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3. Sys Path 2 > Endocrine – Anatomic Pathology > Flashcards

Endocrine – Anatomic Pathology Flashcards

1
Q

Endocrine Pathologic Processes

A
  1. Proliferation
    * Neoplasia
    * Hyperplasia
    > Diffuse (↑ stimulation or ↓ feedback)
    > Multifocal (often idiopathic)
    > Focal (often incidental)
  2. Atrophy
    * Lack of trophic hormone
    * Idiopathic
    * Compression
  3. Inflammation
    * Immune-mediated > infectious
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2
Q

Endocrine Neoplasia - functional vs non-functional effects

A

Functional
* Distant effects, in target tissue(s) of overproduced hormone(s)
> Size doesn’t always matter
<><><>
Non-functional
* Local effects, compression and destruction of adjacent tissues
> Size matters more

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3
Q

Pituitary gland Pathological Processes

A

Adenohypophysis (pars: distalis, intermedia, tuberalis) ie. anterior pituitary
* Cysts
* Neoplasia
* Inflammation
<><><>
Neurohypophysis (pars nervosa) ie. posterior
* Diabetes insipidus
* Neoplasia
> Pituicytoma

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4
Q

pituitary cysts
- where are they derived from
- anatomy
- importance? effects?

A

Derived from different aspects of pituitary gland
* Distal end of the craniopharyngeal duct
* Proximal end of the craniopharyngeal duct
* Failure of differentiation of the oropharyngeal ectoderm of Rathke’s pouch
> Remnants, common

<><><><>
* Typically incidental unless large, but can:
* Exert pressure on other structures
> Consequences dependent on affected structures
> Rupture can lead to inflammation and fibrosis

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5
Q

pituitary
Large or Invasive Tumour/Cyst Consequences

A

Lack of secretion of pituitary trophic hormones:
* Trophic atrophy and subnormal function adrenal cortex
and thyroid gland
* Gonadal atrophy
* Failure to attain somatic maturation
<><><>
Water metabolism disturbances
* Interference with the release and synthesis of antidiuretic hormone (ADH)
<><><>
* Deficits in cranial nerve function
* CNS dysfunction caused by extension into the overlying brain

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6
Q

Juvenile Panhypopituitarism
- what is this? what happens?
- Dx

A
  • Pituitary dwarfism
    <><><><>
  • Dogs, also seen in cats and other species
    > German Shepherds most common
  • Deficiency in GH, TSH, prolactin, and gonadotropins
    > ACTH = N or ↓
  • Normal: birth up to ~2 mos, then…
    > Slower growth rate, retention puppy hair, lack primary guard hairs
    > Bilaterally symmetrical alopecia develops gradually
    > Often progresses to complete alopecia (except for head and tufts of hair on legs)
    > Progressive skin hyperpigmentation, until uniformly brown-black
  • Dx: compare littermates, radiographs (open epiphyseal lines), thyroid function tests, skin biopsy, serum GH or IGF-1
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7
Q

pituitary neoplasia:
Corticotroph (ACTH-secreting) adenoma
- where? effects? who?

A
  • Pars distalis (or pars intermedia) -> produce ACTH -> ↑ cortisol from adrenal gland = pituitary dependent hyperadrenocorticism
  • Dogs
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8
Q

pituitary neoplasia:
Pars intermedia (melanotroph) adenoma
- what happens? who?

A
  • POMC-derived peptides
  • Pituitary pars intermedia dysfunction
    (PPID)
  • Horses
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9
Q

pituitary neoplasia:
Somatotroph adenoma
- what is it? effects?

A
  • Growth hormone (GH)-secreting acidophils (somatotrophs)
  • Infrequent in animals
  • Large, indent hypothalamus, extend into overlying brain
  • Hypersecretion of GH -> acromegaly
  • Insulin-resistant diabetes mellitus in cats
    > Increased GH -> downregulation of insulin receptors
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10
Q

pituitary neoplasia:
Suprasellar germ cell tumour (craniopharyngioma)
- what is it? who gets it? origins?

A

non-functional tumour
* Young animals
* Derived from epithelial remnants of the oropharyngeal ectoderm of the craniopharyngeal duct (Rathke’s pouch)

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11
Q

inflammation of the pituitary can occur how?

A

Systemic disease
* Bacterial septicemia in ruminants
<><><><>
Regional disease (extension)
* Suppurative meningitis
* Trauma from fighting or dehorning
* Inner ear
* Tooth root
* Sinuses

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12
Q

Diabetes Insipidus
- what is it?
- forms?

A

Large volumes of hypotonic urine with polydipsia
* Urine osmolality decreased below normal plasma osmolality
<><><><>
Hypophyseal form
* Inadequate antidiuretic hormone (ADH) production
> Compression and destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus
=> Cysts, neoplasia, granulomas, skull trauma with hemorrhage
<><><>
Nephrogenic form
* Lack of response in target cells to normal or high ADH

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13
Q

Adrenalitis
- what causes it? why here?

A
  • Infectious and parasitic agents
    <><><><>
    Why?
  • High local concentration of anti-inflammatory steroids in the adrenal cortex suppresses local cell-mediated immunity
    > Permits the preferential progressive growth of certain fungi, protozoa, and bacteria
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14
Q

adrenal hemorrhage - when do we see it?

A
  • Newborn animals
  • Stress response
  • Secondary infarct
    > toxemia
    > septicemia
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15
Q

Hyperplasia of the adrenal Medulla
- what we see, when

A
  • Diffuse or nodular
    > Can precede the development of pheochromocytoma in bulls with C-cell tumours
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16
Q

Hyperplasia of the adrenal Cortex
- types we see

A
  • Nodular cortical hyperplasia (and accessory cortical nodules)
    > Common, incidental, non-functional in aged dogs
    <><>
  • Diffuse cortical hyperplasia
17
Q

Hyperadrenocorticism (Cushing’s)
- origins, rates

A
  • Pituitary (functional corticotroph adenoma) = 85%
  • Adrenal (functional adrenal neoplasm) = 15%
    > adenoma or carcinoma
18
Q

Hyperadrenocorticism: Ferret
- anatomic variations
- what it produces
- associated with what other condition?

A

Adrenal enlargement
* Bilateral
> Diffuse or nodular hyperplasia
* Unilateral
> Adrenocortical adenoma/carcinoma
=> Carcinoma more common
=> More common on left
<><><><>
Overproduction of estrogenic steroids
* Estradiol 17-β
<><><><>
1⁄3 ferrets with adrenocortical tumours also have neoplasms derived insulin producing β-cells of the pancreatic islets
* Hypoglycemia

19
Q

Hyperadrenocorticism: Ferret pathogenesis, clinical signs

A

Ferret, pathogenesis:
* Early gonadectomy -> loss of negative feedback on pituitary gonadotrophs -> increase LH secretion -> stimulation & proliferation of zona reticularis of the adrenal cortex -> sex steroids overproduction
<><><><>
Gross/Clinical signs:
* bilaterally symmetrical alopecia, sexual behaviour, swollen vulva

20
Q

Neoplasias of the adrenal Cortex
- what types?
- species? anatomy?

A

Adenomas
* Dogs > years
> Sporadically in horses, cattle sheep
* Single nodules in cortex, can be bilateral
<><>
Carcinoma
* Less common than adenomas, larger than adenomas
* Invasion into surrounding tissues
> Metastasis to liver and lung
* Cattle and older dogs
<><>
Myelolipoma
* Cattle
<><><><>
*Adenomas and carcinomas can be functional or non-functional

21
Q

neoplasia of the adrenal medulla
- Pheochromocytoma
> what is this?
> what does it do?
> anatomy
> species

A

Tumour of chromaffin cells
* Secrete: epinephrine, norepinephrine, or both
> If functional, norepinephrine -> constricts blood vessels -> systemic hypertension, tachycardia, cardiac hypertrophy
<><><><>
* Unilateral or bilateral
* Cattle and dogs
> Bulls can be concurrent with calcitonin-secreting C-cell tumours
of the thyroid gland
* Often large

22
Q

Neoplasias of the adrenal medulla
- their anatomy and characteristics

A

Pheochromocytoma
<><><><>
Neuroblastoma
* Primitive neuroectodermal cells
* Younger animals
* Large intra-abdominal mass
<><><><>
Ganglioneuroma
* Tumour of multipolar ganglion cells and neurofibrils
* Often contain melanin pigment in cattle
* Small
<><><><>
Metastatic
* Common site
* Usually bilateral and in the medulla

23
Q

Hypoadrenocorticism (Addison’s)
- primary definition / cause, general anatomy
- iatrogenic cause

A

Primary
* Idiopathic – possibly immune-mediate inflammatory destruction (other causes of destruction are uncommon)
* Unilateral – productive neoplasm in contralateral gland
<><><><>
Iatrogenic
* Exogenous glucocorticoids + abrupt cessation
* Overdose other drugs (mitotane)

24
Q

Hypoadrenocorticism (Addison’s) pathogenesis (primary)

A

Destruction of adrenal cortex -> mineralocorticoid (aldosterone) & glucocorticoid deficiency -> excessive Na excretion in renal tubules & retention of K and H ions -> hyponatremia -> hypovolemia + hypotension + prerenal azotemia
* Hypovolemic crisis

25
Q

Pathologic Processes of the thyroid gland

A
  • Hypothyroidism
  • Hyperplasia
  • Neoplasia
  • Hyperthyroidism
26
Q

Hypothyroidism - primary - cause, what we see

A

Primary
* Lymphocytic thyroiditis
* Idiopathic follicular collapse
* Bilateral non-functional thyroid tumors
* Severe iodine-deficient hyperplastic goiter

27
Q

thyroid hyperplasia
- causes

A
  • Iodine-deficient diet
  • Goitrogenic compounds that interfere with thyroid hormone synthesis
  • Genetic enzyme defects in biosynthesis of thyroid hormones
    > All above -> inadequate thyroid hormone synthesis -> ↓ T4 & T3 -> detected by hypothalamus and pituitary to increase secretion of TSH -> hypertrophy/hyperplasia of follicular cells
  • Dietary iodide excess
28
Q

Nodular Hyperplasia/Neoplasia of the thyroid

A
  • Follicular Cell or C-Cell
  • Nodular hyperplasia, adenoma
    > Common geriatric horse, incidental
  • Carcinoma
    > Dogs
29
Q

Neoplasia: Thyroid C-Cell Tumour
- who gets it?
- occurs with what else?

A

Adult to aged bulls and horses
* Infrequent in dogs and other species
<><><><>
Bulls
* ~30% aged bulls have C-cell tumours or hyperplasia when fed high Ca diets
* Occurs with bilateral pheochromocytoma &
occasionally pituitary adenoma
> Adrenal medullary hyperplasia precedes pheochromocytoma

30
Q

Hyperthyroidism - what species? anatomy/cause?

A

Cats: multinodular follicular cell hyperplasia or adenomas/adenocarcinomas
* Can be unilateral
* Consequences in other tissues…

31
Q

Pathologic Processes of the parathyroid

A
  • Hyperplasia
  • Neoplasia
  • Hyperparathyroidism
  • Hypoparathyroidism
32
Q

Hyperplasia/Neoplasia of the parathyroid
- types, and their characteristics or causes

A

Focal (nodular) hyperplasia
* Single or multiple nodules in one or both glands
> Poorly defined within the parenchyma
<><><><>
Diffuse hyperplasia
* Uniform enlargement of all parathyroid glands
> Chronic renal failure
> Long-term dietary imbalance (low Ca or high P)
<><><><>
Adenomas/carcinomas
* Can be functional

33
Q

Hyperparathyroidism
- primary vs secondary, causes

A

Primary
* Functional adenomas/carcinomas
> Autonomous hypersecretion of PTH
* Multinodular hyperplasia
> Primary (idiopathic)
=> Dogs
<><><>
Secondary
* Nutritional imbalance
* Chronic renal failure

34
Q

Hyperparathyroidism: Fibrous Osteodystrophy
- what is this?

A

Mineral is removed from the skeleton and replaced by immature fibrous connective tissue

35
Q

Hypercalcemia of Malignancy
- how does this arise? what does it do?

A

Apocrine gland anal sac adenocarcinoma (AGASAC)
* Secrete parathyroid hormone-related peptide (PTHrP)

36
Q

Hypoparathyroidism
- mechanisms

A
  • Lymphocytic parathyroiditis (idiopathic? immune mediated?),
    adult dogs (familial in miniature schnauzers)
  • Invasion or destruction by primary/metastatic neoplasia
  • Injury/removal during thyroidectomy (cats)
    > All above -> ↓ PTH and calcitriol -> ↓ bone resorption -> ↓ blood Ca -> ↑ neuromuscular excitability (spasms) -> tetany
  • Trophic atrophy associated with long-term hypercalcemia
  • Agenesis (rare)

3. Sys Path 2 (47 decks)

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