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Flashcards in Endocrine Deck (67):
1

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

  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

2

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

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)

3

How are steroid hormones excreted from the body?

Via the urine/ bile

4

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

Thyroid > catecholamines

5

From which amino acid are thyroid and catecholamines derived?

Tyrosine

6

What effects can hormones have on target cells?

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

 

7

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

Proteins, peptides, catecholamines, fatty acid derivatives

Used in second messenger systems

8

Which types of hormones are able to activate intracellular receptors?

Steroids and thyroid hormones - these alter transcriptional gene expression

9

Endocrinopathies can be caused by which mechanisms?

  • 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

 

10

Which hormones are released from the adenhypophysis?

FLAT PiG

11

Which hormones are produced in the hypothalamus?

ADH

Oxytocin

Hypophyseotropic releasing hormones

12

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

Acidophilic - growth hormone, prolactin

Basophilic - LH, FSH, TSH, ACTH

13

Diabetes incipidus is caused by deficiency in which hormone?

Outline the difference between central and nephrogenic diabetes insipidus.

ADH

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

Nephrogenic - ADH receptor defect in the collecting duct and DCT

14

Rathke's cysts

Pituitary cysts - can cause dyspnoea if grow too large

15

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

Cyclopia

Arhynencephaly

16

Pituitary dwarfism is caused by a deficiency in which hormone?

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

17

An acidophilic adenoma can cause which conditions in an animal?

Excessive GH and growth

Overgrowth of connective tissue

Diabetes mellitus - GH inhibits insulin receptors

18

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

Atrophy - horse and dog

Pituitary inflammation - abscess formation - due to viral infection

Nodular hyperplasia

Adenoma

19

Pituitary inflammation can be caused by which viral agents?

Borna disease

Classical swine fever

Infectious anaemia

20

Describe the lesion

Q image thumb

The pituitary shows marked increase in size.

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

3x4 cm

 

21

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

Most frequently cause hypersecretion of ACTH

22

Describe the lesion

Q image thumb

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

23

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

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

24

Describe the associated lesions here.

Which condition is associated with these?

Q image thumb

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

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

Q image thumb

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.

Q image thumb

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

A image thumb
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

Q image thumb

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