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Y3 Repro and Endo Pathology > Pathology of the Endocrine system 2 > Flashcards

Pathology of the Endocrine system 2 Flashcards

1
Q

What is the function of the parathyroid glands?

A

Production of parathyroid hormone

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2
Q

What are the functions of parathyroid hormone?

A
  • Mobilisation of calcium from bone
  • Enhances absorption of calcium from the small intestine
  • Suppressed calcium lost in urine
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3
Q

How is calcium mobilised from bone?

A

PTH indirectly stimulates osteoclasts to reabsorb bone mineral, liberating Ca into blood

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4
Q

How does PTH enhance calcium absorption from the SI?

A

Indirectly; by stimulating production of the active form of vitamin D in the kidney; vitamin D induces synthesis of a Ca-binding protein in intestinal epithelial cells that facilitates efficient absorption of Ca into blood

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5
Q

How does PTH supress loos of Ca in urine?

A

PTH stimulates tubular reabsorption of Ca and stimulates loss of phosphate ions in urine

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6
Q

Reduced PTH release leads to?

A

Hypoparathyroidism

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7
Q

What are the consequences of hyperparathyroidism?

A

Hypocalcaemia → increased neuromuscular excitability → spasms, tetany, tremors

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8
Q

Name some causes of hypoparathyroidism

A
  • Agenesis of parathyroid glands
  • Inflammation (autoimmune parathyroiditis; dogs)
  • Surgical excision (eg. with thyroidectomy)
  • Tumour infiltration
  • Trauma
  • Vit D intoxication
  • Postnatal hypocalcaemia in cattle
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9
Q

Describe Postnatal hypocalcaemia in cattle

A
  • Parturient paresis in dairy cattle
  • Complex metabolic disease (characterised by severe hypocalcaemia and hypophosphataemia near time of parturition and initiation of lactation)
  • Ca levels <50% normal (in spite of PTH↑), hardly any bone resorption
  • Influenced by composition of diet
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10
Q

What are the consequences of hyperparathyroidism?

A

Ca mobilisation from bone → hypercalcaemia

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11
Q

Primary hyperparathyroidism is due to?

A

Hyperplasia, adenoma or carcinoma of parathyroid gland

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12
Q

Secondary hyperparathyroidism is due to?

A
  • Consequence of chronic renal insufficiency

- Consequence of dietary Ca/P imbalance

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13
Q

Tertiary hyperparathyroidism is due ti?

A

Final stage kidney disease with non-responsive, autonomous hyperparathyroidism

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14
Q

Describe Pseudohyperparathyroidism

A
  • Humoral malignant hypercalcaemia

- Mainly in dogs with adenocarcinoma of the anal sac (para-anal) gland or lymphomas (release of PTH-like protein!)

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15
Q

How does hyperparathyroidism appear grossly?

A

Gross lesion is of bilaterally enlarged (hyperplastic) parathyroid glands

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16
Q

Describe the mechanisms of renal secondary hyperparathyroidism

A
  • Reduced renal Ca resorption and phosphate secretion
  • Reduced Vit D activation
  • Hyperphosphataemia
  • Hypocalcaemia
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17
Q

What are the two main consequences of renal secondary hyperparathyroidism?

A
  • Fibrous osteodystrophy

- Metastatic calcification: calcium deposited within tissues

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18
Q

What is fibrous osteodystrophy?

A

Calcium is liberated from the bone to return blood calcium back to normal. Mineralised matrix of the bone is replaced by a soft collagenous connective tissue

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19
Q

What are the clinical signs of fibrous osteodystrophy?

A

Bone pain (lameness), loss of teeth, deformity of maxilla and mandible

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20
Q

What are the gross findings of fibrous osteodystrophy?

A

“soft”, demineralised bones [Test skull, ribs!]

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21
Q

Which cells are enhanced in fibrous osteodystrophy?

A

Osteoclasts

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22
Q

What is normal bone substituted by in fibrous osteodystrophy?

A
  • insufficiently mineralized osteoid

- collagenous connective tissue

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23
Q

Atrophy of the parathyroid glands is due to?

A

Goitre or thyroid cysts (compression)

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24
Q

Secondary hyperplasia of the parathyroid glands is due to?

A

Hypocalcaemia

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25
Q

Name some primary tumours of the parathyroid glands

A

Chief cell adenoma, adenocarcinoma (can be hormonally active which would lead to a primary hyperparathyroidism)

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26
Q

Describe the gross appearance of a parathyroid gland adenoma

A

Asymmetrical lesion
One side is large and is secreting hormones
One side is small/atrophic

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27
Q

Name the 3 layers of the adrenal gland

A

capsule
cortex
medulla

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28
Q

Name the 3 layers of the cortex of the adrenal gland

A

Zona glomerulosa
Zone fasciculata
Zona reticularis

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29
Q

Name the hormone secreted by the zona glomerulosa

A

Mineralocorticoids (aldosterone)

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30
Q

Name the hormone secreted by the zona fasciculata

A

Glucocorticoids (cortisol)

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31
Q

Name the hormone secreted by the zona reticularis

A

Sex steroids (androgens, oestrogens, progesterone)

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32
Q

Name the hormone secreted by the adrenal medulla

A

Catecholamines (adrenaline and noradrenaline)

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33
Q

Describe the histology of the adrenal cortex and medulla

A

Zona glomerulosa – cells form distinct arches
Zona fasciculata and zona reticularis – producing steroid based hormones so we see vacuolation of the cytoplasm
Medulla – producing protein based catecholamines so cytoplasm is granular

34
Q

What are the functions of mineralocorticoids (adrenal cortex)

A

Main effects on ion transport of epithelial cells:

  • Lead to loss of potassium (K+) and conservation of sodium (Na+)
  • Most potent: aldosterone; due to: effect on enzymatically controlled electrolyte pumps in -
    a) epithelial cells of distal convoluted renal tubule (cation exchange mechanism, leading to resorption of Na from glomerular filtrate and secretion of K into lumen)
    b) sweat glands
35
Q

What are the functions of glucocorticoids (adrenal cortex)

A
  • Concerned with intermediary metabolism of glucose
  • Acute effects within 15-30 min, before compensatory effect of insulin!
  • Increase glucose production -> hyperglycaemia
36
Q

Glucocorticoids cause hyperglycaemia due to what mechanisms?

A

a) decrease in glucose uptake in adipose tissue, skin, fibroblasts, lymphoid tissue
b) increased glucose catabolism in these tissue and in muscle
c) increased gluconeogenesis (mainly in liver)
d) decreased lipogenesis, increased lipolysis in adipose tissue -> glycerol and free fatty acids
- increase protein catabolism

37
Q

What are the functions of noradrenaline and adrenaline from the adrenal medulla?

A
  • Fight or flight response with sympathetic NS
  • Increased rate and force of contraction of the heart muscle
  • Vasoconstriction
  • Dilation of bronchioles
  • Stimulation of lipolysis of fat cells
  • Increased metabolic rate
  • Dilation of pupils
38
Q

Primary hypoadrenocorticism is also known as?

A

Addisons disease

39
Q

Describe primary hypoadrenocorticism

A
  • Humans, dog, cat, horse, usually idiopathic cortical atrophy
  • Usually all zones of the adrenal cortex affected
  • Non-specific symptoms (mineralo- and glucocorticoids affected)
40
Q

Secondary hypoadrenocorticism is due to?

A

Hypopituitarism (ACTH↓)

41
Q

Hyperadrenocorticism linked to hyperaldosteronism is due to?

A

Nodular hyperplasia, adenoma or carcinoma of zona glomerulosa [endocrine activity]

42
Q

Hyperadrenocorticism linked to hyperaldosteronism has what consequnces?

A

Metabolic acidosis

Oedema

43
Q

Adrenal dependent Hypercortisolism is also known as?

A

Cushings syndrome

44
Q

What are the consequences/clinical signs of Cushings syndrome?

A

Polydipsia, polyuria, polyphagia, obesity (trunk)
Atrophy of skeletal muscle, alopecia, epidermal atrophy
Osteopenia
Secondary diabetes mellitus

45
Q

Describe primary adrenal Cushing syndrome

A

With adenoma or carcinoma of zona fasciculata

46
Q

Describe paraneoplastic Cushing syndrome

A

Ectopic ACTH production in non-pituitary tumours (eg. bronchial carcinoma, thymoma, pancreatic carcinoma)

47
Q

Describe iatrogenic Cushing syndrome

A
  • Side effect of glucocorticoid (or ACTH) therapy
  • Mainly in dogs (and cats) e.g. itchy dogs on chronic prednisolone therapy
  • Will lead to negative feedback at the pituitary gland and bilateral adrenal atrophy. Sudden cessation of therapy results in hypoadrenocorticism due to atrophic glands. Don’t stop steroid therapy suddenly
48
Q

What are some general features of hyperadrenocorticism?

A
  • Increased appetite and food intake
  • Weakened and atrophic muscles (extremities, abdomen)
  • Gradual abdominal enlargement, lordosis, muscle trembling
  • Atrophy of temporal muscles
  • Hepatomegaly (fat and glycogen storage)
  • Skin alterations
49
Q

Describe the gross skin lesions of hyperadrenocorticism

A
  • Progressive bilateral symmetrical alopecia
  • Fine, paper thin, wrinkled texture, hyperpigmentation
  • Mineralisation (calcinosis cutis)
50
Q

Describe the histological skin lesions of hyperadrenocorticism

A
  • Atrophy of epidermis, hair follicles and sebaceous glands
  • Loss of collagen and elastin in dermis and subcutis
  • Inactive hair follicles with infundibular dilatation and hyperkeratosis
  • Diffuse othokeratotic hyperkeratosis
  • Cutaneous mineralisation (calcinosis cutis) (deposition of mineral crystals along collagen and elastin fibres)
51
Q

Describe circulatory disorders of the adrenal glands

A
  • Hyperaemia with intoxications and sepsis

- Haemorrhage in sepsis, intoxication and fatal stress

52
Q

Adrenal cortical insufficiency is also termed?

A

Addisonian crisis

53
Q

Describe adrenal cortical insufficiency

A
  • Stress induced (circulatory, infectious, toxic, traumatic or thermal insults)
  • Often with cortical necrosis
54
Q

What causes adrenal cortical atrophy?

A

Prolonged glucocorticoid therpay

55
Q

Which zone is mostly affected by adrenal cortical atrophy?

A

Zona fasciculata

56
Q

Describe the effects of reduced mineralocorticoid levels in hypoadrenocorticism

A
  • Severe hyperkalaemia, reduced serum Na and Cl
  • Cardiovascular disturbances due to hyperkalaemia
  • Progressive dehydration and haemoconcentration due to loss of Na
57
Q

Describe the effects of reduced glucocorticoid levels in hypoadrenocorticism

A
  • Moderate hypoglycaemia (due to gluconeogenesis↓ and insulin sensitivity↑)
  • Hyperpigmentation of skin (due to increased MSH release)
58
Q

Bilateral cortical hyperplasia (=secondary hyperplasia) is due to?

A

Persistently elevated ACTH levels - pituitary hyperplasia

59
Q

If active cortical adenomas produce?

A

Cushings

60
Q

What is a Phaeochromocytomas?

A

Medullary neoplasm

61
Q

What makes up the endocrine pancreas?

A

Islets of Langerhans (pancreatic islands)

62
Q

Islets of Langerhans (pancreatic islands) are composed of?

A

a) alpha cells [60-70%; insulin]
b) beta cells [20%; glucagon]
c) delta cells [somatostatin]
d) PP cells [pancreatic polypeptide]
e) D1 cells [vasoactive intestinal peptide]
f) enterochromaffin cells [serotonin]

63
Q

Describe the effects of insulin on carbohydrate metabolism

A
  • Facilitates entry of glucose into muscle, adipose and other tissues (facilitated diffusion)
  • Stimulates liver to store glucose as glycogen (activation of several enzymes involved in glycogen synthesis)
  • Decreases glucose concentration in blood
64
Q

Describe the effects of insulin on lipid metabolism

A
  • Promotes synthesis of fatty acids in the liver (when liver is saturated with glycogen, additional glucose is used for synthesis of fatty acids export as lipoproteins
  • Inhibition of breakdown of fat in adipose tissue (inhibition of intracellular lipase -> further accumulation of fat)
65
Q

How are the brain and liver not linked to glucose?

A

Brain and liver do NOT require insulin for efficient glucose uptake - their level of glucose is dependant on blood glucose level

66
Q

A lack of insulin leads to?

A

A catabolic state

67
Q

Describe a catabolic state due to a lack of insulin?

A
  • Increased gluconeogenesis from glycogen and protein -> hyperglycaemia
  • Reduced protein synthesis -> wasting of tissues
  • Increased lipolysis, diminished uptake of free fatty acids in adipose tissue -> hyperlipidaemia
  • hyperosmolarity, profound dehydration, acidosis -> neurological derangement, coma
68
Q

What are the consequences of hyperglycaemia?

A

Increased glucose load in primary urine -> glycosuria, osmotic diuresis, thirst

69
Q

What are the consequences of hyperlipidaemia?

A

Fatty acid metabolisation in the liver via acetyl-CoA, in absence of glucose -> ketoacids -> ketoacidosis

70
Q

Name 3 endocrine pancreas neoplasms

A

a) Insulinoma (β-cell adenoma)
b) Gastrinoma [Zollinger-Ellison syndrome]
c) Glucagenoma [hyperglycaemia, Diabetes mellitus]

71
Q

What are the consequences of insulinomas?

A

Hyperinsulinism, hypoglycaemia, neurological signs

72
Q

What are the clinical signs of an insulinoma?

A

Seizures
Weakness, depression, lethargy
Ataxia, posterior weakness
Polyphagia, anorexia

73
Q

Zollinger-Ellison Syndrome is seen with?

A

Gastrinoma

74
Q

Describe the consequences of a gastrinoma

A

Secretion of gastrin -> gastric hypersecretion -> hyperacidity, mucosal hyperplasia, ulceration

75
Q

Type 1 diabetes is … dependant

A

Insulin

76
Q

Describe type 1 diabetes causes and features

A
  • Severe, absolute lack of insulin due to reduction of beta cell mass
  • Acute onset, but based on chronic autoimmune attack of beta cells
  • Lymphocyte-rich inflammatory infiltrate in islets
77
Q

Describe primary diabetes in different animals

A

With extensive neoplastic destruction of pancreatic tissue
OR
In dogs: a) with acute pancreatic necrosis, chronic fibrosing pancreatitis. b) occasionally early-onset diabetes (purebred dogs) due to islet hypoplasia
- In cats: with islet amyloidosis
- In cattle: with chronic FMD

78
Q

Describe type II diabetes?

A

= non-insulin-dependent DM

Normal insulin production

79
Q

Describe the 2 mechanisms of type II diabetes

A

a) Derangement in beta cell secretion of insulin
b) Decreased response of peripheral tissues to insulin [“insulin resistance”]
- Due to genetic defects of insulin receptor and insulin signalling pathways
- Due to obesity

80
Q

Secondary diabetes mellitus occurs due to?

A

As a consequence or complication of other diseases

Due to antagonism between insulin and other hormones

81
Q

Describe some example causes of secondary diabetes mellitus

A

a) Endogenous progesterone (bitch): persistent corpora lutea
b) Pituitary tumours: due to growth hormone production
c) Cats, dogs: hyperadrenocorticism

82
Q

What lesions are seen with diabetes mellitus?

A
  • Emaciation, (dehydration)
  • Hepatic lipidosis, vacuolation of bile duct epithelium [due to glycogen accumulation]
  • Glycogen nephrosis
  • Cataract (dogs)

Y3 Repro and Endo Pathology (5 decks)

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