease

36
Q

other than the thyroid, Grave’s disease involves TSH receptors found where in the body? what does this result in and why?

A

on fibroblasts behind the eyes and in the ant. tibia; fibroblasts deposit ground substance = myxedema

37
Q

What hormone levels are to be expected in Grave’s disease?

A

^TH, decrease TSH, decrease TRH

38
Q

w/ Grave’s disease, ____ produces ____ which bind TSH receptors and stimulate thyrocytes resulting in ____.

A

type II hypersensitivity; anti-TSH receptor Antibodies; hyperthyroidism

39
Q

Grave’s disease presents w/ a (painful/painless) goiter

A

Painless

40
Q

What is another name for De Quervain Thyroiditis?

A

subacute thyroiditis

41
Q

describe the pathogenesis of subacute thyroiditis.

A
  • viral-like illness and recovery precedes
  • develop painful ant. neck enlargement
  • demonstrate hyperthyroidism signs
  • self-limiting (resolves in weeks/months)
42
Q

what is the pattern of inflammation associated w/ De Quervain thyroiditis? what are the consequences?

A

granulomatous inflammation; inflammation-induced follicle rupture releases TH

43
Q

subacute thyroiditis presents w/ a (painful/painless) goiter

A

Painful/tenderness

44
Q

Histologically, subacute thyroiditis displays ____ of ____ + ____. describe the follicles.

A

granulomas of necrosis + multinucleated giant cells; peripheral colloid-filled follicles

45
Q

Riedel Thyroidits (always/sometimes) trends towards ___.

A

always; Hypothyroidism

46
Q

describe the pathogenesis of Riedel Thyroiditis?

A
  • type III hypersensitivity
  • deposition of immune complexes (IC) into tissue
  • progressive collagenization
47
Q

Histologically, Riedel Thyroiditis involves ____ surrounded by ____

A

very few, very small follicles; scar tissue (ample fibrous CT replaces parenchyma)

48
Q

How does Riedel Thyroidits present clinically?

A

Painless, “woody”, stony palpable feel goiter

49
Q

Which thyroid condition(s) are hyperthyroid?

A

Grave’s disease, De Quervain thyroiditis

50
Q

Which thyroid condition(s) are hypothyroid?

A

Riedel thyroiditis

51
Q

which thyroid condition(s) present with a painful goiter?

A

De Quervain thyroiditis

52
Q

which thyroid condition(s) present with a painless goiter?

A

Grave’s disease, Riedel thyroiditis

53
Q

what distinct SSx are seen in Grave’s disease?

A

Myxedema behind the eyes and on the ant. tibia

54
Q

what distinct SSx are seen in Subacute thyroiditis?

A
  • preceeding viral infection
  • painful goiter
  • self-limiting (resolving w/in weeks/months)
55
Q

what distinct SSx are seen in Riedel thyroiditis?

A

stony, palpable, “woody” thyroid gland / goiter

56
Q

what is pediatric (neonate + infant) hypothyroidism?

A

Cretinism

57
Q

TH is premissive to ___

A

sex hormones; no TH = no puberty

58
Q

what is the etiology of Cretinism

A

multifacoral: maternal hypothyroidism, thyroid agenesis, endemic factors (iodine deficiency)

59
Q

how does Cretinism present?

A
  • large protruding tongue (myxedema deposits in tongue)
  • squaring-off forehead (coarse facial features)
  • low ant. hairline
  • short stature
  • cognitive disability
60
Q

what is the traditional medical treatment of Hypothyroidism?

A

Thyroxone (TH)

61
Q

what is the most common cause of hypothyroidism?

A

Hashimoto’s Thyroiditis

62
Q

how does Hashimoto’s present grossly; how about histologically?

A
  • sm. atrophic gland
  • ample chronic inflammatory cells - mostly lymphocytes, sm. atrophic follicles
63
Q

describe the pathogenesis of Hashimoto’s

A
  • autoimmune destruction of the thyroid (type II + type IV)
  • TSH binds to receptors on fibroblasts throughout the body = general myxedema
64
Q

what homones levels are to be expected in Hashimoto’s?

A

decreased TH, ^TSH, ^TRH

65
Q

describe the physical presentation of Hypothyroidism, why does this occur?

A

general Myxedema - cutaneous presentation of hypothyroidism; result of glycosaminoglycan accumulation in skin + soft tissues due to CT cell activation by ^circulating TSH levels. CT cells posses TSH receptors.

66
Q

what term is given to bulging eyballs due to accumulation of glycosaminoglycans in the post. eye (periorbital fat)?

A

Exophthalamus

67
Q

____ myxedema is a term given to individuals possessing Grave’s disease.

A

Pretibial myxedema

68
Q

what is Pretibial myxedema?

A

non-pitting edema in hyperthyroidism found on the anterior tibia

69
Q

what is the most common thyroid neoplasm?

A

Follicular adenoma (MC of all thyroid neoplasms)

70
Q

what is a follicular adenoma?

A

benign, solitary nodule; “cold” in radioactive uptake

71
Q

how do follicular adenomas present histologically?

A

hyperplastic follicles surrounded by a fibrous capsule. normal, but compressed, follicles on the periphery of the adenoma/its capusle

72
Q

what is the most common thyroid carcinoma?

A

papillary carcinoma (MC of only malignant thyroid neoplasms)

73
Q

what are Papillary carcinomas composed of?

A

Papillae, Orphan Annie nuclei, Psammoma bodies

74
Q

what are Papillae? how do they present histologically in Papillary carcnioma?

A

finger-like protrusions of cells; “Orphan Annie” nuclei

75
Q

what are Psammoma bodies?

A

specific form of Dystrophic Calcification seen as sm. pearl-like basophilic bodies (dense calcopherites - “hard balls of Ca+”)

76
Q

what population do Thyroid conditions most commonly affect?

A

20-50 year old females

77
Q

which Thyroid conditions are Hot on a Thyroid scan?

A

Grave’s disease and De Quervain thyroiditis

78
Q

what gland of the endocrine system might produce kidney stones? what condition is this termed?

A

Parathyroid; Primary Hyperparathyroidism

79
Q

how does Primary Hyperparathyroidism lead to “stones, bones, moans, and groans”?

A

^Ca+. kidney stones + nephrocalcinosis; osteomalacia, osteoporosis, osteitis fibrosa cystica; constipation, acute pancreatitis, peptic ulcer disease; CNS depression = lethargy, fatigue, psychosis, depression.

80
Q

what is the most common cause of Primary Hyperparathyroidism?

A

Parathyroid-secreting tumor/adenoma

81
Q

what are Chvostek’s sign and Trousseau’s sign indicative of? which is more sensitive?

A

Hypoparathyroidism; Trousseau’s sign is more sensitive

82
Q

what is Chvostek’s sign?

A

tapping on side of face/cheek = muscle spasms in ipsi. face

83
Q

what is Trousseau’s sign?

A

filling of BP cuff = wrist flexion and adduction

84
Q

1.5 months following a minor viral illness, a 32-year-old female develops a tender mass on the anterior of her neck. over the next 2 months she loses 14 pounds and begins complaining that she persistently feels as if her “heart is jumping out of her chest.” her heart rate is 104 BPM and her BP is 148/90 mm Hg. she is told “it should go away with no complication.” what condition do you suspect? how would this condition appear histologically?

A

subactue thyroiditis; granulomatous inflammation w/ multinucleated cells

85
Q

What hormone is involved in Cushing’s disease?

A

ACTH

86
Q

What are the clinical features of hyperthyroidism?

A
  • Increased: T3/4, BMR, activity, reflexes, HR, respiratory rate, GI tract (diarrhea), sebaceous gland activation (oily hair, warm oily sweaty skin), auscultations, neurological (anxious), exophthalmus, heat intolerance
  • Decreased: BMI
  • Amennorhea
87
Q

What are the clinical features of Hypothyroidism?

A
  • Increased: BMI
  • Decreased: T3/4, BMR, activity, reflexes, HR, respiratory rate, GI tract (constipation) sebaceous gland activation (queen ann hair sign - lateral loss of eyebrows, dry + brittle hair, cold dry skin), neurological (depressed), cold intolerance
  • Amennorhea

NYCC Visceral Pathology (40 decks)

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