Endocrine Flashcards

(67 cards)

1
Q

Name the four types of hormone and give an example of each.

A
  1. Peptide and protein - insulin, prolactin, ACTH, ADH, oxytocin
  2. Steroids - glucocorticoids, oetrogens, androgens
  3. Amino acid derivatives - catecholamines, thyroid
  4. Fatty acid derived - prostaglandins , leukotrienes
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2
Q

What is the difference between regulated and constitutive secretion of peptide/ protein hormones?

A

Regulated - hormones are stored in secretory granules and released when stimulated

Constitutive - hormones are not stored in cells but secreted as they are synthesized (particularly as protein/ peptide hormones have short half lives)

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3
Q

How are steroid hormones excreted from the body?

A

Via the urine/ bile

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4
Q

How does the half life of thyroid and catecholamine hormones differ?

A

Thyroid > catecholamines

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5
Q

From which amino acid are thyroid and catecholamines derived?

A

Tyrosine

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6
Q

What effects can hormones have on target cells?

A
  1. Activation of enzymes or other dynamic molecule (second messenger systems)
  2. Modulation of gene expression
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7
Q

Which types of hormones are able to activate cell surface receptors?

A

Proteins, peptides, catecholamines, fatty acid derivatives

Used in second messenger systems

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8
Q

Which types of hormones are able to activate intracellular receptors?

A

Steroids and thyroid hormones - these alter transcriptional gene expression

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9
Q

Endocrinopathies can be caused by which mechanisms?

A
  • Primary or secondary hypofunction of the gland
  • Primary or secondary hyperfunction of the gland
  • Hypersecretion of hormones from non-endocrine neoplasms
  • Dysfunction of the target cell
  • Disease of other organs due to endocrine hyperactivity
  • Iatrogenic syndromes of hormonal excess
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10
Q

Which hormones are released from the adenhypophysis?

A

FLAT PiG

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11
Q

Which hormones are produced in the hypothalamus?

A

ADH

Oxytocin

Hypophyseotropic releasing hormones

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12
Q

Acidophilic and basophilic cells of the adenohypophysis cause release of which hormones?

A

Acidophilic - growth hormone, prolactin

Basophilic - LH, FSH, TSH, ACTH

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13
Q

Diabetes incipidus is caused by deficiency in which hormone?

Outline the difference between central and nephrogenic diabetes insipidus.

A

ADH

Central - impaired hypothalamic production, transport, storage and pituitary release

Nephrogenic - ADH receptor defect in the collecting duct and DCT

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14
Q

Rathke’s cysts

A

Pituitary cysts - can cause dyspnoea if grow too large

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15
Q

Hypoplasia or aplasia of the hypothalamo-adenohypophyseal system can cause what conditions in calves?

A

Cyclopia

Arhynencephaly

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16
Q

Pituitary dwarfism is caused by a deficiency in which hormone?

A

Somatotropin hormone - causes decreased growth hormone and failure to differenciate of rathkes pouch

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17
Q

An acidophilic adenoma can cause which conditions in an animal?

A

Excessive GH and growth

Overgrowth of connective tissue

Diabetes mellitus - GH inhibits insulin receptors

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18
Q

Which regressive changes can be seen in the HPA axis with age?

A

Atrophy - horse and dog

Pituitary inflammation - abscess formation - due to viral infection

Nodular hyperplasia

Adenoma

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19
Q

Pituitary inflammation can be caused by which viral agents?

A

Borna disease

Classical swine fever

Infectious anaemia

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20
Q

Describe the lesion

A

The pituitary shows marked increase in size.

Focal grey oval lesion - filled with thick grey - yellow fluid

3x4 cm

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21
Q

Why can adenomas of the adenohypophysis cause cushings in dogs and horses?

A

Most frequently cause hypersecretion of ACTH

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22
Q

Describe the lesion

A

The adenohypophysis of the pituitary is affected.

The gland shows a focal lesion which is red and shows multifocal-coelescing dark red pigmentation.

The round nodule is firm to touch and is approximately 3-4cm in diameter

MD - Pituitary adenoma

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23
Q

In the dog cushings disease is associated with which clinical signs?

A
  • PU/ PD
  • Polyphagia
  • Obesity
  • Skeletal muscle atrophy
  • Bilateral and symmetrical alopecia
  • Epidermal atrophy
  • Osteopenia
  • Secondary DM
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24
Q

Describe the associated lesions here.

Which condition is associated with these?

A

Pituitary - normal tissue has been destroyed and replaced with a round, diffusely reddened nodular, firm mass which is 2x3cm in size

Adrenal gland - the cortex of the adrenal glands show diffuse symmetrical and bilateral thickening (hyperplasia) due to increased stimulation by ACTH released by the tumour

Cushings

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25
Equine Cushings is associated with which pathological mechanism? What clinical presentation would be expected?
ACTH-producing adenohypophysis tumours Space-occupying lesion - hypertichosis, hyperhydrosis, intermittent fever (impedes on neurohypophysis and hypothalamus) ACTH production - PU/PD, polyphagia, hyperglycaemia, glucosuria, immunosupression
26
Outline four primary causes of hypothyroidism.
1. Loss of parenchyma - aplasia, atrophy, neoplasia etc 2. Deficiency of hormone components - iodine 3. Chemical blockage of hormone production 4. Resection of the gland
27
Outline the clinical presentation of primary hypothyroidism.
* Increased body weight * Skin: thin coat, bilateral alopecia, hyperkeratosis, hyperpigmentation * Repro: abnormal cyclic, reduced sperm count * Goitre * Myxoedema: oedema of subcutis and mucosa * Cretinism: disproportionate dwarfism
28
Outline a cause of hyperthyroidism in the cat. What clinical presentation would be expected?
Thyroid multinodular hyperplasia/ adenoma. * Increased basal metabolic rate * Weight loss * Hepatic lipidosis & necrosis (glycogen deficiency) * Left ventricular hypertrophy
29
How would TRH and TSH levels be expected to change with hyperthyroidism?
They are decreased to negative feedback from increased T3 and T4. Atrophy of the thyroid gland
30
Chronic lymphocytic thyroiditis is caused by what?
Autoimmune disorder (Ab against thyroglobin)
31
Name the three main types of neoplasm seen in the thyroid gland and an example of each.
1. Epithelial tumours - adenomas, carcinomas 2. Mesenchymal tumours - fibroma, haemangioma, osteochondroma, fibrosarcoma 3. C cell tumour
32
Describe this histological lesion and predict the gross morphology of the organ
Focal aggregation of cells affecting 40% of the side. The structure contains multiple to coelescing cycstic cavities containing amorphous pale pink proteinaceous fluid. Cells appear well differentiated and there are few mitosis Grossly this appears as a distinct pale tan firm mass which has destructed the normal architecture of the gland. Thyroid adenoma
33
What is the function of parathyroid hormone? (x3)
Increasing serum calcium levels 1. Mobilising calcium from bone - OCl 2. Enhancing absorption of Ca from small intestine - stimulates vit D3 activation in the kidney 3. Supressing Ca loss from urine - renal reabsorption
34
Hypocalcaemia can have what gross effects on the animal?
Increased neuromuscular excitability leading to spasms, tetany and tremors
35
What are the consequences of hyperparathyroidism?
Hypercalcaemia
36
Primary hyperparathyroidism can be caused by what?
Hyperplasia Adenoma/ carcinoma of the parathyroid gland
37
Secondary hyperparathyroidism can be caused by what?
Chronic renal insufficiency Dietry Ca/P
38
Tertiary hyperparathyroidism can be caused by what?
Final stage of secondary with non-responsive autonomous hyperparathyroidism
39
Pseudo hyperparathyroidism can be caused by what?
Malignant hypercalcaemia Anal sac adenocarcinoma which releases PTH-like protein
40
Describe these associated lesions.
Bilateral and symmetrical hyperplasia of the parathyroid gland. Chronic diffuse fibrosing renal insufficiency. Hyperplasia of PTG is secondary to reduced Ca2+ reabsorption and vitD3 caused by chronic renal failure and therefore drop in blood calcium levels
41
Clinically how does renal secondary hyperparathyroidism manifest?
Fibrous osteodystrophy * Lameness * Loss of teeth * Deformity of mandible and maxilla Metastatic calcification - gut mucosa
42
What primary tumours are found in the parathyroid gland?
Chief cell adenoma adenocarcinoma (may be functional - primary hyperparathyroidism)
43
Name the four main zones of the adrenal gland and the hormone they are responsible for secreting.
1. Zona glomerulosa - mineralocorticoids 2. Zona fasciculata - glucocorticoids 3. Zona reticularis - androgen, oestrogens, progesterones 4. Medulla - catecholamines
44
What is the main function of mineralocorticoids?
Aldosterone Loss of potassium and retention of Na+
45
What is the main function of glucocorticoids?
Cortisol Glucose metabolism (before insulin) - they increase glucose production
46
What is the main function of catecholamines?
Fight or flight Increased rate and force of heart contractions Vasoconstriction Bronchodilation Lipolysis Increased metabolic rate Pupil dilation
47
Addisons disease
Primary hypoadrenocorticism
48
Hypopituitarism causes what effects in the adrenal gland?
Secondary hypoadrenocorticism (decreased ACTH)
49
Nodular hyperplasia, adenoma or carcinoma of the Zona glomerulosa can lead to what clinical presentations?
Hyperaldosteronism Metabolic acidosis Oedema
50
What type of tumours can lead to hyperadrenocorticism?
Acidophilic adenohypophysis cell tumour - ACTH producing. Adenoma or carcinoma of the adrenal gland
51
What clinical presentation is often seen in cases of hyperadrenocorticism?
* Increased appetite * Weak/ atrophic muscles - particularly trunk/ abdomen * Abdominal enlargement, lordosis, muscle tremors * Temporal muscle atrphy * Hepatomegaly * Epidermal atrophy * Hyperpigmentation * Calcinosis cutis * Bilateral and symmetrical alopecia
52
Septic shock can lead to which gross changes in the adrenal gland?
Haemorrhage of the cortex
53
What regressive changes are associated with the adrenal gland?
1. Insufficiency - addisonian crisis - stress induced 2. Atrophy - iatrogenic 3. Idiopathic atrophy - autoimmunity
54
What clinical signs would be expected with a) reduced mineralocorticoids and b) reduced glucocorticoids?
1. Mineralocorticoids: hyperkalaemia, reduced serum Na and Cl, cardiovascular disturbences, dehydration and haemoconcentration (Na+ loss) 2. Glucocorticoids: Hypoglycaemia, hyperpigmentation
55
Describe the lesion
The adrenal cortex is diffusely affected and shows marked enlargement. The normal architecture is diffusely whitened and firm to touch. The enlargement of the cortex is impeding upon the normal medullary architechture.
56
Phaeochromocytoma
Medullary tumour
57
What hormones are secreted by the endocrine pancreas and by which cells?
1. Insulin - beta 2. Glucagon - alpha 3. Somatostatin - delta 4. Pancreatic polypeptide - PP cells 5. Vasoactive intestinal peptide - D1 cells 6. Serotonin - Enterochromaffin cells
58
What are the main roles of insulin?
1. Carbohydrate metabolism: glucose into muscle, glycogenesis 2. Lipid metabolism: fatty acid synthesis, inhibits breakdown of adipose tissue 3. Uptake of amino acids 4. K, Mg and P ion permeability increased in cells
59
A lack of insulin has what effects on the body?
Catabolism * Gluconeogenesis - hyperglycaemia * Reduced protein synthesis - muscle wastage * Lipolysis - hyperlipidaemia * Acidosis * Dehydration
60
Chronic pancreatitis can lead to what regressive changes?
Islet atrophy and fibrosis
61
FIP can lead to what regressive changes in the pancreas?
Focal granulomatous- necrotising pancreatitis
62
Insulinoma
Beta cell adenoma - functional tumour leads to hyperinsulinism, hypoglycaemia, neurological signs
63
Zollinger-Ellison tumour
Gastrinoma - leads to hypersecretion of acid into the duodenum and ulcerative necrosis
64
Glucagonoma
Hyperglycaemia and DM
65
What can cause primary diabetes mellitus in the dog, cat and cow?
1. Dog: acute pancreatic necrosis, chronic fibrosing pancreatitis,neoplastic destruction 2. Cat: islet amyloidosis 3. Cow: chronic FMD
66
Secondary dibetes mellitus can be caused by ...
1. Persistent CL -\> P4 -\> GH -\> Insulin inhibition 2. Pituitary tumour - GH 3. Hyperadrenocorticism
67
What clinical presentation may be expected with diabetes mellitus in the dog?
* Emaciation * Hepatic lipidosis * Glycogen accumulation in the bile duct cells - vacuolation * Glycogen nephrosis * Glomerulosclerosis - chronic * Cataracts