Vet Path 250-215 Endocrine Pathology

Front 1

Pituitary starts here

Back 1

Pituitary starts here

Front 2

Briefly, what 3 categories of pituitary pathology occur? (this is a broad overview question)

Back 2

Developmental disorders
- aplasia, hypoplasia
- - - - inherited, toxic, infectious
- pituitary cysts

Inflammation
- systemic D or extension from face/orbit

Neoplasia
- non-functional or functional adenomas
- others

Front 3

What is the typical concentration of hormones in the blood?

How does this compare with other chemicals?

Back 3

Typically 10-10 -> 10-11 for hormones
compared to 10-3 - 10-5 for others

Hormones are active at these concentrations due to high affinity receptors

Front 4

There are 3 types of cells in the pituitary.

Name them, the different cell types in each category and the products of each

Back 4

Acidophils
- somatotrophs - GH*
- luteotrophs - prolactin

Basophils
- gonadotrophs - LH, FSH
- thyrotrophs - TSH

Chromophobes (don't stain)
- corticotrophs - ACTH*
- melanotrophs - MSH

Front 5

Sketch and briefly discuss the regulation of pituitary hormones

Back 5

Now, write in the RF and SH for corticosteroids

Front 6

Where is the pituitary. What structures is a space occupying lesion likely to effect?

Back 6

The pituitary lies in a bony depression at the base of the brain (sella turcica).

Enlargement of the pituitary is likely to effect the hypothalamus and optic chiasm.

Front 7

Failure of pituitary development
- what 3 mechanisms are most common?

Back 7

Genetic: aplasia -> prologoned gestation in several cattle breeds

Toxicities in utero: hypoplasia -> Veratrum californicum in ewes

Infectious in utero: viral

Front 8

How does Veratrum californicum lead to developmental disorders of ewes?

(I don't think this is v-imp but the process of pathogenesis is an interesting exercise that can be applied to any damage of the hypothalamus)

Back 8

Exposure to skunk cabbage between d9-14 of gestation inhibits neural tube formation.

Absent/malformed hypothalamus -> lack of releasing factors from hypo -> lack of stimulating H from pit -> target organ hypoplasia -> CS

Front 9

Discuss the aetiology & pathogenesis of pituitary dwarfism

Back 9

Inherited in several dog breeds (esp GSD)

Pituitary cyst formation

Clinically progressive: GH> TSH but ACTH generally not affected

CS: proportional dwarfism, cretinism, puppy coat retained

Front 10

Do pituitary cysts always lead to pituitary dwarfism?

Back 10

No, they can be incidental findings

Front 11

What are the two general mechanisms for pituitary inflammation?

Back 11

1. Systemic inflammatory diseases

2. Local extension from face or nose dt bacterial or mycotic infection

Front 12

Pituitary adenomas are classified in two ways.

What are they?

Back 12

Non-functional - hormonally inactive

Functional - hormonally active

Front 13

Briefly, what are 5 potential consequences of a non-functional pituitary adenoma?

Why do they occur?

Back 13

Clinical signs dt
- functional loss of pituitary, and/or
- compression of adjacent tissues

Potential consequences
- adult onset panhypopituitarism dt decr. secretion of trophic hormones)

- pituitary cachexia dt loss of protein anabolic effects of GH

- blindness dt compression of optic nerves or optic chiasm

- diabetes insipidus dt effect on posterior pituitary

- CNS dysfunction dt effects on hypothalamus

Front 14

List the 3 most common functional tumours, the cells & species affected.

Back 14

Chromophobe adenoma in dogs -> pituitary dependent Cushings

Chromophobe adenoma in horses -> CS referable to hypothalamic compression, occ. pit-dep Cushings

Acidophils tumours in cats -> excess GH -> acromegaly

Front 15

Chromophobe adenoma in dogs
- cause
- breeds
- clinical signs

Back 15

PItuitary dependent Cushings
- excess ACTH -> excess cortisol
- Boxers, Terriers, Dachshunds
- bilateral enlargement of adrenal glands
- PUPD, thin skin, obesity, pot belly, alopecia, may progress to DM

Front 16

How is chromophobe adenoma of horses different to dogs?

Back 16

CS usually dt hypothalamic derangement. If functional, MSH, endorphins in excess NOT ACTH.

Striking feature is hairiness

Front 17

Acromegaly is dogs occurs via a different mechanism to that most commonly seen in cats. Discuss

Back 17

In dogs, acromegaly is associated with excess progestin exposure.

This triggers hyperplasia of the mammary gland and excess GH

In cats, acromegaly is usually dt a functional pituitary adenoma affecting the somatotrophs (GH)

Front 18

List 5 common CS of acromegaly

Back 18

1. Thickened CT -> heavy facial features

2. Thickened bones, subcutis, visceral enlargement

3. Insulin dependent DM

4. PUPD

5. Large body mass

Front 19

What are the two main mechanisms leading to diabetes insipidus?

Back 19

1. Central - defect in posterior pituitary leading to decr. ADH

2. Peripheral aka "nephrogenic DI" - defect in kidneys leading to decr response to ADH

Front 20

What is the key diagnostic feature of central diabetes insipidus?

Back 20

Polyuria in the abscence of renal disease

Front 21

Central diabetes insipidus can be dt lesions in hypothalamus or the posterior pituitary. Why?

Back 21

Remember that the posterior pituitary is neural tissue. The hormones ADH and oxytocin and made in the large & small nuclei of the hypothalamus and transported to the post-pit.

Front 22

List 8 effects of hypothalamic destruction

Back 22

PUPD
hirsuitism
altered appetitie
insulin resistant hyperglycaemia
weakness
incoordination, tremors
somnolences
blindness
hyperhidrosis (sweating)
aggression/mood swings

Front 23

Now, write a summary of the endocrine pathology of the pituitary gland - mechanisms, conditions, species most affected

Back 23

Front 24

These are litter mates.

What is the aetiology and pathogenesis?

Back 24

Pituitary hypoplasia dt pituitary cyst

Progressive loss: GH> MSH (ACTH rarely affected)

Inherited disorder in several dog breeds incl GSD

Front 25

What is the aetiology & pathogenesis?

Back 25

Acromegaly in dogs. Usually dt excessive progestin exposure > mammary hyperplasia > excessive GH

Overall enlargement of soft & bony tissues seen as increased mass and facial thickenings

Front 26

What is this image suggesting?

Back 26

Functional pituitary adenoma (chromotroph = corticotrophs) -> excess ACTH -> bilateral hyperadrenocortisim.

This animal most likely showed clinical signs of pituitary dependent hyperadrenocorticism (Cushings)

Front 27

What is wrong with this horse? (It shouldn't be this hairy)

Back 27

Most likely pituitary chromophobe adenoma. In horses, effects are dt hypothalamic derangement. If functional, MSH & endorphins most likely affected. Unlike dogs, ACTH not usually affected

Front 28

Thyroid starts here

Back 28

Thyroid starts here

Front 29

Thyroid:
what are the 3 categories of dysfunction for the thyroid

Back 29

Hypothryoidism

Hyperthyroidism

Neoplasia

Front 30

What are the two broad mechanisms by which hypothryoidism may occur?

Back 30

Decreased functional thyroid mass

Ineffective thyroid hormone production

Front 31

Hyperthyroidism is most commonly seen in which species?

How does this usually arise?

Back 31

Cats, esp. > 8 yo

Functional hyperplasia or adenomas

Front 32

In which species are thryoid carcinomas commonly seen?

What are the usually sequelae?

Back 32

Dogs, predisposition for beagles, boxers, goldies

Compression effects, metastasis to lung, 10% are functional

Front 33

Hypothyroidism dt decreased functional mass;

give 5 mechanisms by which this might occur?

Which are the two most common mechanisms in dogs?

Back 33

lymphocytic thyroiditis (auto-immune = Hashimotos) **** dogs

idiopathic follicular atrophy **** dogs

aplasia/ hypoplasia
neoplasia (causing destruction)
secondary to pituitary damage (decr. TSH)

Front 34

Hypothyroidism can also occur dt ineffective thyroid hormone production.

What is this called?

What forms can it take?

Give three causes

Back 34

Goitre - diffuse, colloid, nodular

I deficiency
I excess
goitrogenic compounds

Front 35

What are the two main types of thyroid neoplasia?

What are the most common effects of each?

Back 35

Thyroid adenoma - benign

Thyroid carcinoma - compression effects, metastases to lung, 10% functional

Front 36

Define adenoma

Back 36

A benign epithelial tumour in which the cells form recognisable glandular structures

or

in which the cells are derived from glandular epithelium

Front 37

Define carcinoma

Back 37

Malignant new growth made up of epithelial cells tending to infiltrate surrounding tissues and to give rise to metastases.

Front 38

Create a summary of endocrine pathology of the thyroid gland

Back 38

Well done! (add pic)

Front 39

What are the products of the thyroid gland?

Back 39

T3 & T4 from thyroid epithelial cells

Calcitonin from the parafollicular C cells

Front 40

List 4 main functions of T3 & T4

Back 40

Increases BMR

Increases synthesis & catabolism

Acts with GH in musculoskeletal & NS development in young animals

Increases HR, CO

Front 41

List 6 clinical signs of hypothyroidism in dogs

Back 41

Decreased BMR, lethargy, dullness, inactivity

cretinism in neonates & juvenilles

rat-tail, dry hair coat

symmetrical alopecia

seborrhoea

myxoedema "tragic facial expression"

Peripheral neuropathies, myopathies

Reproductive failure in females

Front 42

What are the two main causes of hypothyroidism in dogs?

Back 42

Lymphocytic thyroiditis (Hasimoto's)
- inherited autoimmune

Idiopathic follicular atrophy

Front 43

List 3 other causes of hypothyroidism

Back 43

Hypoplasia/aplasia
Atrophy
Destruction dt neoplasia
Sx removal
Secondary to pituitary disease
Ineffective production (conditions leading to goitre)

Front 44

What is goitre?

How is it manifest differently in cats?

Back 44

Non-neoplastic, non-inflammatory thyroid enlargement

TYPICALLY associated with HYPOTHYROIDISM

Associated with hyperthryoidism in cats

Front 45

What are the 3 forms of goitre?

Back 45

Diffuse (hyperplastic)

Nodular

Colloid

Front 46

What situations lead to goitre?

Back 46

Iodine deficiency

Iodine excess

Exposure to goitrogens

Front 47

How is it that iodine excess can lead to goitre?

Back 47

Inhibits iodide uptake by thryoid gland

Low T3, T4

TSH secretion continues

Hyperplasia of epithelial cells without functional hormone production

Front 48

What is linked to the increased incidence of hyperthryoidism in cats over the last 40 years

Back 48

Tinned cat food and excess iodine in diet

Front 49

What clinical signs are associated with feline hyperthryoidism (give 6)

Back 49

Weight loss
Polyphagia
PUPD
Alopecia
Scurfy appearance
Tachycardia
Hyperactivity, nervousness, aggression

Front 50

Name 2 potentially devastating sequelae of hyperthyroidism in cats

Back 50

Left ventricular concentric myocardial hypertrophy dt system hypertension

Retinal aneurysm or detachment dt systemic hypertension

Front 51

In what species is C cells hyperplasia & neoplasia most common?

What is the outcome?

Back 51

Horse - C cell adenomas common in older animals

Often non-functional and incidental finding

Front 52

Now, write a summary of the endocrine pathology of the thyroid gland - mechanisms, conditions, species most affected

Back 52

add pic here

Front 53

Parathyroid starts here

Back 53

Parathyroid starts here

Front 54

List actions of parathyroid hormone at three main sites

Back 54

PTH is released in response to low plasma Ca
PTH has roles in Ca homeostasis & in the calcification of bone

1. Bone: incr osteoclast activity & osteoblast no.

2. Kidney: activation of VitD, incr absorption of Ca in proximal tubules

3.Gut: incr Ca absorption (dt VitD activation)

Front 55

Which is seen more commonly - hypoparathyroidism or hyperparathyroidism

Back 55

HYPERparathyroidism

Front 56

What are the causes of hypoparathyroidism?

Back 56

Primary:
- autoimmune -> decr. PTH

Secondary
- neoplasia
- hypoplasia
- atrophy following sustained HYPERcalcaemai
- gland destruction (eg sx)

Front 57

What's milk fever got to do with any of this?

Back 57

Acute hypocalcaemia at parturition usually following a period of high Ca during preg (PTH atrophy) and then low Ca at parturition -> PT unable to respond appropriately

Barely mentioned by Ron but included here for completeness

Front 58

List the primary & secondary causes of hyperparathyroidism

Back 58

Primary: functional tumour or hyperplasia -> excess PTH

Secondary
- nutritional
- renal
- paraneoplastic

Front 59

What are the causes & effects of hyperparathyroidims in dogs and horses?

Back 59

For both species -> secondary hyperparathyroidism -> fibrous osteodystrophy = excessive fibrous material in bone esp facial. Also see calcification of soft tissues

Dogs: renal secondary hyperparathryoidism

Horses: nutritional secondary hyperparathyroidism

Front 60

Now, write a summary of the endocrine pathology of the parathyroid gland - mechanisms, conditions, species most affected

Back 60

add pic here

Front 61

Discuss likely aetiology & pathogenesis for this dog?

Back 61

Front 62

What's the likely aetiology & pathogeneis for this dog?

Back 62

Fibrous osteodystrophy dt secondary renal hyperparathyroidism

Front 63

What's the likely aetiology & pathogeneis for this horse?

Back 63

Fibrous osteodystrophy dt secondary nutritional hyperparathyroidism

Front 64

What's the likely aetiology & pathogeneis for this sheep?

Back 64

Hyperplastic goitre possible dt
- mother grazing pasture with insufficient iodine
- mother grazing pasture with plants containing goitrogens

Front 65

Samples form a scurfy cat. What's being shown here?

Back 65

For extra points, explain how systemic hypertension leads to LV concentric myocardial hypertrophy

Hint 65

systemic HT -> incr. BP -> incr. P against which left heart contracts -> incr. work of LV -> concentric myocardial hypertrophy (response to chronic P overload)

Front 66

Histology of various thyroids. What's being shown here?

Back 66

Front 67

Adrenals start here

Back 67

Adrenals start here

Front 68

3 zones of adrenal cortex & products

Back 68

?

Front 69

Main functions of adrenal cortex products

Back 69

?

Front 70

List 3 developmental anomalies of the adrenal gland

Back 70

Agenesis: unilateral or bilateral (-> death)

Hypoplasia dt hypothalamus or pituitary deficit

Accessory adrenal tissue

Front 71

List 3 degenerative lesions of the adrenal gland

Back 71

Mineralisation
Amyloidosis (both oft incidental)

Haemorrhage

Front 72

What situations can lead to adrenocortical haemorrhage?

Back 72

DIC

Shock

Septicaemias

Neonates: hypoxia, birth trauma, cold stress

Front 73

What are the 2 mechanisms for enlargement of the adrenal glands?

Back 73

Hyperplasia

Neoplasia

Front 74

List the 5 types of hyperplasia of the adrenal cortex

Back 74

Accessory nodules

Nodular

Diffuse cortical

Hyperplasia of the zona glomerulosa -> hyperaldosteronism
- primary (idiopathic)
- secondary (dt renal D, hypoT, Na depletion)

Front 75

What are the two types of adrenal cortical neoplasia?

What are the usual sequelae?

Back 75

Adenomas:
- common, usually non-functional

Carcinomas:
- often invasive (aorta, VC) and metastasize,
- usually non-functional

A small no. can be functional leading to adrenal dependent hyperadrenocorticism (Cushings)

Front 76

What are the 3 main causes of hyperadrenocorticism (Cushings)?

- proportion?
- uni/bilateral?
- breeds affected?

Back 76

Pituitary-dependent
- 85% in dogs
- bilateral
- small breed

Adreno-dependent
- 15%
- usually unilateral
- med-large breeds

Iatrogenic
- excess exogenous cortisol

Front 77

List 12 clinical signs of hyperadrenocorticism in dogs

Make sure you can sketch a brief pathogenesis for each

Back 77

PUPD
polyphagia
enlarged abdomen
thin skin
calcinosis cutis
delayed wound healing
hepatomegaly
DM
Muscle weakness
Endocrine dermatosis
Secondary infections
Lethargy
Wasting

Front 78

How does diabetes mellitus develop in response to hyperadrenocorticism?

Back 78

Cortisol antagonises insulin leading to the development of insulin resistance, hyperglycaemia and eventually DM

Note: the most common clinical signs in dogs/cats when concurrent disease presents are referable to the DM: PUPD, polyphagia with weight loss

Front 79

List 3 key points about hyperadrenocorticism in cats

Back 79

Rare
Most dt functional pituitary tumour (95%)
Mostly old cats (> 10y)

Front 80

List the 4 types of hypoadrenocorticism

Back 80

Primary (Addisons)
Secondary to pit/hypo deficits
Iatrogenic (mitotane tx for hyperA)
Idiopathic

Front 81

What is a phaeochromocytoma and why should you care?

Back 81

Phaeochromocytoma = "dusky coloured cell tumour"

Tumour of the adrenal medulla (most common, esp dogs, cattle)
Tan/brown often with haemorrhage
Invasion of vena cava with tracking to the heart is common with malignancies

Front 82

What's typical of phaeochromocytomas in bulls?

Back 82

Develop concurrently with calcitonin C-cell tumours of the thyroid gland (same embryological origin)

Front 83

Now, write a summary of the endocrine pathology of the adrenal gland - mechanisms, conditions, species most affected

Back 83

Front 84

Pancreas starts here

Back 84

Pancreas starts here

Front 85

There's only really one tumour of the pancreas that you NTK now.

What is it?
Who gets it?
What effects does it have?

Back 85

Insulinomas (beta-cells of the pancreas)

Middle aged - older dogs esp GSD, fox terriers, standard poodles, boxers, irish setters

Effects mostly referable to glucose depletion: episodic seizures, weakness, collapse

Front 86

Transected adrenals from small white fluffy dog with thin skin and pot-belly. What's the likely aetiology & pathogenesis?

Back 86

Unilateral adrenals thus adrenal-dependent hyperadrenocorticism (hyperA) dt functinoal neoplasia (adenoma or carcinoma). Excess cortisol leads to clinical signs

Front 87

Organs from a Cushingoid dog. Explain the aetiology of each

Back 87

Front 88

Dog: adrenal gland growth invading the hepatic artery. What's it likely to be?

Back 88

Phaeochromocytoma (tumour of the adrenal medulla)

Front 89

Pancreas of a dog showing episodic seuizures. What's it likely to be>

Back 89

Insulinoma -> hypoglycaemia

Front 90

Ox adrenal. What's the arrow likely pointing to?

Back 90

Phaeochromocytoma (tumour of the adrenal medulla)

Front 91

Pix & Q from autotutorial start here

Back 91

Pix & Q from autotutorial start here

Front 92

Thyroid from cat

What's the condition? Why is it different for a cat?

What's the likely clinical signs?

What's a likely sequelae?

Back 92

Nodular hyperplasia of the thryoid.
Often functional (hormonally active) in cats

CS: weight loss, polyphagia, PUPD, anxiety, scruffy coat.

In cats, can develop into functional adenomas.

Front 93

Lamb with bilateral large masses

Condition?

4 main causes

Back 93

colloidal goitre (involutary stage of diffuse hyperplastic goitre)

Goitre:
I deficiency
I excess
Goitrogenic compounds
Congenital dyshormonogenetic