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3 Path Unit > Endocrine I and II > Flashcards

Endocrine I and II Flashcards

1
Q

What 2 things function as the conductor of most of our endocrine function?

A

Hypothalamus and Anterior pituitary

parathyroid excluded

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2
Q

Hypothalamic function govern anterior pituitary output of what 6 hormones?

A 
prolactin
GH
ACTH
TSH
FSH
LH
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3
Q

M:F ratio of pituitary adenoma?

A

1:2

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4
Q

What are the characteristics of a macro adenoma?

A

> 1cm and can invade locally

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5
Q

What are the all the symptom effects of a pituitary tumor from?

A
  1. Hormone production
  2. pressure effects (optic chiasm, sinus)
  3. Carcinoma (rare)
  4. atypical adenoma seen occasionally
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6
Q

What is the most common adenoma?

A

Null cell, non-secreting

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7
Q

What is the most common functioning adenomas?

A

prolactinomas (30%)

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8
Q

What is a mammosomatotroph adenoma?

A

Prolactin-GH bihormonal adenoma

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9
Q

Prolactinoma causes what?

A

galactorhea, amenorrhea, loss of libido, infertility

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10
Q

GH releasing adenoma causes what?

A

Young: gigantism
Old: acromegaly,

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11
Q

ACTH releasing adenoma causes what?

A

cushings

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12
Q

A Thyrotroph ademona causes what?

A

thyrotoxicosis

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13
Q

What does a gonadotroph adenoma cause?

A

UP FSH AND LH–> abnormal menses, loss of libido, often asymptomatic

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14
Q

Review- what 3 cells are found in anterior pituitary to help us know what it is ?

A

chromophobes
acidophils
basophils

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15
Q

What 2 things does the posterior pituitary secrete?

A
  1. Oxytocin

2. vasopressin/Antidiuretic Hormone

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16
Q

Does vasopressin effect movement of electrolytes?

A

No- just H20

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17
Q

What comes from ADH deficiency?

A

Diabetes insipidus- thirst, low specific gravity polyuria, serum Na/osmol UP,

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18
Q

What comes from excess ADH release?
What type of injury would cause this?
What else can cause?

A
  1. Syndrome of inappropriate ADH secretion- Hyponatremia, cerebral edema
  2. injury to HYPOTHALAMUS
  3. Ectopic secreting tumors (small cell carcinoma in lung)
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19
Q

What is a normal functioning thyroid called even though it has pathology, goiter, adenoma etc?

A

Euthyroid

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20
Q

What is the result of thyroid hyper function? hypo function?

A
  1. thyrotoxicosis

2. myxedema

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21
Q

Can the thyroid be inflamed? have tumors?

A

yes 1. acute and chronic 2. Primary (benign and malignant), secondary

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22
Q

What are the 3 most common causes of thyrotoxicosis?

A
  1. Graves 85%
  2. Toxic multinodular goiter
  3. Toxic Adenoma

[Others–postpartum, thyroiditis, thyroid carcinoma, TSH pituitary tumor, Struma ovarii, exogenous iodine or thyroxin ingestion]

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23
Q

What is th M:F ratio of Grave’s?
MHC classes- for review?
What gene polymorphism prevents T cell response to self antigens?

A
  1. -1:7
  2. HLA-B8, HLA-DR3
  3. CTLA-4
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24
Q

What are the 3 TSH receptor antibodies?

A
  1. TSI- specific to graves
  2. Thyroid growth stimulating Ig
  3. TSH binding inhibitors- mimic TSH [weird]
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25
Q

Review the list of Grave’s disease signs– they are a little different- just BUZZ WORDS

A
  1. Exophthalmos
  2. Pretibial edema, NON-PITTING
  3. Enlarged gland- bruit
  4. HOT AND SKINNY
  5. Tremor
  6. Fine Hair

cut surface uniform, hemorrhages, proliferating follicular cells RAGGED SCALLOPED WATERY COLLOID

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26
Q

What is cretinism due to?

A

hypothyroidism

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27
Q

What is cretinism?

A

severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones (congenital hypothyroidism) due to maternal nutritional deficiency of iodine.

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28
Q

What is myxedema from?

A

Hypothyroidism

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29
Q

What is the primary cause of loss of thyroid tissue? secondary?

A
  1. Di george

2. Hashimoto’s, irradiation

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30
Q

Besides loss of thyroid tissue, what are some other causes of myxedema?

A
  1. pituitary- low TSH
  2. Hypothalamus- low TRH
  3. Reduced thyroid synthesis- error, autoimmune, dietary
  4. Thyroid hormone resistant syndrome- receptor mutation
  5. Mutations in TSH receptor- hypoplasia
  6. other mutations—>thyroid agenesis and cleft
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31
Q

Review the following list of hypothyroid signs- you already know but just some extras

A
  1. Cold Slug
  2. weakness
  3. loss of lateral eyebrow
  4. myxedema madness
  5. Coarse brittle hair
  6. pallor
  7. large tongue
    8 hoarseness (edema in larynx)
  8. cardiomegaly (myxedema)
  9. gastric atrphy, constipation
  10. PERIPHERAL EDEMA
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32
Q

What are the acute causes of thyroiditis?

A

bacteria, fungi, virus

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33
Q

What are the chronic causes of thyroiditis? 4

A
  1. Hashimoto’s- lymphocytic thyroiditis
  2. Subacute granulomatous- de quervain’s
  3. Subacute lymphocytic thyroiditis
  4. Reidel’s fibrous thyroiditis
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34
Q

Hashimoto’s thyroiditis is more common in men or women? HLAs for review

A

women 10-20x

HLA-DR3, HLA-DR5

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35
Q

Hashimoto’s thyroiditis –what are the antibodies to?

A

thyroid peroxidase, thyroglobulin, TSH receptor

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36
Q

Hashimoto’s thyroiditis - we see an increased incidence of what other disease?

A

b-cell lymphoma

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37
Q

Hashimoto’s thyroiditis – adaptive immune involvement?

A
  • T4 helper cells B cell Ab: antibody dependent cytotoxic
  • T4 cells induce cytokines
  • T4 cells may induce cytotoxic T8
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38
Q

What are 4 things we can Identify or can look for in biopsy image of hashimoto’s thyroiditis?

A
  1. Lymphocytic infiltrate
  2. Germinal Centers
  3. destruction of thyroid follicles
  4. Hurthle cell change/oncocytic
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39
Q

What is a Hurthle cell?

A

Hürthle cells are characterized as enlarged epithelial cells with abundant eosinophilic granular cytoplasm as a result of altered mitochondria

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40
Q

What are 4 key points of Subacute granulomatous thyroiditis?

A
  1. Viral etiology
  2. irregularly enlarged
  3. acute, granulomatous or chronic
  4. Will resolve
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41
Q

What are 5 key points of subacute lymphocytic thyroiditis? what is an important thing to remember?

A
  1. Hyperthyroidism is transient, enlarged, no antibodies, self-limiting, can occur post partum
  2. Associated with HLA-DR3 and DR5, familial history of Hashimoto’s, can present later with obvious hashimoto’s.
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42
Q

What are the 3 types of goiter?

A
  1. diffuse non-toxic
  2. multinodular (non-toxic)
  3. Toxic multinodular
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43
Q

Answer the following questions about diffuse non-toxic goiter

  1. What intake is reduced?
  2. what are the goitrogenic foods?
  3. What hormone is increased and which is decreased?
  4. what are the 4 listed metabolic abnormalities ?
A
  1. reduced iodine intake
  2. cabbage, cauliflower, Brussels, sprouts, cassava
  3. Raised TSH, Low T4/T3
  4. Iodide transport, organizational, dehalogenase, iodotyrosine coupling defects
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44
Q

Answer the following questions about multi nodular goiter

  1. Why might it progress from diffuse goiter?
  2. Is it hyper, euthyroid or hypothyroid?
  3. What local structures are compressed?
  4. Hemorrhages occur and fibrous healing leads to?
A
  1. possible clonal response to TSH
  2. Can be any of those
  3. dysphagia occurs and trachea is compressed
  4. scarring–> fibrous bands–>leads to nodularity
45
Q

Is a follicular adenoma encapsulated? Do they become malignant? Use core biopsy?

A
  1. yes, by definition- key think to look on slide
  2. No
  3. No-Fine needle aspirate
46
Q

Order the following in regards to the most common?

anaplastic thyroid carcinoma, follicular carcinoma, medulary thyroid carcinoma, papillary thyroid carcinoma?

A

papillary> Follicular> medullary> anaplastic

47
Q

What are the risks to developing thyroid carcinoma?

A
  1. ionizing radiation
  2. autoimmune thyroid disease
  3. RET/PTC oncogene, RET proto-oncogen
48
Q

In a papillary thyroid carcinoma do we remove the entire gland?

  1. does it have a capsule?
  2. The prognosis is good, when is it bad?
  3. Men or female more?
    • what type of metastasis?
  5. Genetics review
A
  1. remove entire gland
  2. does not have to have capsule
  3. age over 45, female, parithyroid invasion, distant metastasis
  4. F>M
  5. lymphatic- delta node
  6. PTC oncogene, RET proto-oncogene on Chr 10 and NTRK1, mutations on BRAF oncogene, mutations of RAS
49
Q

What 3 important things can we find in papillary thyroid biopsy slide?

A
  1. nuclear overlapping
  2. orphan annie nucleie
    3, nuclear groove
50
Q

In a follicular thyroid carcinoma (more common in middle age females)- what defines malignancy? Where does metastases go?

A
  1. capsule invasion and/or vessel invasion

2. lungs/hematogenous

51
Q

What is the medullary thyroid carcinoma derived from? what all can it secrete?

A
  1. thyroid neuroendocrine cells- C cells (calcitonin)

2. somatostatin, prostoglandins, serotonin, ACTH, histamine etc.

52
Q

What is the medullary thyroid carcinoma associated with genetically? how man are sporadic mutations? what are the major non-sporadic?

A
  1. RET proto-oncogene, long arm of Chr 10
  2. 80%
  3. MEN IIA, MENIIB and familiatl MTC
53
Q

Does medullary thyroid carcinoma have a good or bad prognosis?

A

Bad

54
Q

Anaplastic carcinomas—- are the aggressive? when do most deaths occur if they do? how many have previous multinodular goiter? they are usually older individuals with what mutation?

A
  1. very aggressive
  2. first year
  3. 50%
  4. p53
55
Q

Generally with hyperparathyroidism we see osteoporosis, pathological fractures, claculi in renal and gallbladder areas, and cardiac valve calcification—-what do we get neurologically? muscularly?

A
  1. Depression, lethargy, seizures

2. fatigue, muscle weakness

56
Q

T-F– primary hyperparathyroidism is normally due to primary hyperplasia?

A

False-adenoma = 75-85% and hyperplasia is 10-15%

57
Q

primary hyperparathyroidism has what chromosomal abnormalities normally? is carcinoma common?

A
  1. PRAD1, Chr11, 20% of sporadic adenomas
  2. MENI muation in 20% of sporadic, Chr11
  3. <5%
58
Q

How many of the parathyroid glands is enlarged in parathyroid adenoma?

A

only one

59
Q

Are the inferior or superior parathyroids more commonly associated with adenoma?

A

inferior

60
Q

What is the most common cause of secondary hyperparathyroidism? others?

A
  1. renal dysfunction

2. Vit D def., Low Ca high PTH,

61
Q

In secondary hyperparathyroidism– how many glands are involved?

A

All 4- hyperplasia

62
Q

What is tertiary hyperparathyroidism?

A

pseudohyperparathyroidism- organ failure

63
Q

What are the 3 common causes of primary hypoparathyroidism?

A
  1. congenital absence- DiGeorge
  2. idiopathic atrophy
  3. familial (
64
Q

What are the 2 common causes of secondary hypoparathyroidism?

A
  1. post-operative

2. Auto-immune

65
Q

What are 6 signs we should look for in hypoparathyroidism?

A
  1. neuromuscular irritability/tetany
  2. circumoral tingling
  3. laryngospasm
  4. seizures
  5. CHVOSTEK’s sign
  6. TROUSSEAU’s sign
66
Q

What is chvostek’s sign?

A

tapping face just in front of ear and watching facial muscles twitch

67
Q

What is trousseau’s sign?

A

inflate BP cuff around arm–wrist flexion, extension of fingers with flexion of the thumb against palm

68
Q

What are the 3 types of adrenal gland cortex hyper function and their released hormones ?

A
  1. Cushing’s- cortisol
  2. Conn’s–aldosterone
  3. Adrenogenital/virilzation syndromes- androgen overproduction
69
Q

What are the 4 possibilities of causes of cushing’s syndrome?

A
  1. Cushing’s disease of the pituitary ACTH
  2. Adrenal gland hyperplasia, adenoma
  3. Ectopic ACTH or CRH
  4. Exogenous cortisol (iatrogenic–> low ACTH)
70
Q

What are the common clinical findings of Cushing’s syndrome—JUST REVIEW

A
  1. Central obesity with buffalo hump
  2. moon facies, muscular fatigue
  3. hypertension, glucose intolerance
  4. hirsutism, skin striae
  5. osteoporosis
  6. neuropsychiatric state
    7 menstrual irregularities
71
Q

Is cushing’s disease in the pituitary (hyperplasia or ademona) more common in women or men?
What is increased? Does dexamethasone suppress?

A
  1. Women- 20-30s
  2. ACTH, cortisol
  3. does not at low doses but does at high doses
72
Q

Cushing’s syndrome of the adrenal gland has raised cortisol levels and diminished what? what are the 3 main causes?

A
  1. ACTH

2. cortical hyperplasia (uncommon), and cortical adenoma(50%), cortical carcinoma

73
Q

What common tumors do we see ectopic cushing’s coming from?

A
  1. lung, pancreas, adrenal medulla, medullary thyroid carcinoma, and neuroendocrine tumors
74
Q

What levels are increased in Cushing’s syndrome of ectopic production?

A

ACTH, CRH, Cortisol

75
Q

What is a KEY radiological finding for ectopic cushing’s?

A

BILATERAL adrenal cortical hyperplasia

76
Q

Conn’s Syndrome—Primary hyperaldosteronism is a problem where? secondary?

A
  1. adrenal

2. renal

77
Q

What are the key diagnostic criteria for primary hyperaldosteronism- renin levels, Na levels, K levels, BP?

A
  1. Low renin
  2. High Na
  3. Low K
  4. Hypertension
78
Q

What are the key diagnostic criteria for secondary hyperaldosteronism- renin levels, Na levels, K levels, BP?

A
  1. High renin
  2. High Na
  3. Low K
  4. Hypertension
79
Q

What is the etiology of Conn’s primary hyperaldosteronism?

A

adenoma (65-80%)

adrenal cortical hyperplasia (20-30%)

80
Q

What is the etiology of Conn’s secondary hyperaldosteronism? 5

A

poor renal perfusion, renal ischemia, chronic edematous state, hypoalbuminemia, renin producing tumors

81
Q

What is the most common form of adrenogenital syndromes? What is the overall effect?

A
  1. 21 hydroxylase deficiency

2. drives steroidogenesis towards androgens

82
Q

Adrenogenital syndromes have 3 different key types: what are they characterize by ? [think main levels–may be just for review]

A
  1. low aldosterone, low cortisol, high testosterone with salt wasting in infants. Virilization in female infants.
  2. Simple virilization without salt wasting, normal aldosterone, high testosterone, low cortisol, high ACTH
  3. Late onset, raised ACTH and cortisol, aldosterone is near normal, androgens very high
83
Q

When do we see acute primary adrenocortical insufficiency? 3

A
  1. rapid steroid withdrawal
  2. Addison’s disease crisis
  3. destruction of glands
84
Q

What is waterhouse-friderichsen syndrome?

A
  1. bleeding into adrenal glands
  2. septicemia (BACTERIA CAUSE)
  3. petechia
  4. CV collaps
  5. DIC
85
Q

What is primary chronic adrenocortical insufficiency? Most common cause? 2nd and 3rd?

A
  1. Addison’s disease
  2. Idiopathic Autoimmune 70%
  3. TB- 15% Metastatic Disease-15%
86
Q

In addison’s, how much of the glands need to be destroyed, clinically speaking?

A

90%

87
Q

What are the clinical signs of Addison’s?

A
  1. fatigue, nausea, vomit, diarrhea
  2. weight loss
  3. hypotension
  4. Hyperpigmentation of skin and mucosa
  5. Salt craving
88
Q

In addison’s, what are the cortisol levels? CRH levels? Na, Cl, HCO3 and glucose levels? K levels.

A
  1. cortisol down
  2. CRH up
  3. Na etc. down
  4. K up
89
Q

In addison’s do we see an increase in cortisol with ACTH?

A

No

90
Q

CRH release in addison’s leads to what 2 specific things?

A
  1. up ACTH

2. up MTH- melanotropic hormone–>pigmentation

91
Q

In secondary adrenocortical insuffiency- disorder of hypothalamic pituitary axis—where the CRH levels?

A

Low- so low ACTH and MTH

92
Q

In secondary adrenocortical insuffiency- disorder of hypothalamic pituitary axis— what happens to cortisol with ACTH therapy?

A

It will increase

93
Q

In secondary adrenocortical insuffiency- disorder of hypothalamic pituitary axis–what does aldosterone, Na and K all look like?

A

may all be normal

94
Q

What are the 4 types of tumors of the adrenal medulla?

A
  1. pheochromocytoma
  2. neuroblastoma
  3. ganglioneuroblastoma
  4. ganglioneuroma
95
Q

Clinical speaking, is weight loss more likely with adrenal cortical adenoma or carcinoma ?

A

carcinoma

96
Q

Clinically speaking, is metastases more likely with adrenal cortical adenoma or carcinoma?

A

carcinoma

97
Q

Do more males or females have pheochromocytoma? what percentage are sporadic?

A

females -40-60 years

90%

98
Q

In pheochromocytoma do we see hypertension?

A

Yes— unstable catecholamine release

99
Q

Review the following syndromic causes of pheochromocytoma

A

10%
younger people

MEN syndrome
Neurofibromatosis
Sturge-wever syndrome
Von-hippel-lindau

100
Q

What are the 3 types of adrenal medulla tumors in children?

A
  1. Neuroblastoma- 0-50% ganglion cells [undifferentiated, poorly, differentiating]
  2. Ganglioneuroblastoma- >50% [nodular, intermixed]
  3. Ganglioneuroma- no neuroblasts [mature, maturing]
101
Q

MEN I is what syndrome?

A

Wermer’s

102
Q

MEN IIA is what syndrome?

A

Sipple’s

103
Q

MEN IIB is what syndrome?

A

Mucosal neuroma syndrome

104
Q

What is the MEN I mutation?

A

Chr11(11q13) loss of tumor suppressor gene

105
Q

In MEN I we are supposed to think of the 3 P’s what are they?

A
  1. parathyroid hyperplasia or adenoma
  2. pancreatic islet hyperplasia/adenoma/carcinoma
  3. Pituitary adenomas - NON FUNCTIONAL
106
Q

Are the pituitary adenomas of MEN I functional?

A

No

107
Q

Is MEN II A or B a single amino acid change?

A

B–both are RET proto-oncogene associated, but A is Chr 10 GOF

108
Q

Does MENII A or B have medullary thyroid carcinoma? Pheochromocytoma? parathyroid hyperplasia/adenoma? mucosal neuromas/ ganglioneuromas? marfanoid habitus?

A
  1. both
  2. both
  3. both but MEN II B doesn’t have to have
  4. MENIIB
  5. MENIIB

3 Path Unit (5 decks)

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