Endocrinology and eye pathology Flashcards

(94 cards)

1
Q

With respect to the anatomy of the eye define the terms; Blepharo, Dacryo, Kerato, Ophthalmo and Sicca ?

A

Definition of the anatomy of the eye

Blepharo = eyelid
Dacryo = tear lacrimation
Irido = iris
Kerato = cornea
Ophthalmo = globe or eye
Sicca = dry

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2
Q

Define a cataract, Descemetocele and Glaucoma ?

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Definitions of the eye
Cataract = any opacity of the lens or its capsule or both

Desscemetocele = A deep corneal ulcer characterised by exposure and possible protrusion of the Descements memebrane.

Glaucoma = Abnormal increase in intraocular pressure

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3
Q

Define the meaning of the terms Uvea, Anterior uveitis, Miosis and Mydriasis ?

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Definition of terms
Uvea = vascular layer of the eye, iris, cililary body and choroid

Anterior uveititis = inflammation within the iris and cilliary body

Miosis = constriction of the pupil

Mydriasis = dilation of the pupil

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4
Q

Define the terms Ptosis, Aniscora and Epiphora ?

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Definitions related to the eye

Ptosis = drooping of the upper eyelid

Aniscora = different sized pupils

Epiphora = overflow of tears onto the face

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5
Q

Describe the potential defences of the eye ?

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Defences of the eye
The globe is a fluid filled sphere protected by
- bony orbit, mobile eyelids
- palpebral reflex blink, menace reflex and corneal reflex
- thick fibrous sclera and tough multi layed cornea
- antimicrobial substances in lacrimal secretions
- lubrication and constant eye washing by tear film
- Blood eye barrier

These defences make the eye susceptable to perpetuation of injury
- prevents drainage of injurous agents, debris, exudates
- chemical mediators for inflammation can cause damage to normal structures

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6
Q

Define the congenital conditions of Anophthalmia, Microphthalmia and Cyclopia / Synophthalmia ?

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7
Q

Define the congenital condition of corneal endothelial dystrophy and persistent pupillary membranes ?

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Definitions

Corneal endothelial dystrophy
- inherited disease with the progressive loss of corneal endothelial cells which leads to corneal oedema.

Persistant pupillary membranes
Failure of complete regression of the embryonic lenticular vasculature. Sometimes will adhere to the lens or cornea and may cause cataracts or irritation

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8
Q

What is a dermoid ?

A

Dermoid

A congenital abnormality of the eye where skin/hair grows from the surface of the eye.

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9
Q

Define conjunctivitis,and identify some potential causes ?

A

Conjunctivitis

This is inflammation of the conjuntiva
- oedema, chemosis
- erythema
- epiphora
- common esp young animals; kittens and pups

cattle infectious bovine Rhinotracheitis
Cats Feline Herpesvirus 1, Chlamydia
Horses Habronemiasis

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10
Q

Describe the disorders of the third eyelid; Horners syndrome and cherry eye ?

A

Abnormalities of the third eyelid

Protruding third eyelid
- systemic illness especially in cats (Horner’s syndrome)
Horner’s syndrome
- prolapsed third eyelid, enophthalmos, ptosis and pupillary miosis
- eg middle ear infection, tick paralysis may be idiopathic

Cherry eye
- prolapse of the gland of the third eyelid (nictitating membrane)

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11
Q

Define Blepharitis, Ectopic cilia and Distichiasis ?

A

Definitions telated to the eye

Blepharitis
- inflammation of the eyelids eg allergy pyoderma

Distichiasis
- Cilia originating from the Meibomian glands
- can irritate the cornea

Ectopic cilia
- cilia protruding through the palprebral conjunctiva
- can irritate the cornea

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12
Q

Define the terms Entropian and Ectropian eye pathology ?

A

Eye pathology

Entropian
Infolding of the eyelid margin
- irritation of the cornea by eyelashes
- eg Sharpeis, Rottweilers

Ectropian
Outward rolling of the eyelid which exposes the conjunctiva
- eg bloodhounds and Mastiffs

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13
Q

Identify this pathology ?

A

Meibomian adenoma
Meibomian adenomas are very common benign neolplasms

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14
Q

Identify this pathology ?

A

Squamous cell carcinoma

Predisposing factors = UV light, and poor pigmentation of the eye lids and conjunctiva.

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15
Q

Identify this pathology ?

A

Corneal oedema
This is increased fluid in the corneal stroma
- thus reducing the transparency of the cornea

There are a number of common causes involving injury to the corneal epithelium
- ulcers keratitis causing fluid absorption from the tear film
- lens luxation, glaucoma
- immune mediated CAV-1, absorbs fluid from the aqueous humor

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16
Q

Describe non specific inflammation of the cornea, and its possible pathology ?

A

Keratitis = inflammation of the cornea
Non specific chronic keratitis with epidermalization (cutaneous metaplasia)
There are many possible causes
- entropian, protruding pug eyes

Pathology
If it is non specific indicates a persistant corneal injury
- epithelial hyperplasia
- keratinisation
- pigmentation
- stromal fibrosis
- vascularisation

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17
Q

Identify this pathology and describe its causes ?

A

Chronic superficial keratitis (pannus)
Chronically distinctive keratitis in GSD and sight hounds

  • suspected immune mediated response
  • likely a genetic component (it is reccomended to not breed from afflicted dogs)
  • exacerbated by UV light
  • both eyes are usually affected but not symetrically
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18
Q

Identify and describe this pathology ?

A

Kertoconjunctivitis sicca (KCS): Dry eye

This is caused by a lack of lacrimal secretions
- most commonly due to an immune mediated disorder
- common in dogs
- prone to getting corneal ulcers
- chronic dessication may result in cutaneous metaplasia

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19
Q

Describe the possible pathology of infectious keratitis ?

A

Keratitis = inflammation of the cornea

Infectious Keratitis
- can be an extension of infectious conjunctivitis

Infectious Bovine keratoconjunctivitis (pink eye)
- cause Moraxella bovis
- worldwide contagious disease
- gram negative coccobacillis
- often transmitted by flies
- conjunctivitis - keratitis - corneal ulceration - suppurative - keratomalacia

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20
Q

Define the pathology of a Keratomalacia and Descemetocoele ?

A

Corneal ulcers
Corneal necrosis: epithelial +/- stromal loss
- injuries which occur to rapidly for cutaneous metaplasia to occur
- rappid desiccation, traumatic injuries, chemicals, infections (Feline herpes virus-1, Morexalla bovis in cattle)
- focal corneal stromal oedema
- stains with fluorescein stains

Keratomalacia
Stromal necrosis “contaminated ulcer” neurophils
- melting ulcer

Descemetocoele
Deep loss of stroma down to the descements membrane
- bulges anteriorly into the defect
- won’t take up stain

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21
Q

Identify and describe this pathology ?

A

Corneal sequestrum
Necrosis of the corneal stroma

  • this often occurs after chronic corneal ulceration
  • cats (especially in flat faced breeds)
  • characteristic corneal dark brown, leathery pigment
  • pigment in tears caused by an infiltrate of dead stromal tissue
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22
Q

What is corneal Sclerosis

A

Corneal Sclerosis
Age related change
The centre of the lens becomes denser with age
- imparts a blue grey appearance
- visual impairment not generally noted

The lens
- biconvex disc made up of transparent lens fibres and held in place by the zonular ligaments.
(limited response to injury)

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23
Q

Describe the pathology of a cataract ?

A

Cataracts

A change in the opacity of the lens
There are numerous causes
- hereditary
- senile
- diabetes
- inflamation (uveitis)

Approximately 50% of untreated dogs with diabetes mellitus will get cataracts within 6 months
(lens may rupture if the swelling is very rapid)

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24
Q

Describe the pathology of lens laxation ?

A

Lens laxation

Anterior luxation
- lens falls forward into the anterior chamber
- more serious
- predisposes to glaucoma
Posterior luxation
- falls backward into the vitreous chamber

Primary
inhereditied predispositin esp young terrior dogs
Secondary
trauma, glaucoma,uveitis, neoplasm

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25
What is uveitis and what is its causes and microscopic manifestations ?
Uveitis Inflammation of the uvea The uvea is made of the iris , ciliary body and choroid Causes of uveitis - infectious viral, fungal or bacterial disease - trauma - immune mediated eg uveodermatologic syndrome - idiopathic Macroscopic manifestations - iris swelling and colour change, hyperemia, oedema and inflammation - Hypopyon; neutrophils and fibrin settle in the anterior chamber - Conjunctival reddening; hyperemia
26
Describe the consequences of uveitis ?
27
Identify this pathology ?
28
Describe the pathology of a primary and secondary glycoma ?
Glycoma Is a sustained increase in intraocular pressure - causes ocular pain - detrimental to the retina, optic nerve - atrophy - blindness - several causes which are all due to the inability to remove of aqueous humor - mydriasis, corneal odema, conjunctival swelling, blindness and globe enlargement. Primary glycoma - developmental defect in aqueous drainage pathways (iridocorneal angle) - pure breed dogs are more predisposed Secondary glycoma - synechia - intraocular neoplasm - lens luxation - inflammation uveitis / trauma
29
Describe the consequences of glycoma ?
30
Define retinal atrophy, retinitis and retinal detachment ?
Disorders of the retina Retinal atrophy - inheretid disease eg canine progressive retinal atrophy - may be secondary to conditions such as glycoma Retinitis - usually an extension of uveitis or haematogenous infection Retinal detachment - seen with many ocular disease - collie eye anomalie CEA (inheritied) - uveitis - neoplasia
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Answer = D
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Corneal sequestion
33
Protrusion of the third eye lid and unilateral miosis reduced size of the pupil
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39
Describe the 7 possible pathogenic mechanisms of endocrine disease ?
Mechanisms of endocrine disease 1. Hypofunction of endocrine organ (primary, secondary). 2. Hyperfunction of endocrine organ (primary, secondary) 3. Hypersecretion of hormone by a non endocrine neoplasm 4. Failure of target cell response 5. Hyperactivity due to disease of other organs 6. Abnormal degradation of hormone 7. Latrogenic (medical treatment)
40
# hj Define primary and secondary hyperfunction of an endocrine organ ?
Hypofunction Primary hypofunction Reduced secretion of hormone - Destruction of endocrine cells eg neoplasia, immune mediated - Failure of endocrine cells to develop (eg pituitary dwarfism) - Defect in hormone synthesis Secondary hypofunction Reduced secretion of tropic hormones - causes a reduced function of the target endocrine cells - - secondary reduced secretion of hormone - eg non functional pituitary tumour - reduced ACTH - atrophy of adrenal cortex and reduced secretion of cortisol
41
Define primary and secondary hyperfunction of an endocrine organ ?
Primary hyperfunction Excessive synthesis and secretion of a hormone - eg adrenal adenoma or carcinoma Secondary Hyperfunction Increased secretion of trophic hormone - secondary excessive secretion of endocrine hormone - eg Functional pituitary tumor secreting ACTH > excess cortisol from adrenals
42
Describe the anatomy of the pituitary gland ?
The pituitary gland Adenohypophysis (anterior pituitary) - pars distalis, pars tuberalis and pars intermedia -prolactin, gonadotropins, TSH, ACTH, GH, MSH and endorphins Neurohypophysis (posterior pituitary) - oxytocin - ADH vasopressin
43
Describe the pathology behind hypopituitarism causing prolonged gestation and aplasia ?
Aplasia and prolonged gestation Hypopituitarism Hypoplastic endocrine organs - incomplete or underdevelopment of the pituitary gland - genetic predisposition in Guernseys and Jersey cows - lacks pituitary tropic hormone secretion during third trimester - hypoplasia of target organs (adrenal cortex, thyroid follicular cells.) - lack of cortisol prolongs gestation Potential secondary cause Ewes eating Corn lily = malformed CNS
44
Identify this pathological cyst and its pathology ?
Pituitary cyst Hypopituitarism = panhypopituitarism A lack of growth hormone secretion Failure of ectoderm of the rathkes pouch to develop into functioning endocrine cells This results in = dwarfism - Recessive gene common in German Shepherd dogs - Appear normal upto 8 weeks of age - slow growth - retention of puppy coat - bilateral progressive alopecia and skin hyperpigmentation - diagnose via a growth hormone assay
45
Describe the pathogenesis of of a non-secreting neoplasia in the anterior pituitary and the clinical signs ?
Non secreting neoplasm of the anterior pituitary Non-function adenoma, Craniopharyngiomas, pituitary gland carcinoma Pathology Compression of adjacent pituitary and brain tissue - reduces function - reduced hormone production Clinical signs - panhypopituitarism - diabetes insipidus - CNS disturbances - Blindness through compression of the optic nerve
46
Describe the pathology and clinical signs of a pars intermedia adenoma ?
Pars intermedia adenoma Hyperpituitary - secreting neoplasm (farely rare in most species Horses Many symptoms are due to hypothalamus compression (inactive) and deranged homeostatic regulation. Elevated cortisol and ACTH - PU/PD diabetes insipidus - polyphagia - muscle weakness - Hirsutism - Hyperglycaemia Dogs May be inactive (hypopituitarism and diabetes insipidus) or secrete excessive amounts of ACTH (Cushings syndrome)
47
Identify this pathology in a horse ?
Functional pituitary adenoma in the horse. Resulting in hypersecretion from the anterior pituitary.
48
Describe the pathology underlying Cushings in a dog ?
Hyperpituitarism = Adenohypophysis / anterior ACTH secreting tumour of the anterior pituitary. ACTH secreting adenomas - Corticotroph secreting cells; as well as pars intermedia - older dogs usually - Adrenal glands secrete excess cortisol > hyperadrenocorticism
49
Describe the pathology underlying Diabetes insipidus ?
Diabetes insipidus Pathology two forms May result from disorders of the neurohypophysis, hypopituitary Reduced secretion of ADH/ vasopressin (may also occur in a nephrogenic form, target kidney cells do not respond to ADH/vasopressin). Clinical signs PU/PD Large volumes of dilute urine Pathology
50
Describe the three layers of the adrenal cortexand medulla, and what hormones are produced ?
Adrenal anatomy Adrenal cortex 1. Zona glomerulosa = mineralocorticoids (aldosterone). 2. Zona fasciculata = glucocorticoids (cortisol) 3. 3. Zona reticularis = sex hormones (progesterone, oestrogen and androgens). Adrenal medulla Catecholamines (Noradrenalaine)
51
Describe the common primary and secondary causes of Addison's disease ?
Addison's disease (adrenal insufficiency; hypoadrenacorticism) Primary causes 1. Adrenalitis (inflammation) 2. Haemorrhage (Waterhouse-Friderichsen syndrome) 3. Idiopathic atrophy - young dogs Secondary causes 1. Pituitary disease 2. 2. Exogenous glucocorticoids (negative feedback)
52
Identify this lesion and describe its pathology ?
Adrenocortical atrophy (addison's) Adrenal insufficiency Idiopathic atrophy - usually immune mediated - young adult dogs - all layers of the cortex are affected DDX pituitary lesions that reduce ACTH - atrophy of the zona fasciculata and reticularis only.
53
Identify this lesion and describe its pathology ?
Adrenalitis Clinical signs - loss of zones within the cortex of the adrenal gland - inflammatory cells - eosinophilic inclusion bodies Pathology Inflammation of the adrenal gland causes adrenal insufficiency and Addison's disease - various bacteria, viral and parasitic pathogens.
54
Identify this lesion and describe its pathology ?
Adrenocortical haemorrhage = Waterhouse Friderichsen syndrome Pathology Uncommon but fatal consequences of sepsis, endotoxic shock and trauma
55
Desribe the pathophysiology and clinical signs of Hypoadrenocorticism ?
Hypoadrenocortism; Addison's disease Pathophysiology and clinical signs The common presentation - Collapsed in hypovolamic shock - often following a period of stress This occurs due to deficiencies in 1. Mineralocorticoids (aldosterone) 2. Glucocorticoids (cortisol) 3. Sex steroids Mineralocorticoid deficiency results in - Inability to excrete potassium, and retain Na (stay K; see ya later Na). - hyperkalaemia (high potassium in blood stream) > brachycardia and muscle weakness - Hypoatremia (abnormally low sodium in blood) and hypochloraemia > fluid loss and dehydration Glucocorticoid (cortisol) deficiency - Inability to respond to stress - Reduced glucogenesis - Increased insulin sensitivity - Hypoglycaemia (low blood glucose) - lethargy, vomiting and diarrhoea
56
Describe the primary and secondary causes of Hyperadrenocorticism ?
Hyperadrenocorticism / Cushing's disease (excessive secretion of glucocorticoids, cortisol). Primary causes 1. Nodular hyperplasia 2. Adrenal gland neoplasia; Cortical adenoma, Cortical carcinoma Secondary causes 1. Pituitary functional adenoma or hyperplasia 2. Iatrogenic (corticosteroid administration)
57
58
Identify this lesion of the adrenal gland and describe its pathology ?
Nodular adrenal cortical hyperplasia (Cushings = hyperadrenocorticism) Nodular hyperplasia - old daogs, cats and horses
59
Identify this lesion and describe its pathology ?
Adrenocortical Adenoma (hyperadrenocorticism; Cushings disease) Cortical adenoma - potential increased secretion of cortisol - old dogs, ferrets and occasionally other species - well demarcated with a fibrous capsule, may be functional (Cushings).
60
Identify this lesion and describe its pathology ?
Adrenocortical carcinoma and contralateral cortical atrophy. Pathology - old dogs, ferrets, cattle and occasionally other species - invasive to surrounding tissue - may be functional eg Cushing's excessive cortisol synthesis
61
What are the clinical signs of Cushing's ?
Cushing's Excessive cortisol production Clinical signs - Pot-belly - Obesity - Muscle weakness - Skin atrophy - Alopecia - Rat's tail - Calcinosis cutis - Infections - Poor healing - PU/PD - Polphagia (excessive eating)
62
Describe the pathophysiology of Cushing's disease ?
Cushing's disease - excessive secretion of cortisol Most common endocrine disorder of older dogs Insidious, progressive disease. Most clinical signs are due to altered CHO, protein and lipid metabolism. Hepatomegally (glycogen storage) = pot belly Lipolysis Thoracic and abdominal obesity - pot belly Protein catabolism - muscle wastage Anti inflammatory and immunosupressive = lymphocyte lysis Reduced fibroplasia = delayed wound healing.
63
Identify this lesion of the adrenal medulla and its potential consequences ?
Adrenal medulla hyperplasia - diffuse or nodular - Chromaffin cells proliferate (may preceed the formation of a paheochromocytoma. Excessive catecholamines = tachycardia, cardiac hypertrophy, oedema.
64
Identify this lesion and describe its pathology ?
Phaeochromocytoma Most common neoplasm of the medulla - cattle and dogs - may secrete catecholomines = tachycardia, cardiac hypertrophy and oedema - may become malignant
65
Describe the anatomy of the thyroid gland and what hormone each cell type produces ?
**Thyroid and parathyroid gland ** ** Thyroid gland** Thyroid follicular cells - thyroid hormones T3 and T4 - determines the metabolic rate **Thyroid parafollicular cells (C)** - Calcitonin - calcium and phosphate balance - reduction of serum calcium **Parathyroid gland** - Parathyroid hormone (PTH) - calcium and phosphate balance - Parathyroid chief cells act to increase serum calcium
66
Describe how calcium balance is maintained by the thyroid and parathyroid gland ?
Thyroid and parathyroid gland (calcium balance) Too musch serum calcium The parafolicular / C cells of the thyroid gland release calcitonin to reduce serum calcium. Too litle serum calcium Parathyroid gland Chief cells release Parathyroid hormone (PTH) to increase serum calcium.
67
Describe the many physiological affects of the thyroid hormones T3 and T4 ?
Physiological effects of the thyroid gland. (regulation of metabolic rate) Glucose - glycolysis - glucogenesis - increase intestinal uptake of glucose Lipids - regulate lipid metabolism - conversion of cholesterol to bile - regulate lipoprotein lipase - increase sensitivity of adipose tissue to lipolysis Protein - Regulate protein systhesis
68
Describe the common causes of Hypothyroidism ?
The common causes of hyperthyroidism Causes are usually primary - Idiopathic follicular atrophy - immune mediated (lymphocytic) thyroiditis Less common causes - neoplasia - iodine deficient gitre - pituitary lesions - hypothalamic lesions **The consequences of a hypoactive thyroid gland** Reduced production of thyroid hormones (T3 and T4) - reduced metabolic rate > reduced lipolysis, glycogenesis (less glucose available for energy).
69
Identify this lesion of the thyroid gland and describe its pathology ?
Idiopathic follicular atrophy (Small thyroid glands) results in hypothyroidism - progressive loss of follicular cells and replacement with adipose tissue. - (Picture on the left - thyroid gland reduced so much in size it is now the equivalent of the parathyroid gland). - arrises spontaneously and the cause remains unknown
70
identify this lesion of the thyroid gland and describe its pathology ?
Immune mediated Thyroiditis (results in hypothyroidism) Immune mediated thyroiditis - thyroglobulin autoantibodies in 48% of dogs - possible a inherited disorder of dogs - lymphocytes, plasma cells and macrophages infiltrate.
71
Describe the clinical signs of a hypoactive thyroid gland ?
Hypothyroidism the clinical signs - lethargy - weight gain or abeseity (not always with increased appetite) - Skin disease - dry skin, hyperpigmentation, hyperkeratosis - hair loss (trunk and tail) - Myxoedema (increased glycosaminoglycans (GAGS) and hyaluronic acid bind water in the skin) - cold intolerance - bradycardia - reduced reproductive function - behavioural changes - mild non regenerative anaemia - hypercholesterolaemia
72
Describe the potential causes which may result in Hyperthyroidism ?
Hyperthyroidism This condition is more common in cats - middle to older cats - From a range of proliferative lesions - multinodular hyperplasia - adenomas Rare in dogs - Thyroid neoplasia (adenomas and carcinomas of follicular and C cells) The physiological effects of increased circulating T3 and T4 - increased basal metabolic rate - increased heart rate and cardiac output - increased gluconeogenesis and glycolysis - increased muscle (protein) catabolism
73
Identify this lesion of the thyroid gland and describe its pathology ?
Multinodular hyperplasia (Potential cause of a hyperactive thyroid gland) This causes an increased stimulation of TSH signaling pathways throigh Ig - elevated T3 and T4 disturbs calcium homeostasis (down Ca and up P) - concomitant chief cell hyperplasia and increased PTH secretion Changes observed - decreased size of colloid - increased cell numbers
74
Describe the signs of a hyperactive thyroid gland ?
Hyperactive thyroid gland Clinical signs Old, skinny hungry cats - weight loss - polyphagia - PUPD - nervousness, excitability, aggression - muscle weakness - heat intolerance - vomiting / diarrhoea - poor unkempt hair coat - Tachycardia - Dyspnoea (pulmonary oedema).
75
Identify this lesion and discuss its pathology ?
Goitre (Thyroid hyperplasia and hypertrophy) Goitre is a non neoplastic, non inflammatory enlargement of the thyroid gland. There are many possible causes of Goitre - iodine deficient diets - excess iodine in the diet - goitrogenic compounds - genetic defects in thyroid hormone synthesis The consequences of Goitre Suboptimal production of thyroid hormones (hypothyroidism) - decreased circulating T3 and T4 - hypothalamus stimulates pituitary to increase TSH - hyperplasia of follicular cells
76
Describe the various types of Goitre ?
Types of Goitre 1. Diffuse hyperplastic Goitre - Dietary iodine deficiency 2. Colloid Goitre - involutionary phase of hyperplastic goitre (after replacing iodine in diet) 3. Multifocal nodular hyperplasia - unencapsulated, hyperplastic nodules with variable amounts of colloid 4. Dyshormongenetic Goitre (pictured below). - recessive gene; sheep, cattle and goats - inadequate thyroglobulin synthesis
77
Describe the pathology of follicular cell neoplasia in the Thyroid gland ?
Follicular cell neoplasia Adenomas - small white to tan solid nodules with a fibrous capsule - more common in cats and often functional = hyperthyroidism. Carcinomas - rapid growth, invasive compression of trachea
78
Describe the types of neoplasm of C cells in the thyroid and there effect ?
Parafollicular cell neoplasm Adenoma small, discrete grey to tan nodules with a capsule Carcinomas Extensive multinodular enlargement - depicted below; thyroid and cervical lymph nodes in a Holstein bull.
79
Describe the potential endocrine affects of adipose tissue ?
Adipose tissue is endocrine tissue Leptin = Appetite suppression, heat generation and pro-inflammatory Adiponectin = Enhances glucose uptake and metabolism, anti inflammatory
80
Identify this lesion ?
Parathyroid cyst (developmental) common in dogs; remanant of the embryonic duct.
81
Describe the pathology of Hypoparathyroidism ?
Hypoparathyroidism Inadequte secretion of PTH or ineffective action on target cells The potential cause - common in small dogs terriers - lymphocytic parathyroiditis - neoplasia - chronic hypercalcaemia Pathophysiology Reduced PTH > reduced bone resorption > reduced blood calcium
82
What are the clinical signs of Hypoparathyroidism ?
Hypoparathyroidism Clinical signs Muscle excitability tremors tetany anxiety seizures
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Describe the pathology behine primary hyperparathyroidism ?
Primary hyperthyroidism Functional chief cell neoplasms - adenomas more common than carcinomas - often secrete increased amounts of PTH
84
Describe the pathology and clinical signs of hyperparathyroidism ?
Hyperparathyroidism Pathology Secrete increased amounts of PTH - increases bone resorption - bone replaced by fibrous tissue - fibrous osteodystrophy (maxilla, mandible and long bones) - increased blood calcium Clinical signs - Lameness due to fractures - motor and/or sensory nerve dysfunction - facial hyperostosis (thickening of bone) - losse teeth - vomiting, constipation - anorexia - PU/PD - Muscle weakness
85
Describe the secondary disorders of hyperparathyroidism ?
Secondary disorders of hyperparathyroidism (more common) 1. Nutritional imbalance - low calcium - excess phosphorous in the diet - chief cell hyperplasia and hypertrophy - grain heavy diets - poor roughage - Fibrous osteodystrophy; hyperostotic maxilla and mandibles (big head) 2. Renal disease - chronic renal failure - fibrous osteodystropy; Osteoporotic maxilla and mandible "rubber jaw"
86
Identify this lesion and describe its pathology ?
Secondary renal hyperparathyroidism
87
Describe the pathology of hyperparathyroidism ?
Pseudo- hyperparathyroidism Humeral hypercalcaemia Secrete PTH like protein - results in atrophy of the parathyroid gland and C cell hyperplasia. The cause neoplasms - lymphosarcoma - apocrine gland adenocarcinoma (anal gland) - metastases of solid neoplasms to bone
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Describe the clinical signs of Pseudo-hyperparathyroidism ?
Pseudo-hyperparathyroidism Humeral hypercalcaemia of malignancy Secretes PTH like protein Clinical signs are due to calcification - PU/PD - anorexia - constipation - weakness - shivering - twitching - vomiting - stiff gait
89
Describe the pathology and clinical signs underlying peri-parturient hypocalcaemia ?
Peri-parturient hypocalcaemia Pathology - high producing dairy cows - high calcium diet prior to partuition increases risk - calcium decreases PTH secretion - minimal bone resorption - interupted calcium supply - combined with increased calcium output due to calving via lactation profound hypocalcaemia Symptoms muscle paresis, fatal if not treated
90
Describe the pathology and clinical signs underlying post-parturient hypocalcaemia ?
91
What hormones are produced by the pancreas ?
Disorder of pancreatic Islet Cells Hypofunction Diabetes mellitus - insufficient insulin Hyperfunctions Insulinomas - B (insulin secreting) islet cell neoplasms Gastrinomas - Non B (gastrin secreting) islet cell neoplasms
92
Describe the pathology behind diabetes ?
Pancreatic Hypofunction - Diabetes Mellitus Causes - chronic relapsing pancreatitis - idiopathic atrophy of the pancreas; young dogs (islet cell aplasia or hypoplasia) - immune mediated damage to B islet cells - deposition of amyloid in cats Pathology - mostly mature dogs - female dogs twice as often as males
93
Describe type one and type two Diabetes mellitus ?
94
Describe the pathophysiology and clinical signs of diabetes mellitus ?
Hypofunction - Diabetes Mellitus Glucose - glucosuria, hyperglycaemia Protein - negative nitrogen balance Lipids - metabolic acidosis Clinical signs PU/PD - weight loss - Weakness and depression, confusion - Bilateral cataracts - Hepatomegaly - Chronic renal disease, blindness - Recurrent infections