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Pathology II > Lecture 1: Endocrine > Flashcards

Lecture 1: Endocrine Flashcards

1
Q

What are endocrine glands

A

Specialized secretory epithelial cells arranged in cords, packets, or follicles (thyroid) supported by fine fibrovascular stroma

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2
Q

What is the function of endocrine glands

A

Synthesis, store and secrete products into bloodstream—> produce signals with distant physiological effects

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3
Q

What does endocrine mean

A

Cell secretes a product that acts on distant cells (systemic effects)

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4
Q

What is autocrine

A

Cells secrete a product that acts on itself

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5
Q

What is paracrine

A

Cells secrete a product that acts on a neighbor cell

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6
Q

What is primary hypofunction

A

Endocrine organ not making hormone because of direct damage

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7
Q

What are some examples of primary hypofunction

A
  1. Organ destroyed (ex: abscess)
  2. Organ not developed (aplasia)
  3. Organ defect (goiter)
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8
Q

What is secondary hypofunction

A

Endocrine organ not making hormone because lack of stimulation by hormones from another endocrine organ

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9
Q

What is the mechanism of endocrine disease on adrenal gland: pituitary gland is destroyed and now the adrenal gland is not stimulated

A

Secondary hypofunction

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10
Q

What is primary hyperfunction

A

Endocrine organ is making too much hormone because of functional tumor/ hyperplasia

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11
Q

What are some examples of primary hyperfunction

A
  1. Functional cortical adenoma of adrenal gland
  2. Functional thyroid gland adenoma
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12
Q

What is a secondary hyperfunction

A

Endocrine organ making too much hormone because overstimulated by hormones

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13
Q

What are the mechanisms of endocrine disease: pituitary gland dependent Cushing overstimulating the adrenal gland by tumor in pituitary

A

Pituitary: primary hyperfunction
Adrenal: secondary hyperfunction

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14
Q

What is hyper secretion of hormones or hormone like factors by nonendocrine neoplasms

A

Non- endocrine organs make substances that are new hormones or are hormones that resemble existing hormones produced by normal endocrine organs

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15
Q

What is the mechanism of endocrine disease: humoral hypercalcemia of malignancy due to PTHrP. PTHp is produced by tumor cells and resembles normal PTH and will function similarly (increase Ca2+)

A

Hyper secretion of hormones or hormone like factors by non-endocrine neoplasms

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16
Q

What is the mechanism of endocrine disease: secondary hyperparathyroidism due to chronic renal disease or nutritional imbalance

A

Endocrine hyperactivity due to disease of other organs

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17
Q

Is a functional endocrine neoplasm more likely to be benign or malignant

A

Benign

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18
Q

Hyperplasia/adenoma or carcinoma: regional invasion and destruction, metastasis

A

Carcinoma

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19
Q

What type of tissue is this? Identify green, blue and yellow outlined areas

A

tissue: pituitary gland
Green: pars distalis
Blue: pars intermedia
Yellow: pars nervosa

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20
Q

What do somatotrophs make

A

Growth hormone

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21
Q

What do lactotrophs make

A

Prolactin

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22
Q

What do corticotrophs make

A

ACTH

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23
Q

What do thyrotrophs make

A

TSH

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24
Q

What do gonadotrophs make

A

FSH and LH

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25
Q

The pars nervosa is responsible for releasing what hormones

A

Vasopressin (ADH)
Oxytocin

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26
Q

Images from old female goat, what is wrong and what is the mechanism of endocrine disease

A

Brain: pituitary tumor
Mammary gland: increased size due to increased prolactin being released by pituitary

Diagnosis: functional lactotroph adenoma with hyper secretion of prolactin

Mechanism: primary hyperfunction of pituitary gland

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27
Q

Describe the HPA axis

A
  1. Hypothalamus releases CRH
  2. Pituitary gland releases ACTH (pars distalis)
  3. Adrenal gland releases cortisol
  4. Negative feedback to hypothalamus to decrease release of CRH
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28
Q

What mechanism of endocrine disease would occur with if the pituitary gland was destroyed by inflammation and non-functional tumors

A

Primary hypofunction

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29
Q

What mechanism of endocrine disease would occur with a congenital/hereditary maldevelopment of pituitary

A

Primary hypofunction

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30
Q

What mechanism of endocrine disease would occur with functional pituitary tumors

A

Primary hyperfunction

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31
Q

What produces ADH and what is the function

A

Produced by pituitary gland pars nervosa and acts on kidneys to reabsorb water

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32
Q

Patient presents with PU/PD to determine type of diabetes insipidus you add exogenous ADH, if the patient is able to concentrate their urine, what type of DI do they have? What structure is likely destroyed and what is the host level of ADH

A

Central DI
Pars nervosa destroyed
ADH is low

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33
Q

Patient presents with PU/PD to determine type of diabetes insipidus you add exogenous ADH, if the patient is not able to concentrate their urine, what type of DI do they have? What structure is likely intact and what is the host level of ADH

A

Nephrogenic DI
Pars nervosa intact
ADH high-kidney not responsive

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34
Q

What are some reasons an animal might have central DI

A

Pituitary tumor or abscess

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35
Q

What species commonly gets somatotroph adenoma

A

Cats

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36
Q

What hormone is affected with somatotroph adenoma and what are some clinical signs of this

A
  1. GH increased
  2. Acromegaly and adult onset DM
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37
Q

What hormone is affected in cortciotroph adenoma. What two organs does that hormone affect and what is the mechanism of endocrine disease for each organ

A
  1. Increase ACTH- primary hyperfunction
  2. Bilateral symmetric adrenal gland cortical hyperplasia of ZF and ZR- secondary hyperfunction
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38
Q

What are some gross findings of the pituitary gland and adrenal glands in patients with pituitary dependent cushings

A
  1. Big pituitary gland
  2. Bilateral symmetric, big cortices of adrenal glands
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39
Q

Based on these findings what is top differential

A

Corticotroph adenoma- pituitary dependent cushings

40
Q

What is the mechanism of endocrine disease for a pituitary gland carcinoma

A

Primary Hypofunction

41
Q

What part of the pituitary is affected in horses with PPID

A

Pars intermedia

42
Q

What is the pathogenesis/outcome from PPID causing compression of hypothalamus

A
  1. Hypothalamic or neurohypophyseal dysfunction
  2. Intermittent hyperpyrexia, polyphasic, hirsutism
43
Q

What is the pathogenesis/outcome of PPID being endocrinologically active

A
  1. Excess POMC
  2. Increase CLIP, MSH, beta-endorphin
  3. Increase ACTH
  4. Adrenal gland cortical hyperplasia (secondary hyperfunction)
44
Q

Why is pituitary hypofunction/ aplasia in fetuses a problem in pregnant animals

A
  1. Fetal hormones needed for final growth/ development
  2. Parturition not activated—> prolonged gestation
45
Q

What is the pathogenesis of pituitary cysts and pituitary dwarfism

A
  1. Failure of pars distalis to develop
  2. Cysts replace portion or all of adenohypohysis
  3. Juvenile panhypopituitarism
  4. Hyposomatotrophism- no growth hormone- no patient growth
46
Q

What pituitary hormone is most affected in pituitary dwarfism

A

Somatrophs- don’t produce enough GH

47
Q

Brain from an abnormally small “adult” German shepherd. What is wrong

A

Cyst on pars distalis causing decreased production of GH

Pars nervosa is okay

48
Q

What does the zona glomerulosa produce

A

Mineralcorticoids/ aldosterone

49
Q

What does the zona fasisculata produce

A

Glucocorticoids/ cortisol

50
Q

What does the zona reticularis produce

A

Sex hormones

51
Q

Which layer of the adrenal gland cortex is not under ACTH control

A

Zona glomerulosa

52
Q

What does the adrenal medulla produce

A

Epinephrine and norepinephrine

53
Q

What is the cause of Addison disease

A

Immune mediated

54
Q

How is Na+ and K+ affected in Addison disease and why

A

Na+ decreases and K+ decreases because Addisons disease destroys all cortical layers of adrenal gland, including ZG which produces aldosterone which normally retains Na+ and removes K+

55
Q

Based on these images- what is top differential

A

addisons disease

56
Q

What is the cause of secondary hypoadrenocorticism

A

Iatrogenic or pituitary gland damage

57
Q

How is Na+ and K+ affected in secondary hypoadrenocortisim and why

A

Normal, because secondary hypoadrenocortisim only affects ZF and ZR, not ZG which produces aldosterone

58
Q

Based on this image and the fact that electrolytes were normal, what is likely dx

A

Secondary hypoadrenocortisim

59
Q

Adrenal gland- in general, what is wrong

A

hypoadrenocortisim- cortex much smaller than medulla

60
Q

Describe the HPA axis when there is a pituitary dependent hyperadrenocorticism

A
  1. Increase ACTH release
  2. Adrenal cortical hyperplasia and increase cortisol
  3. No feedback loop because tumor will continue to release ACTH
61
Q

Describe the HPA axis with adrenal gland dependent hyperadrenocorticism due to cortical adenoma in right adrenal gland

A

1.normal ACTH released from pituitary
2. Lots of cortisol released from right adrenal gland, decreased cortisol release from left adrenal gland (atrophy of left adrenal cortex and some atrophy on right side of affected areas)
3. Negative feedback loop decrease ACTH (results in atrophy of the unaffected adrenal glands)

62
Q

What are some signs of Cushings disease

A
  1. Polyphagia
  2. Distended abdomen
  3. Hepatomegaly
  4. Calcinosis cutis
  5. Immunosuppression- UTI’s and pneumonia
63
Q

These findings are consistent with what dz

A

hyperadrenocorticism/ cushings

64
Q

What is Conn’s syndrome in cats/ pathogenesis

A
  1. Functional tumor of the ZG or hyperplasia of ZG
  2. Increase aldosterone
  3. Increase Na+ and decrease K+
  4. Hypertension and polymyopathy
65
Q

How does the electrolyte balance differ in Conn’s syndrome vs primary hypoadrenocorticism (Addisons)

A

Conn’s syndrome: increase aldosterone—> increase Na+ and decrease K+

Addisons: decrease aldosterone—> decrease Na+ and increase K+

66
Q

What is the pathogenesis/ outcome of phreochromocytoma

A
  1. Increase production of catecholamines
  2. Hypertension, tachycardia, left sided concentric ventricular hypertrophy, cardiomyopathy
67
Q

What is the #1 adrenal gland medullary tumor

A

Pheochromocytoma

68
Q

Which one is malignant

A

A

69
Q

What to components are needed to form T3/T4

A

Iodine and thyroglobulin

70
Q

What do C cells produce and what is the effect

A

Calcitonin- decrease Ca2+ (released when hypercalcemia)

71
Q

What can cause acquired goiter

A

Iodine deficient or excess, goitrogenic compounds

72
Q

What can cause inherited goiter

A

Congenital dyshormonogenetic

73
Q

Does goiter cause hypo or hyperthyroidism

A

Hypo

74
Q

What tissue is this, which is normal vs abnormal (what wrong)

A

Left: C-cell hyperplasia
Right: normal

75
Q

What wrong

A

Lymphocytic thyroiditis

76
Q

How is T3/T4 and TSH affected in hypothyroidism

A

Decrease T3/T4 and increase TSH

77
Q

What are some signs of hypothyroidism

A

Weight gain, alopecia, atherosclerosis, hepatomegaly

78
Q

What are 3 examples that cause thyroid tissue loss and therefore hypothyroidism

A
  1. Idiopathic follicular atrophy/ collapse
  2. Lymphocytic thyroiditis
  3. Destroyed by non-functional tumor
79
Q

What is the pathogenesis for congenital dyshormonogentic/ inherited goiter

A
  1. Inherited autosomal recessive mutation
  2. Abnormal pathway
  3. Decrease T3/T4 due to mutations preventing iodothyronine production
  4. Increase TRH and TSH
  5. Thyroid gland hyperplasia and colloid endocytosis
  6. Goiter and hypothyroidism
80
Q

How does a functional adenoma or thyroid hyperplasia affect T3/T4 and what does it cause

A

Increase T3/T4–> hyperthyroidism

81
Q

What are some signs of hyperthyroidism

A

Weight loss, triangular shaped face, nervousness, tachycardia, dysrythmia, ventricular hypertrophy

82
Q

Dog presents with thyroid gland mass, what is it most likely

A

Carcinoma

83
Q

Cats with thyroid gland mass what is it most likely

A

Hyperplasia or adenoma

84
Q

How does PTH affect Ca2+ and phosphorus

A

Increase Ca2+ and decrease phosphorus

85
Q

How does vitamin D affect Ca2+ and phosphorus

A

Increase both

86
Q

How does calcitonin affect phosphorus and Ca2+

A

Decrease both

87
Q

What cells produce PTH and why

A

Chief cells in response to hypocalcemia

88
Q

What is the pathogenesis of parathyroid gland insufficiency

A
  1. Decrease PTH
  2. Progressive decrease of blood Ca2+ and increase phosphorus
  3. Hypokalemia and hyperphosphatemia
  4. Neuromuscular tetany and excitability
89
Q

What does primary hyperparathyroidms look like

A

Functional tumor, asymmetrically enlarged glands

90
Q

What does secondary hyperparathyroidism look like

A

Hyperplasia, symmetrically enlarged glands

91
Q

What are some causes of secondary hyperparathyroidism

A

Nutritional imbalance
Chronic renal failure

92
Q

How does primary hyperparathyroidism affect Ca2+ and phosphorus

A

Hypercalcemia and low to normal phosphorus

93
Q

How can nutrition cause secondary hyperparathyroidism

A
  1. Low calcium, high phosphorus
  2. PTH increase activity via chief cell hyperplasia
  3. Bone resorption and fibrous osteodystrophy
94
Q

How can chronic renal failure cause secondary hyperparathyroidism

A
  1. Decrease vitamin D3 and chronic increase phosphorus
  2. Decrease Ca2+
  3. PTH increases via chief cell hyperplasia
  4. Bone resorption
95
Q

What are some causes of pseudohyperparathyroidism

A
  1. Carcinoma
  2. Lymphoma
  3. Anal sac apocrine gland adenocarcinoma
  4. Plasma cell myeloma
96
Q

What happens during pseudohyperparathyroidism

A
  1. Secrete biologically active PTHrP
  2. Action mimics normal PTH
  3. Hypercalcemia and low to normal phosphate is

Pathology II (8 decks)

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